Cancer Research and Treatment

Original Articles

The Profile of Gut Microbiota in Carcinogenesis Driven by Mutant EGFR in Non-Small Cell Lung Cancer: Da-Som Kim, Eun Hye Kim, Ji Yong Kim, Dong Ha Kim, Yun Jung Choi, Jaeyi Jeong, Young Hoon Sung, Dong-Cheol Woo, Chong Jai Kim, Jae Cheol Lee, Miyong Yun, Jin-Yong Jeong, Jin Kyung Rho; Received December 9, 2024 Accepted March 2, 2025 Published online March 4, 2025; DOI: https://doi.org/10.4143/crt.2024.1177 [Accepted]

Abstract PDF: Purpose
Accumulating evidence has clarified that gut dysbiosis is involved in lung cancer development and progression. Although the relationship between tumors and gut microbiota has been extensively studied using clinical samples, no studies have examined the association between mutant EGFR-induced lung carcinogenesis and dysbiosis in gut microbiota. Therefore, we investigated the gut microbiota profiles in stool samples from human lung-specific conditional EGFR-mutant transgenic mice during lung tumor carcinogenesis.
Materials and Methods
Stool samples were collected before tamoxifen treatment (V1) and at each time point following mutant EGFR expression in lung tissue (V2) and lung tumor appearance (V3). Fecal 16S rRNA taxonomy was analyzed to assess microbial diversity, composition, and dynamic changes at each time point.
Results
We found that microbiota richness and diversity were significantly elevated when tumors developed and grew in the lung. Phylogenetic analysis of the microbial community revealed that Lachnospiraceae, Ruminococcaceae, Porphyromonadaceae, Rhodospirillaceae, Odoribacteraceae, and Desulfovibrionaceae showed a significant increase at the V3 stage compared to the V1 stage at the family level. In contrast, Lactobacillaceae, Bacteroidaceae, Muribaculaceae, Coriobacteriaceae, and Rikenellaceae significantly decreased at the V3 stage compared to the V1 stage. Furthermore, Lactobacillus species, also known as SCFA-producing bacteria, were relatively abundant at the V1 stage but were depleted with the occurrence of lung tumors at the V3 stage.
Conclusion
Changes in gut microbiota, such as Lactobacillus species, may be a predictive factor for the emergence and progression of tumors in an animal model of lung adenocarcinoma induced by mutant EGFR.

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Sex-specific Molecular Markers NRF2 and PD-L1 in Colon Carcinogenesis: Implications for Right-sided Colon Cancer: Chin-Hee Song, Yonghoon Choi, Nayoung Kim, Ryoung Hee Nam, Jin Won Kim, Jae Young Jang, Eun Hye Kim, Sungchan Ha, Ha-Na Lee; Received August 22, 2024 Accepted December 26, 2024 Published online December 27, 2024; DOI: https://doi.org/10.4143/crt.2024.818 [Accepted]

Abstract PDF: Purpose
This study examined the roles of nuclear factor erythroid 2-related factor 2 (NRF2) and programmed death ligand 1 (PD-L1) in colon carcinogenesis, underscoring on sex and differences in tumor location.
Materials and Methods
A total of 378 participants were enrolled from Seoul National University Bundang Hospital: 88 healthy controls (HC), 139 patients with colorectal adenoma (AD), and 151 patients with colorectal cancer (CRC). Quantitative real-time polymerase chain reaction (PCR), methylation-specific PCR, and immunohistochemistry (IHC) were performed utilizing tumor samples from patients and normal mucosa in the HC group.
Results
NRF2 mRNA expression was higher in the CRC group than in the HC and AD groups, with decreased NRF2 methylation in the AD and CRC groups. NRF2 protein expression, as evaluated by IHC, increased in the AD and CRC groups relative to that in the HC group. PD-L1 protein expression was remarkably higher in the CRC group than in the HC and AD groups. These patterns were consistent in both males and females. In sex- and CRC location-specific analyses, NRF2 methylation was lower in female than in male patients with CRC. NRF2 protein expression was significantly higher in females, particularly in patients with right-sided CRC. Moreover, females exhibited increased PD-L1 mRNA expression compared to males in the AD group, and PD-L1 mRNA levels were higher in females with right-sided CRC than in those with cancer at other locations.
Conclusion
Differences in NRF2 and PD-L1 expression indicate site-specific colon carcinogenesis based on sex, particularly in females with right-sided CRC.

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Genitourinary cancer

Clear Cell Adenocarcinoma of Urethra: Clinical and Pathologic Implications and Characterization of Molecular Aberrations: Boram Song, Seok Hyun Lee, Jeong Hwan Park, Kyung Chul Moon; Cancer Res Treat. 2024;56(1):280-293. Published online September 11, 2023; DOI: https://doi.org/10.4143/crt.2023.577

Abstract PDF Supplementary Material PubReader ePub

Purpose
This study aimed to evaluate the molecular features of clear cell adenocarcinoma (CCA) of the urinary tract and investigate its pathogenic pathways and possible actionable targets.
Materials and Methods
We retrospectively collected the data of patients with CCA between January 1999 and December 2016; the data were independently reviewed by two pathologists. We selected five cases of urinary CCA, based on the clinicopathological features. We analyzed these five cases by whole exome sequencing (WES) and subsequent bioinformatics analyses to determine the mutational spectrum and possible pathogenic pathways.
Results
All patients were female with a median age of 62 years. All tumors were located in the urethra and showed aggressive behavior with disease progression. WES revealed several genetic alterations, including driver gene mutations (AMER1, ARID1A, CHD4, KMT2D, KRAS, PBRM1, and PIK3R1) and mutations in other important genes with tumor-suppressive and oncogenic roles (CSMD3, KEAP1, SMARCA4, and CACNA1D). We suggest putative pathogenic pathways (chromatin remodeling pathway, mitogen-activated protein kinase signaling pathway, phosphoinositide 3-kinase/AKT/mammalian target of rapamycin pathway, and Wnt/β-catenin pathway) as candidates for targeted therapies.
Conclusion
Our findings shed light on the molecular background of this extremely rare tumor with poor prognosis and can help improve treatment options.

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Urethral clear cell adenocarcinoma in an adult female: A rare case report
Yacob Sheiferawe Seman, Michael Teklehaimanot Abera, Fadil Nuredin Abrar, Tesfaye Kebede Legesse, Mesfin Asefa Tola, Tsiyon Nigusie Alemu
Urology Case Reports.2025; 58: 102882. CrossRef
Two rare cases of primary clear cell adenocarcinoma of the urethra: clinical experience, case report and literature review
Bohao Jiang, Jiyuan Hu, Benqiao Wang, Xujia Liu, Ling Tong, Yitong Xu, Hao Zhang
Frontiers in Oncology.2025;[Epub] CrossRef
Association between CACNA1D polymorphisms and hypospadias in a southern Chinese population
Ye He, Binyao Li, Xinying Zhao, Lingling Pan, Yanqing Liu, Chaoting Lan, Fuming Deng, Wen Fu, Yan Zhang, Xiaoyu Zuo
Journal of Pediatric Urology.2024; 20(3): 438.e1. CrossRef
The L‐type calcium channel CaV1.3: A potential target for cancer therapy
Xuerun Liu, Boqiang Shen, Jingyi Zhou, Juan Hao, Jianliu Wang
Journal of Cellular and Molecular Medicine.2024;[Epub] CrossRef

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Breast cancer

Short-term Impact of Hormone Replacement Therapy on Risk of Breast Cancer in BRCA Mutation Carriers: A Nationwide Study in South Korea: Hye Yeon Kim, Jisoo Park, Seok Joo Moon, Sohyeon Jeong, Jin Hwa Hong, Jae Kwan Lee, Geum Joon Cho, Hyun-Woong Cho; Cancer Res Treat. 2024;56(1):143-148. Published online August 16, 2023; DOI: https://doi.org/10.4143/crt.2023.653

Abstract PDF PubReader ePub

Purpose
BRCA1/2 mutations are well-known risk factors for breast and ovarian cancers in women. Risk-reducing salpingo-oophorectomy (RRSO) is the standard treatment for preventing ovarian cancer with BRCA mutations. Postmenopausal syndrome (symptoms after RRSO can be alleviated by hormone replacement therapy (HRT); however, the use of HRT in carriers of BRCA mutations has been controversial because of the concern that HRT increases the risk of breast cancer. This study aimed to evaluate the effects of HRT in BRCA mutation carriers who underwent RRSO.
Materials and Methods
A total of 151 carriers, who underwent RRSO between 2013 and 2020 after the diagnosis of BRCA1 or BRCA2 mutations were selected and followed up for a median of 3.03 years. Patients were divided into two groups: those who received HRT after RRSO (n=33) and those who did not (n=118). We compared the incidence of breast cancer over time between these two groups.
Results
There was no significant difference in the incidence of breast cancer between women who received HRT and those who did not (p=0.229). Multivariate logistic regression analysis, adjusted for age and parity revealed no significant difference in the risk of breast cancer between these two groups (hazard ratio, 0.312; 95% confidence interval, 0.039 to 2.480; p=0.278).
Conclusion
In this study, we found no relationship between post-RRSO HRT and breast cancer in the population with BRCA mutations. Therefore, healthcare providers may consider the alleviation of symptoms of postmenopausal syndrome through HRT in patients who underwent RRSO.

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A contemporary review of breast cancer risk factors and the role of artificial intelligence
Orietta Nicolis, Denisse De Los Angeles, Carla Taramasco
Frontiers in Oncology.2024;[Epub] CrossRef

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Clinical Significance of Major Angiogenesis-Related Effectors in Patients with Metastatic Breast Cancer Treated with Trastuzumab-Based Regimens: Helen P. Kourea, Foteinos-Ioannis Dimitrakopoulos, Georgia-Angeliki Koliou, Anna Batistatou, Kyriaki Papadopoulou, Mattheos Bobos, Anthoula Asimaki-Vlachopoulou, Sofia Chrisafi, Kitty Pavlakis, Kyriakos Chatzopoulos, Eleni Galani, George Pentheroudakis, Dimitrios Pectasides, Dimitrios Bafaloukos, Eleni Res, Pavlos Papakostas, Angelos Koutras, Vassiliki Kotoula, George Fountzilas; Cancer Res Treat. 2022;54(4):1053-1064. Published online November 17, 2021; DOI: https://doi.org/10.4143/crt.2021.748

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Purpose
Angiogenesis is a crucial phenomenon in the development and progression of breast cancer (BC), but the clinical significance of angiogenesis-related proteins in metastatic BC remains unknown. This study investigates the prognostic value of vascular endothelial growth factor receptors 1, 2, 3 (VEGFR1, VEGFR2, VEGFR3) as well as vascular endothelial growth factors A and C (VEGFA and VEGFC) in metastatic BC patients treated with trastuzumab-based regimens.
Materials and Methods
Two hundred female patients were included. Protein and mRNA expression of the studied angiogenesis-related factors were evaluated by immunohistochemistry and quantitative polymerase chain reaction, respectively.
Results
High expression of VEGFA, VEGFC, VEGFR1, VEGFR2, and VEGFR3 in the tumor cells was observed in 43.5%, 24.2%, 36%, 29.5%, and 43%, respectively. Stromal elements expressed high levels of VEGFA, VEGFC, VEGFR1, VEGFR2, and VEGFR3 in 78.9%, 93.3%, 90.7%, 90.2%, and 74.8% of tumors with available data. High tumor cell expression of VEGFR1 was a favorable prognosticator for survival among patients with human epidermal growth factor receptor 2 (HER2)–positive tumors (hazard ratio [HR], 0.55; p=0.013). A trend towards longer progression-free survival was detected univariately for patients with HER2-negative tumors and high expression of VEGFR2 (HR, 0.60; p=0.059).
Conclusion
VEGFR1 and VEGFR2 seem to have significant prognostic value in BC patients with metastatic disease treated with trastuzumab-based regimens.

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Apatinib beyond first progression is associated with prolonged overall survival in patients with advanced breast cancer: Results from an observational study
Jing Wang, Jinghao Jia, Jingjing Liu, Xuemin Yao, Zhiyong Yuan
Experimental and Therapeutic Medicine.2024;[Epub] CrossRef

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Pediatric cancer

The Broad Variability in Dental Age Observed among Childhood Survivors Is Cancer Specific: Patrycja Proc, Joanna Szczepańska, Małgorzata Zubowska, Beata Zalewska-Szewczyk, Wojciech Młynarski; Cancer Res Treat. 2021;53(1):252-260. Published online August 24, 2020; DOI: https://doi.org/10.4143/crt.2020.275

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Purpose
The study aimed to assess the differences in dental maturation between childhood cancer survivors and healthy children.
Materials and Methods
Fifty-nine cancer patients including 16 (27.1%) girls and 43 (72.8%) boys, aged between 4 and 16 years, underwent dental and radiographic examinations. The mean duration of anticancer therapy was 16.8 months (range, 1 to 47 months), and 4.6 years (range, 8 to 123 months) had passed since the termination of disease. The control group consisted of 177 panoramic radiographs of age- and sex-matched healthy individuals. Dental age (DA) was estimated with Demirjian’s scale and delta age, i.e., DA–chronological age (CA), was used to compare groups.
Results
The DA of cancer survivors was accelerated by almost 1 year compared to their CA (9.9±3.1 vs. 8.9±2.8, p=0.040). The greatest difference was observed among patients with brain tumor: delta (DA–CA) was 2.2±1.1 years. Among all cancer patients, only children with familial adenomatous polyposis (FAP)-associated hepatoblastoma (HP) demonstrated delayed DA, with regard to both other cancer survivors (p=0.011) and healthy patients (p=0.037). All four patients with HP suffered from FAP, and three of them had documented adenomatous polyposis coli (APC) genes mutation. The DA of cancer patients having teeth with short roots was significantly greater than that of the cancer survivors without this anomaly (12.8±3.2 vs. 9.0±2.4, p < 0.001).
Conclusion
DA in children may be altered by cancer disease.

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Dental management of long-term childhood cancer survivors: a systematic review
K. Seremidi, S. Gizani, G. Dahllöf, M. Barr-Agholme, D. Kloukos, G. Tsilingaridis
European Archives of Paediatric Dentistry.2024; 25(5): 611. CrossRef
Dental age estimation in children that have undergone antineoplastic treatment
A. Mitsea, K. Seremidi, A. Tsiligianni, S. Gizani
European Archives of Paediatric Dentistry.2022; 23(2): 243. CrossRef
Comparative Study of Malocclusions between Cancer Patients and Healthy Peers
Patrycja Proc, Joanna Szczepanska, Anna Herud, Malgorzata Zubowska, Wojciech Fendler, Monika Lukomska-Szymanska, Wojciech Mlynarski
International Journal of Environmental Research and Public Health.2022; 19(7): 4045. CrossRef

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A Radiosensitivity Gene Signature and PD-L1 Status Predict Clinical Outcome of Patients with Glioblastoma Multiforme in The Cancer Genome Atlas Dataset: Bum-Sup Jang, In Ah Kim; Cancer Res Treat. 2020;52(2):530-542. Published online November 20, 2019; DOI: https://doi.org/10.4143/crt.2019.440

Abstract PDF Supplementary Material PubReader ePub

Purpose
Combination of radiotherapy and immune checkpoint blockade such as programmed death- 1 (PD-1) or programmed death-ligand 1 (PD-L1) blockade is being actively tested in clinical trial. We aimed to identify a subset of patients that could potentially benefit from this strategy using The Cancer Genome Atlas (TCGA) dataset for glioblastoma (GBM).
Materials and Methods
A total of 399 cases were clustered into radiosensitive versus radioresistant (RR) groups based on a radiosensitivity gene signature and were also stratified as PD-L1 high versus PD-L1 low groups by expression of CD274 mRNA. Differential and integrated analyses with expression and methylation data were performed. CIBERSORT was used to enumerate the immune repertoire that resulted from transcriptome profiles.
Results
We identified a subset of GBM, PD-L1-high-RR group which showed worse survival compared to others. In PD-L1-high-RR, differentially expressed genes (DEG) were highly enriched for immune response and mapped into activation of phosphoinositide 3-kinase–AKT and mitogen-activated protein kinase (MAPK) signaling pathways. Integration of DEG and differentially methylated region identified that the kinase MAP3K8-involved in T-cell receptor signaling was upregulated and BAI1, a factor which inhibits angiogenesis, was silenced. CIBERSORT showed that a higher infiltration of the immune repertoire, which included M2 macrophages and regulatory T cells.
Conclusion
Taken together, PD-L1-high-RR group could potentially benefit from radiotherapy combined with PD-1/PD-L1 blockade and angiogenesis inhibition.

Citations

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Clinical Biomarkers of Tumour Radiosensitivity and Predicting Benefit from Radiotherapy: A Systematic Review
Christopher W. Bleaney, Hebatalla Abdelaal, Mark Reardon, Carmel Anandadas, Peter Hoskin, Ananya Choudhury, Laura Forker
Cancers.2024; 16(10): 1942. CrossRef
A retrospective cohort study of neoadjuvant chemoradiotherapy combined with immune checkpoint inhibitors in locally advanced rectal cancer
Zhuo Chen, Zhuoling Zou, Min Qian, Qin Xu, Guojuan Xue, Juan Yang, Tinglan Luo, Lianjie Hu, Bin Wang
Translational Oncology.2024; 44: 101955. CrossRef
Understanding the immunosuppressive microenvironment of glioma: mechanistic insights and clinical perspectives
Hao Lin, Chaxian Liu, Ankang Hu, Duanwu Zhang, Hui Yang, Ying Mao
Journal of Hematology & Oncology.2024;[Epub] CrossRef
PSF-lncRNA interaction as a target for novel targeted anticancer therapies
Ren Liu, Xiaojing Wang, Min Zhou, Jingfang Zhai, Jie Sun
Biomedicine & Pharmacotherapy.2024; 180: 117491. CrossRef
Bladder Cancer Treatments in the Age of Personalized Medicine: A Comprehensive Review of Potential Radiosensitivity Biomarkers
Charbel Feghaly, Rafka Challita, Hanine Bou Hadir, Tala Mobayed, Tarek Al Bitar, Mohammad Harbi, Hala Ghorayeb, Rana El-Hassan, Larry Bodgi
Biomarker Insights.2024;[Epub] CrossRef
Improving the efficacy of combined radiotherapy and immunotherapy: focusing on the effects of radiosensitivity
Zhiru Gao, Qian Zhao, Yiyue Xu, Linlin Wang
Radiation Oncology.2023;[Epub] CrossRef
In Vivo Evaluation of Near-Infrared Fluorescent Probe for TIM3 Targeting in Mouse Glioma
Michael Zhang, Quan Zhou, Chinghsin Huang, Carmel T. Chan, Wei Wu, Gordon Li, Michael Lim, Sanjiv S. Gambhir, Heike E. Daldrup-Link
Molecular Imaging and Biology.2022; 24(2): 280. CrossRef
Relationship between Macrophage and Radiosensitivity in Human Primary and Recurrent Glioblastoma: In Silico Analysis with Publicly Available Datasets
Bum-Sup Jang, In Ah Kim
Biomedicines.2022; 10(2): 292. CrossRef
Optimal management of recurrent and metastatic upper tract urothelial carcinoma: Implications of intensity modulated radiation therapy
Mi Sun Kim, Woong Sub Koom, Jae Ho Cho, Se-Young Kim, Ik Jae Lee
Radiation Oncology.2022;[Epub] CrossRef
Translational landscape of glioblastoma immunotherapy for physicians: guiding clinical practice with basic scientific evidence
Daniel Kreatsoulas, Chelsea Bolyard, Bill X. Wu, Hakan Cam, Pierre Giglio, Zihai Li
Journal of Hematology & Oncology.2022;[Epub] CrossRef
The Next Frontier in Health Disparities—A Closer Look at Exploring Sex Differences in Glioma Data and Omics Analysis, from Bench to Bedside and Back
Maria Diaz Rosario, Harpreet Kaur, Erdal Tasci, Uma Shankavaram, Mary Sproull, Ying Zhuge, Kevin Camphausen, Andra Krauze
Biomolecules.2022; 12(9): 1203. CrossRef
Immunosuppression in Gliomas via PD-1/PD-L1 Axis and Adenosine Pathway
Thamiris Becker Scheffel, Nathália Grave, Pedro Vargas, Fernando Mendonça Diz, Liliana Rockenbach, Fernanda Bueno Morrone
Frontiers in Oncology.2021;[Epub] CrossRef
The Combination of Radiotherapy With Immunotherapy and Potential Predictive Biomarkers for Treatment of Non-Small Cell Lung Cancer Patients
Lu Meng, Jianfang Xu, Ying Ye, Yingying Wang, Shilan Luo, Xiaomei Gong
Frontiers in Immunology.2021;[Epub] CrossRef
Explore association of genes in PDL1/PD1 pathway to radiotherapy survival benefit based on interaction model strategy
Junjie Shen, Jingfang Liu, Huijun Li, Lu Bai, Zixuan Du, Ruirui Geng, Jianping Cao, Peng Sun, Zaixiang Tang
Radiation Oncology.2021;[Epub] CrossRef
Combination of Radiosensitivity Gene Signature and PD-L1 Status Predicts Clinical Outcome of Patients With Locally Advanced Head and Neck Squamous Cell Carcinoma: A Study Based on The Cancer Genome Atlas Dataset
Dongjun Dai, Yinglu Guo, Yongjie Shui, Jinfan Li, Biao Jiang, Qichun Wei
Frontiers in Molecular Biosciences.2021;[Epub] CrossRef
Prognostic Values of Radiosensitivity Genes and CD19 Status in Gastric Cancer: A Retrospective Study Using TCGA Database

Li-Bo Liang, Xin-Yan Huang, He He, Ji-Yan Liu
Pharmacogenomics and Personalized Medicine.2020; Volume 13: 365. CrossRef
Gene signature based on B cell predicts clinical outcome of radiotherapy and immunotherapy for patients with lung adenocarcinoma
Linzhi Han, Hongjie Shi, Yuan Luo, Wenjie Sun, Shuying Li, Nannan Zhang, Xueping Jiang, Yan Gong, Conghua Xie
Cancer Medicine.2020; 9(24): 9581. CrossRef

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Apatinib Combined with Local Irradiation Leads to Systemic Tumor Control via Reversal of Immunosuppressive Tumor Microenvironment in Lung Cancer: Li-jun Liang, Chen-xi Hu, Yi-xuan Wen, Xiao-wei Geng, Ting Chen, Guo-qing Gu, Lei Wang, You-you Xia, Yong Liu, Jia-yan Fei, Jie Dong, Feng-hua Zhao, Yiliyar Ahongjiang, Kai-yuan Hui, Xiao-dong Jiang; Cancer Res Treat. 2020;52(2):406-418. Published online September 3, 2019; DOI: https://doi.org/10.4143/crt.2019.296

Abstract PDF Supplementary Material PubReader ePub

Purpose
This study aimed to investigate the potential systemic antitumor effects of stereotactic ablative radiotherapy (SABR) and apatinib (a novel vascular endothelial growth factor receptor 2 inhibitor) via reversing the immunosuppressive tumor microenvironment for lung carcinoma.
Materials and Methods
Lewis lung cancer cells were injected into C57BL/6 mice in the left hindlimb (primary tumor; irradiated) and in the right flank (secondary tumor; nonirradiated). When both tumors grew to the touchable size, mice were randomly divided into eight treatment groups. These groups received normal saline or three distinct doses of apatinib (50 mg/kg, 150 mg/kg, and 200 mg/kg) daily for 7 days, in combination with a single dose of 15 Gy radiotherapy or not to the primary tumor. The further tumor growth/regression of mice were followed and observed.
Results
For the single 15 Gy modality, tumor growth delay could only be observed at the primary tumor. When combining SABR and apatinib 200 mg/kg, significant retardation of both primary and secondary tumor growth could be observed, indicated an abscopal effect was induced. Mechanism analysis suggested that programmed death-ligand 1 expression increased with SABR was counteract by additional apatinib therapy. Furthermore, when apatinib was combined with SABR, the composition of immune cells could be changed. More importantly, this two-pronged approach evoked tumor antigen–specific immune responses and the mice were resistant to another tumor rechallenge, finally, long-term survival was improved.
Conclusion
Our results suggested that the tumor microenvironment could be managed with apatinib, which was effective in eliciting an abscopal effect induced by SABR.

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Comparison of Efficacy and Safety of Different Second-line Therapies for Patients With Advanced Thymic Carcinoma
K. Shao, Y. Hao, M. Xu, Z. Shi, G. Lin, C. Xu, Y. Zhang, Z. Song
Clinical Oncology.2024; 36(11): 710. CrossRef
Immune effect and prognosis of transcatheter arterial chemoembolization and tyrosine kinase inhibitors therapy in patients with hepatocellular carcinoma
Yuan Guo, Ru-Chun Li, Wei-Li Xia, Xiong Yang, Wen-Bo Zhu, Fang-Ting Li, Hong-Tao Hu, Hai-Liang Li
World Journal of Gastrointestinal Oncology.2024; 16(7): 3256. CrossRef
A disintegrin and metalloproteinase domain 10 expression inhibition by the small molecules adenosine, cordycepin and N6, N6-dimethyladenosine and immune regulation in malignant cancers
Wenqian Zhang, Jiewen Fu, Jiaman Du, Xiaoyan Liu, Jingliang Cheng, Chunli Wei, Youhua Xu, Junjiang Fu
Frontiers in Immunology.2024;[Epub] CrossRef
Antiangiogenic Treatment Facilitates the Abscopal Effect of Radiation Therapy Combined With Anti-PD-1 in Hepatocellular Carcinoma
Hailong Sheng, Yongyi Luo, Liting Zhong, Zhiyi Wang, Zhichao Sun, Xinna Gao, Xinrong He, Zhenru Zhu, Dehua Wu, Jingyuan Sun, Chuanhui Cao
International Journal of Radiation Oncology*Biology*Physics.2024;[Epub] CrossRef
Low‐ dose Apatinib promotes vascular normalization and hypoxia reduction and sensitizes radiotherapy in lung cancer
Shanshan Jiang, Yue Zhou, Liqing Zou, Li Chu, Xiao Chu, Jianjiao Ni, Yida Li, Tiantian Guo, Xi Yang, Zhengfei Zhu
Cancer Medicine.2023; 12(4): 4434. CrossRef
Local Destruction of Tumors and Systemic Immune Effects
Karl-Göran Tranberg
Frontiers in Oncology.2021;[Epub] CrossRef
A novel role for apatinib in enhancing radiosensitivity in non-small cell lung cancer cells by suppressing the AKT and ERK pathways
Lin Li, Yuexian Li, Huawei Zou
PeerJ.2021; 9: e12356. CrossRef

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KIF11 Functions as an Oncogene and Is Associated with Poor Outcomes from Breast Cancer: Juan Zhou, Wei-Rong Chen, Li-Chao Yang, Jun Wang, Jia-Yuan Sun, Wen-Wen Zhang, Zhen-Yu He, San-Gang Wu; Cancer Res Treat. 2019;51(3):1207-1221. Published online December 27, 2018; DOI: https://doi.org/10.4143/crt.2018.460

Abstract PDF Supplementary Material PubReader ePub

Purpose
The study aimed to search and identify genes that were differentially expressed in breast cancer, and their roles in cancer growth and progression.
Materials and Methods
The Gene Expression Omnibus (Oncomine) and The Cancer Genome Atlas databases (https://cancergenome.nih.gov/) were screened for genes that were expressed differentially in breast cancer and were closely related to a poor prognosis. Gene expressions were verified by quantitative real-time polymerase chain reaction, and genes were knocked down by a lentivirus-based system. Cell growth and motility were evaluated and in vivo nude mice were used to confirm the in vitro roles of genes. Markers of epithelial-to-mesenchymal transition and the associations of KIF11 with the classical cancer signaling pathways were detected by Western blot.
Results
A series of genes expressed differentially in patients with breast cancer. The prognosis associated with high KIF11 expression was poor, and the expression of KIF11 increased significantly in high stage and malignant tumor cells. Inhibiting KIF11 expression in lentivirus-suppressed cells revealed that KIF11 inhibition significantly reduced cell viability and colony formation, inhibited migration and invasion, but promoted apoptosis. The sizes and weights of KIF11-inhibited tumors in nude mice were significantly lower than in the negative controls. Western blot showed that E-cadherin in breast cancer was significantly upregulated in KIF-inhibited cells and tumor tissues, whereas N-cadherin and vimentin were significantly downregulated. BT549 and MDA231 cells with KIF11 knockdown exhibited decreased ERK, AMPK, AKT, and CREB phosphorylation.
Conclusion
KIF11 acts as a potential oncogene that regulates the development and progression of breast cancer.

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HELLS Knockdown Inhibits the Malignant Progression of Lung Adenocarcinoma Via Blocking Akt/CREB Pathway by Downregulating KIF11
Gang Yang, Jinsong Fu, Jiawei Wang, Mei Ding
Molecular Biotechnology.2025; 67(2): 548. CrossRef
Identification of potential biomarkers for 2022 Mpox virus infection: a transcriptomic network analysis and machine learning approach
Joy Prokash Debnath, Kabir Hossen, Sabrina Bintay Sayed, Md. Sayeam Khandaker, Preonath Chondrow Dev, Saifuddin Sarker, Tanvir Hossain
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Lu Wang, Na Li, Yang Chen, Yehua Qiao, Yaolin Song, Xiangyan Zhang, Han Zhao, Wenwen Ran, Guangqi Li, Xiaoming Xing
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Biying Wang, Lunmin Bao, Xiaoduo Li, Guang Sun, Wu Yang, Nanzi Xie, Ling Lei, Wei Chen, Hailong Zhang, Man Chen, Xing Zhao, Xiufang Wan, Rui Yuan, Hongmei Jiang
Journal of Translational Medicine.2025;[Epub] CrossRef
Integrative analysis of T cell-mediated tumor killing-related genes reveals KIF11 as a novel therapeutic target in esophageal squamous cell carcinoma
Xinxin Cheng, Huihui Zhao, Zhangwang Li, Liping Yan, Qingjie Min, Qingnan Wu, Qimin Zhan
Journal of Translational Medicine.2025;[Epub] CrossRef
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Paulina Antosik, Justyna Durślewicz, Marta Smolińska-Świtała, Jonasz Podemski, Edyta Podemska, Izabela Neska-Długosz, Jakub Jóźwicki, Dariusz Grzanka
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The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside
Kai Zhao, Xiangyu Li, Yunxiang Feng, Jianming Wang, Wei Yao
Biomarker Research.2024;[Epub] CrossRef
Mitotic Functions and Characters of KIF11 in Cancers
Wanting Gao, Junjie Lu, Zitao Yang, Enmin Li, Yufei Cao, Lei Xie
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Kinesin 26B modulates M2 polarization of macrophage by activating cancer-associated fibroblasts to aggravate gastric cancer occurrence and metastasis
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World Journal of Gastroenterology.2024; 30(20): 2689. CrossRef
Di-(2-ethylhexyl) phthalate promotes benign prostatic hyperplasia through KIF11-Wnt/β-catenin signaling pathway
Pan Song, Dong Lv, Luchen Yang, Jing Zhou, Xin Yan, Zhenghuan Liu, Kai Ma, Yunfei Yu, Xiaoyang Liu, Qiang Dong
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Genetic Risk Score, Combined Lifestyle Factors and Risk of Colorectal Cancer: Young Ae Cho, Jeonghee Lee, Jae Hwan Oh, Hee Jin Chang, Dae Kyung Sohn, Aesun Shin, Jeongseon Kim; Cancer Res Treat. 2019;51(3):1033-1040. Published online October 18, 2018; DOI: https://doi.org/10.4143/crt.2018.447

Abstract PDF Supplementary Material PubReader ePub

Purpose
Both genetic and lifestyle factors contribute to the risk of colorectal cancer, but each individual factor has a limited effect. Therefore, we investigated the association between colorectal cancer and the combined effects of genetic factors or/and lifestyle risk factors.
Materials and Methods
In a case-control study of 632 colorectal cancer patients and 1,295 healthy controls, we quantified the genetic risk score for colorectal cancer using 13 polymorphisms. Furthermore, we determined a combined lifestyle risk score including obesity, physical activity, smoking, alcohol consumption, and dietary inflammatory index. The associations between colorectal cancer and risk score using these factors were examined using a logistic regression model.
Results
Higher genetic risk scores were associated with an increased risk of colorectal cancer (odds ratio [OR], 2.57; 95% confidence interval [CI], 1.89 to 3.49 for the highest tertile vs. lowest tertile). Among the modifiable factors, previous body mass index, physical inactivity, heavy alcohol consumption, and a high inflammatory diet were associated with an increased risk of colorectal cancer. A higher lifestyle risk score was associated with an increased risk of colorectal cancer (OR, 5.82; 95% CI, 4.02 to 8.44 for the highest tertile vs. lowest tertile). This association was similar in each genetic risk category.
Conclusion
Adherence to a healthy lifestyle is associated with a substantially reduced risk of colorectal cancer regardless of individuals’ genetic risk.

Citations

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Clinical and Genetic Characteristics of BRCA1/2 Mutation in Korean Ovarian Cancer Patients: A Multicenter Study and Literature Review: Byung Su Kwon, Jung Mi Byun, Hyun Joo Lee, Dae Hoon Jeong, Tae Hwa Lee, Kyung-Hwa Shin, Dong Soo Suh, Ki Hyung Kim; Cancer Res Treat. 2019;51(3):941-950. Published online October 8, 2018; DOI: https://doi.org/10.4143/crt.2018.312

Abstract PDF Supplementary Material PubReader ePub

Purpose
We investigated the clinical relevance and spectrum of BRCA1/2 mutations in Korean ovarian cancer (KoOC) patients.
Materials and Methods
Two hundred seventy-nine KoOC patients were enrolled from three university hospitals between 2012 and 2017. Their peripheral blood samples were obtained for BRCA1/2 mutation analysis by direct sequencing. Clinicopathological characteristics were retrospectively reviewed, and spectrum analyses of BRCA1/2 mutation were assessed by systematic literature review.
Results
Frequency of BRCA1/2 mutations was 16.5% in KoOC patients. BRCA1/2 mutations were significantly associated with family history of breast/ovarian cancer (p<0.001), serous histology (p=0.044), and advanced International Federation of Gynecology and Obstetrics (FIGO) stage (III/IV, p=0.018) but not with early age-of-onset (age < 50, p=0.729). Literature review of BRCA1/2 mutations in KoOC patients found 111 (55 distinct) mutations with high proportion of Korean-specific mutations (24/55, 43.6%). Comparing the spectrum of BRCA1/2 mutation between KoOC and Korean breast cancer (KoBC) patients, the ratio of BRCA1-to-BRCA2 mutations was different, with BRCA1 (78.4%) being predominant in KoOC and BRCA2 in KoBC (59.2%). The most common mutation also differed between the two (c.3627insA of BRCA1 in KoOC and c.7480C>T of BRCA2 in KoBC).
Conclusion
The clinical relevance of BRCA1/2 mutations in KoOC patients was confirmed but that of early age-of-onset was not. Possible inconsistency in the ratio of BRCA1-to-BRCA2 mutations and the most common mutation between KoOC and KoBC may probably suggest presence of mutation sequence-associated penetrance tendency in hereditary Korean breast and ovarian cancer. These data may provide insights for optimal genetic counseling and prophylactic treatment for at-risk relatives of KoOC patients.

Citations

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Exploring the effect of BRCA1/2 status on chemotherapy-induced hematologic toxicity in patients with ovarian cancer
In Hee Lee, Soo Jung Lee, Juhyung Kim, Yoon Hee Lee, Gun Oh Chong, Jong Mi Kim, Juhun Lee, Nan Young Lee, Seo Young Park, Dea Gy Hong, Yee Soo Chae
Cancer Chemotherapy and Pharmacology.2024; 94(1): 103. CrossRef
Utility of Next-Generation Sequencing Panel Including Hereditary Breast and Ovarian Cancer-Related Genes for Pathogenic Variant Detection
Jae Hee Lee, Do-Hoon Kim
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Basic knowledge for counseling patients undergoing risk-reducing salpingo-oophorectomy
Jihye Kim, Chel Hun Choi
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Prevalence of BRCA1 and BRCA2 mutations in ovarian cancer patients from Yunnan Province in southwest China
Yongmei Peng, Jiaqian Liao, Xian He, Yongchun Zhou, Lei Zhang, Yue Jia, Hongying Yang
European Journal of Cancer Prevention.2024;[Epub] CrossRef
Validation of multi-gene panel next-generation sequencing for the detection of BRCA mutation in formalin-fixed, paraffin-embedded epithelial ovarian cancer tissues
Eun Taeg Kim, Ha Eun Jeong, Hyung Joon Yoon, Ki Hyung Kim, Dong Soo Suh
Taiwanese Journal of Obstetrics and Gynecology.2023; 62(1): 66. CrossRef
Using species richness calculations to model the global profile of unsampled pathogenic variants: Examples from BRCA1 and BRCA2
Nandana D. Rao, Brian H. Shirts, Alvaro Galli
PLOS ONE.2023; 18(2): e0278010. CrossRef
Mutational Analysis of BRCA1 and BRCA2 Genes in Breast Cancer Patients from Eastern Sicily
Stefania Stella, Silvia Rita Vitale, Federica Martorana, Michele Massimino, Giuliana Pavone, Katia Lanzafame, Sebastiano Bianca, Chiara Barone, Cristina Gorgone, Marco Fichera, Livia Manzella
Cancer Management and Research.2022; Volume 14: 1341. CrossRef
How to start niraparib in real-world Asian ovarian cancer patients?
Sook-Hee Hong
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Identification of BRCA1:c.5470_5477del as a Founder Mutation in Chinese Ovarian Cancer Patients
Jun Li, Sile Han, Cuiyun Zhang, Yanlin Luo, Li Wang, Ping Wang, Yi Wang, Qingxin Xia, Xiaoyan Wang, Bing Wei, Jie Ma, Hongle Li, Yongjun Guo
Frontiers in Oncology.2021;[Epub] CrossRef
Prevalence and clinical characterization of BRCA1 and BRCA2 mutations in Korean patients with epithelial ovarian cancer
E Sun Paik, Eun Jin Heo, Chel Hun Choi, Jae‐Hoon Kim, Jae‐Weon Kim, Yong‐Man Kim, Sang‐Yoon Park, Jeong‐Won Lee, Jong‐Won Kim, Byoung‐Gie Kim
Cancer Science.2021; 112(12): 5055. CrossRef
Impact of proactive high-throughput functional assay data on BRCA1 variant interpretation in 3684 patients with breast or ovarian cancer
Hyun-Ki Kim, Eun Jin Lee, Young-Jae Lee, Jisun Kim, Yongsub Kim, Kyunggon Kim, Shin-Wha Lee, Suhwan Chang, Young Joo Lee, Jong Won Lee, Woochang Lee, Sail Chun, Byung Ho Son, Kyung Hae Jung, Yong-Man Kim, Won-Ki Min, Sei-Hyun Ahn
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Clinical and histopathologic analysis of gynecological cancer: a single institute experience over 7 years
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Yeungnam University Journal of Medicine.2020; 37(3): 179. CrossRef

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Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL: Chunhui Cui, Duanyang Zhai, Lianxu Cai, Qiaobin Duan, Lang Xie, Jinlong Yu; Cancer Res Treat. 2018;50(3):992-1008. Published online October 30, 2017; DOI: https://doi.org/10.4143/crt.2017.226

Abstract PDF PubReader ePub

Purpose
Studies have found that long noncoding RNA HEIH (lncRNA-HEIH) is upregulated and facilitates hepatocellular carcinoma tumor growth. However, its clinical significances, roles, and action mechanism in colorectal cancer (CRC) remains unidentified.
Materials and Methods
lncRNA-HEIH expression in CRC tissues and cell lines was measured by quantitative real-time polymerase chain reaction. Cell CountingKit-8, ethynyl deoxyuridine incorporation assay, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and nude mice xenografts assays were performed to investigate the roles of lncRNA-HEIH. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays were performed to investigate the action mechanisms of lncRNA-HEIH.
Results
In this study, we found that lncRNA-HEIH is significantly increased in CRC tissues and cell lines. lncRNA-HEIH expression is positively associated with tumor size, invasion depth, and poor prognosis of CRC patients. Enhanced expression of lncRNA-HEIH promotes CRC cell proliferation and decreases apoptosis in vitro, and promotes CRC tumor growth in vivo. Whereas knockdown of lncRNA-HEIH inhibits CRC cell proliferation and induces apoptosis in vitro, and suppresses CRC tumor growth in vivo. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor κB (NF-κB), increases the binding of NF-κB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL. Moreover, Bcl-xL expression is positively associatedwith lncRNA-HEIH in CRC tissues. Blocking the interaction between lncRNA-HEIH and miR-939 abolishes the effects of lncRNA-HEIH on CRC tumorigenesis.
Conclusion
This study demonstrated that lncRNA-HEIH promotes CRC tumorigenesis through counteracting miR-939‒mediated transcriptional repression of Bcl-xL, and suggested that lncRNA-HEIH may serve as a prognostic biomarker and therapeutic target for CRC.

Citations

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Clinical Risk Factors Influencing Dental Developmental Disturbances in Childhood Cancer Survivors: Chung-Min Kang, Seung Min Hahn, Hyo Sun Kim, Chuhl Joo Lyu, Jae-Ho Lee, Jinae Lee, Jung Woo Han; Cancer Res Treat. 2018;50(3):926-935. Published online October 10, 2017; DOI: https://doi.org/10.4143/crt.2017.296

Abstract PDF Supplementary Material PubReader ePub

Purpose
Although studies regarding dental developmental disturbances after childhood cancer treatment have increased, they have many limitations. Studies analyzing the significance of independent clinical risk factors with regard to the dental health status are also rare. We aimed to investigate the risk factors for dental developmental disturbances, particularly severe disturbances, in childhood cancer survivors (CCS).
Materials and Methods
Oral examinations and retrospective reviews of medical and panoramic radiographs were performed for 196 CCS (mean age, 15.6 years). Cancer type, age at diagnosis, treatment modality, type and accumulated dose of administered drugs, and dose and site of radiation were recorded. Dental developmental disturbances were diagnosed using panoramic radiographs and graded for severity according to the Modified Dental Defect Index (MDDI). Descriptive statistics and multivariate analyseswere performed to determine the association between dental abnormalities and clinical factors.
Results
In total, 109 CCS (55.6%) exhibited at least one dental anomaly, and the median value of MDDI was 2.5. Microdontia (30.6%) was the most prevalent anomaly, followed by tooth agenesis (20.4%), V-shaped roots (14.8%), and taurodontism (10.2%). Multivariate analysis revealed that a young age at diagnosis (≤ 3 years), a history of hematopoietic stem cell transplantation, the use of multiple classes of chemotherapeutic agents (≥ 4 classes), and the use of heavy metal agents were significant risk factors for severe dental disturbances.
Conclusion
CCS with any of the above risk factors for severe developmental disturbances should be comprehensively followed up to minimize adverse consequences to their dental development and preserve their future dental health.

Citations

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Comparison of Ion Personal Genome Machine Platforms for the Detection of Variants in BRCA1 and BRCA2: Sang Mee Hwang, Ki Chan Lee, Min Seob Lee, Kyoung Un Park; Cancer Res Treat. 2018;50(1):255-264. Published online April 7, 2017; DOI: https://doi.org/10.4143/crt.2017.062

Abstract PDF Supplementary Material PubReader ePub

Purpose
Transition to next generation sequencing (NGS) for BRCA1/BRCA2 analysis in clinical laboratories is ongoing but different platforms and/or data analysis pipelines give different results resulting in difficulties in implementation. We have evaluated the Ion Personal Genome Machine (PGM) Platforms (Ion PGM, Ion PGM Dx, Thermo Fisher Scientific) for the analysis of BRCA1/2.
Materials and Methods
The results of Ion PGM with OTG-snpcaller, a pipeline based on Torrent mapping alignment program and Genome Analysis Toolkit, from 75 clinical samples and 14 reference DNA samples were compared with Sanger sequencing for BRCA1/BRCA2. Ten clinical samples and 14 reference DNA samples were additionally sequenced by Ion PGM Dx with Torrent Suite.
Results
Fifty types of variants including 18 pathogenic or variants of unknown significance were identified from 75 clinical samples and known variants of the reference samples were confirmed by Sanger sequencing and/or NGS. One false-negative results were present for Ion PGM/OTG-snpcaller for an indel variant misidentified as a single nucleotide variant. However, eight discordant results were present for Ion PGM Dx/Torrent Suite with both falsepositive and -negative results. A 40-bp deletion, a 4-bp deletion and a 1-bp deletion variant was not called and a false-positive deletion was identified. Four other variants were misidentified as another variant.
Conclusion
Ion PGM/OTG-snpcaller showed acceptable performance with good concordance with Sanger sequencing. However, Ion PGM Dx/Torrent Suite showed many discrepant results not suitable for use in a clinical laboratory, requiring further optimization of the data analysis for calling variants.

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Review Article

Anti-angiogenic Therapy in Patients with Advanced Gastric and Gastroesophageal Junction Cancer: A Systematic Review: Li-Tzong Chen, Do-Youn Oh, Min-Hee Ryu, Kun-Huei Yeh, Winnie Yeo, Roberto Carlesi, Rebecca Cheng, Jongseok Kim, Mauro Orlando, Yoon-Koo Kang; Cancer Res Treat. 2017;49(4):851-868. Published online January 3, 2017; DOI: https://doi.org/10.4143/crt.2016.176

Abstract PDF Supplementary Material PubReader ePub

Despite advancements in therapy for advanced gastric and gastroesophageal junction cancers, their prognosis remains dismal. Tumor angiogenesis plays a key role in cancer growth and metastasis, and recent studies indicate that pharmacologic blockade of angiogenesis is a promising approach to therapy. In this systematic review, we summarize current literature on the clinical benefit of anti-angiogenic agents in advanced gastric cancer. We conducted a systematic search of PubMed and conference proceedings including the American Society of Clinical Oncology, the European Society for Medical Oncology, and the European Cancer Congress. Included studies aimed to prospectively evaluate the efficacy and safety of anti-angiogenic agents in advanced gastric or gastroesophageal junction cancer. Each trial investigated at least one of the following endpoints: overall survival, progression-free survival/time to progression, and/or objective response rate. Our search yielded 139 publications. Forty-two met the predefined inclusion criteria. Included studies reported outcomes with apatinib, axitinib, bevacizumab, orantinib, pazopanib, ramucirumab, regorafenib, sorafenib, sunitinib, telatinib, and vandetanib. Second-line therapy with ramucirumab and third-line therapy with apatinib are the only anti-angiogenic agents so far shown to significantly improve survival of patients with advanced gastric cancer. Overall, agents that specifically target the vascular endothelial growth factor ligand or receptor have better safety profile compared to multi-target tyrosine kinase inhibitors.

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Original Articles

Underexpression of HOXA11 Is Associated with Treatment Resistance and Poor Prognosis in Glioblastoma: Young-Bem Se, Seung Hyun Kim, Ji Young Kim, Ja Eun Kim, Yun-Sik Dho, Jin Wook Kim, Yong Hwy Kim, Hyun Goo Woo, Se-Hyuk Kim, Shin-Hyuk Kang, Hak Jae Kim, Tae Min Kim, Soon-Tae Lee, Seung Hong Choi, Sung-Hye Park, Il Han Kim, Dong Gyu Kim, Chul-Kee Park; Cancer Res Treat. 2017;49(2):387-398. Published online July 19, 2016; DOI: https://doi.org/10.4143/crt.2016.106

Abstract PDF Supplementary Material PubReader ePub

Purpose
Homeobox (HOX) genes are essential developmental regulators that should normally be in the silenced state in an adult brain. The aberrant expression of HOX genes has been associated with the prognosis of many cancer types, including glioblastoma (GBM). This study examined the identity and role of HOX genes affecting GBM prognosis and treatment resistance.
Materials and Methods
The full series of HOX genes of five pairs of initial and recurrent human GBM samples were screened by microarray analysis to determine the most plausible candidate responsible for GBM prognosis. Another 20 newly diagnosed GBM samples were used for prognostic validation. In vitro experiments were performed to confirm the role of HOX in treatment resistance. Mediators involved in HOX gene regulation were searched using differentially expressed gene analysis, gene set enrichment tests, and network analysis.
Results
The underexpression of HOXA11 was identified as a consistent signature for a poor prognosis among the HOX genes. The overall survival of the GBM patients indicated a significantly favorable prognosis in patients with high HOXA11 expression (31±15.3 months) compared to the prognoses in thosewith lowHOXA11 expression (18±7.3 months, p=0.03). When HOXA11 was suppressed in the GBM cell lines, the anticancer effect of radiotherapy and/or temozolomide declined. In addition, five candidate mediators (TGFBR2, CRIM1, TXNIP, DPYSL2, and CRMP1) that may confer an oncologic effect after HOXA11 suppression were identified.
Conclusion
The treatment resistance induced by the underexpression of HOXA11 can contribute to a poor prognosis in GBM. Further investigation will be needed to confirm the value of HOXA11 as a potential target for overcoming the treatment resistance by developing chemo- or radiosensitizers.

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Jinyun Li, Meng Ye, Chongchang Zhou
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Methylation in HOX Clusters and Its Applications in Cancer Therapy
Ana Paço, Simone Aparecida de Bessa Garcia, Renata Freitas
Cells.2020; 9(7): 1613. CrossRef
N6-Methylandenosine-Related lncRNAs Are Potential Biomarkers for Predicting the Overall Survival of Lower-Grade Glioma Patients
Zewei Tu, Lei Wu, Peng Wang, Qing Hu, Chuming Tao, Kuangxun Li, Kai Huang, Xingen Zhu
Frontiers in Cell and Developmental Biology.2020;[Epub] CrossRef
Targeting HOX/PBX dimer formation as a potential therapeutic option in esophageal squamous cell carcinoma
Lu‐Yan Shen, Ting Zhou, Ya‐Bing Du, Qi Shi, Ke‐Neng Chen
Cancer Science.2019; 110(5): 1735. CrossRef
An inverse interaction betweenHOXA11andHOXA11-ASis associated with cisplatin resistance in lung adenocarcinoma
Youwei Zhang, Yuan Yuan, Yang Li, Peiying Zhang, Pingsheng Chen, Sanyuan Sun
Epigenetics.2019; 14(10): 949. CrossRef
Long noncoding RNA HOXA11-AS promotes gastric cancer cell proliferation and invasion via SRSF1 and functions as a biomarker in gastric cancer
Yun Liu, Yu-Mei Zhang, Feng-Bo Ma, Su-Rong Pan, Bao-Zhen Liu
World Journal of Gastroenterology.2019; 25(22): 2763. CrossRef
DNA methylation changes following DNA damage in prostate cancer cells
Laura P. Sutton, Sarah A. Jeffreys, Jessica L. Phillips, Phillippa C. Taberlay, Adele F. Holloway, Mark Ambrose, Ji-Hoon E. Joo, Arabella Young, Rachael Berry, Marketa Skala, Kate H. Brettingham-Moore
Epigenetics.2019; 14(10): 989. CrossRef
MicroRNA‐128/homeobox B8 axis regulates ovarian cancer cell progression
Rui Li, Lingling Gong, Pin Li, Jing Wang, Liangliang Bi
Basic & Clinical Pharmacology & Toxicology.2019; 125(6): 499. CrossRef
Evaluation of the HOXA11 level in patients with lung squamous cancer and insights into potential molecular pathways via bioinformatics analysis
Rui Zhang, Tong-tong Zhang, Gao-qiang Zhai, Xian-yu Guo, Yuan Qin, Ting-qing Gan, Yu Zhang, Gang Chen, Wei-jia Mo, Zhen-bo Feng
World Journal of Surgical Oncology.2018;[Epub] CrossRef
HOXA11 antisense long noncoding RNA (HOXA11‐AS): A promising lncRNA in human cancers
Cheng‐Wei Lu, Dan‐Dan Zhou, Tian Xie, Ji‐Long Hao, Om Prakash Pant, Cheng‐Bo Lu, Xiu‐Fen Liu
Cancer Medicine.2018; 7(8): 3792. CrossRef
Identification of radiation responsive genes and transcriptome profiling via complete RNA sequencing in a stable radioresistant U87 glioblastoma model
Ninh B. Doan, Ha S. Nguyen, Hisham S. Alhajala, Basem Jaber, Mona M. Al-Gizawiy, Eun-Young Erin Ahn, Wade M. Mueller, Christopher R. Chitambar, Shama P. Mirza, Kathleen M. Schmainda
Oncotarget.2018; 9(34): 23532. CrossRef
Upregulation of HOXA11 during the progression of lung adenocarcinoma detected via multiple approaches
Xia Yang, Yun Deng, Rong‑Quan He, Xiao‑Jiao Li, Jie Ma, Gang Chen, Xiao‑Hua Hu
International Journal of Molecular Medicine.2018;[Epub] CrossRef
Clinical Significance and Effect of lncRNA HOXA11-AS in NSCLC: A Study Based on Bioinformatics, In Vitro and in Vivo Verification
Yu Zhang, Wen-jie Chen, Ting-qing Gan, Xiu-ling Zhang, Zu-cheng Xie, Zhi-hua Ye, Yun Deng, Ze-feng Wang, Kai-teng Cai, Shi-kang Li, Dian-zhong Luo, Gang Chen
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Functional analysis of HOXA10 and HOXB4 in human medulloblastoma cell lines
Ricardo Bonfim-Silva, Fernanda Ursoli Ferreira Melo, Carolina Hassibe Thomé, Kuruvilla Joseph Abraham, Fábio Augusto Labre De Souza, Fernando Silva Ramalho, Hélio Rubens Machado, Ricardo Santos De Oliveira, Angelo A. Cardoso, Dimas Tadeu Covas, Aparecida
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Long non-coding RNA HOXA11-AS promotes cell proliferation and metastasis in human breast cancer
Jian-Chun Su, Xue-Feng Hu
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Identification of skin-related lncRNAs as potential biomarkers that are involved in Wnt pathways in keloids
Xiao-Jie Sun, Qiang Wang, Baofeng Guo, Xian-Ying Liu, Bing Wang
Oncotarget.2017; 8(21): 34236. CrossRef
Microarray-based analysis and clinical validation identify ubiquitin-conjugating enzyme E2E1 (UBE2E1) as a prognostic factor in acute myeloid leukemia
Hongmei Luo, Yu Qin, Frederic Reu, Sujuan Ye, Yang Dai, Jingcao Huang, Fangfang Wang, Dan Zhang, Ling Pan, Huanling Zhu, Yu Wu, Ting Niu, Zhijian Xiao, Yuhuan Zheng, Ting Liu
Journal of Hematology & Oncology.2016;[Epub] CrossRef

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Gastric Carcinogenesis in the miR-222/221 Transgenic Mouse Model: Boram Choi, Jieun Yu, Tae-Su Han, Young-Kook Kim, Keun Hur, Byeong-Cheol Kang, Woo-Ho Kim, Dae-Yong Kim, Hyuk-Joon Lee, V. Narry Kim, Han-Kwang Yang; Cancer Res Treat. 2017;49(1):150-160. Published online June 23, 2016; DOI: https://doi.org/10.4143/crt.2015.462

Abstract PDF Supplementary Material PubReader ePub

Purpose
MicroRNAs (miRNAs) regulate various cellular functions, including development, cell proliferation, apoptosis, and tumorigenesis. Different signatures associated with various tissue types, diagnosis, progression, prognosis, staging, and treatment response have been identified by miRNA expression profiling of human tumors. miRNAs function as oncogenes or as tumor suppressors. The relationship between gastric cancer and miRNA garnered attention due to the high incidence of gastric cancer in Asian countries. miR-222/221 expression increases in gastric tumor tissues. The oncogenic effect of miR-222/221 was previously determined in functional studies and xenograft models. In this study, transgenic mice overexpressing miR-222/221 were generated to confirm the effect of miR-222/221 on gastric carcinogenesis. Materials and Methods At 6 weeks of age, 65 transgenic mice and 53 wild-type mice were given drinking water containing N-nitroso-N-methylurea (MNU) for 5 alternating weeks to induce gastric cancer. The mice were euthanized at 36 weeks of age and histologic analysis was performed.
Results
Hyperplasia was observed in 3.77% of the wild-type mice and in 18.46% of the transgenic mice (p=0.020). Adenoma was observed in 20.75% of the wild-type mice and 26.15% of the transgenic mice (p=0.522). Carcinoma was observed in 32.08% of the wild-type mice and 41.54% of the transgenic mice (p=0.341). The frequency of hyperplasia, adenoma, and carcinoma was higher in transgenic mice, but the difference was statistically significant only in hyperplasia. Conclusion These results suggest that hyperplasia, a gastric pre-cancerous lesion, is associated with miR-222/221 expression but miR-222/221 expression does not affect tumorigenesis itself.

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The Mechanism of miR-222 Targets Matrix Metalloproteinase 1 in Regulating Fibroblast Proliferation in Hypertrophic Scars
Yi Zhang, Wei-Long Hong, Zhi-Ming Li, Qi-Yu Zhang, Kang Zeng
Aesthetic Plastic Surgery.2021; 45(2): 749. CrossRef
Fraser extracellular matrix complex subunit 1 promotes liver metastasis of gastric cancer
Shinichi Umeda, Mitsuro Kanda, Takashi Miwa, Haruyoshi Tanaka, Chie Tanaka, Daisuke Kobayashi, Masamichi Hayashi, Suguru Yamada, Goro Nakayama, Masahiko Koike, Yasuhiro Kodera
International Journal of Cancer.2020; 146(10): 2865. CrossRef
Aldehyde dehydrogenase 1, a target of miR‑222, is expressed at elevated levels in cervical cancer
Changde Liu, Yan Zhang, Shanghua Liang, Yuhua Ying
Experimental and Therapeutic Medicine.2020;[Epub] CrossRef
Expression and regulatory role of miRNA-222 in intervertebral disc degeneration (IDD)
Chen Ge, Changwei Li
Biotechnology & Biotechnological Equipment.2019; 33(1): 1553. CrossRef
MicroRNA-222 regulates the viability of fibroblasts in hypertrophic scars via matrix metalloproteinase 1
Yi Zhang, Xiaohua Lin, Li Zhang, Weilong Hong, Kang Zeng
Experimental and Therapeutic Medicine.2017;[Epub] CrossRef

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Use of a High-Throughput Genotyping Platform (OncoMap) for RAS Mutational Analysis to Predict Cetuximab Efficacy in Patients with Metastatic Colorectal Cancer: Dalyong Kim, Yong Sang Hong, Jeong Eun Kim, Kyu-pyo Kim, Jae-Lyun Lee, Sung-Min Chun, Jihun Kim, Se Jin Jang, Tae Won Kim; Cancer Res Treat. 2017;49(1):37-43. Published online April 27, 2016; DOI: https://doi.org/10.4143/crt.2016.069

Abstract PDF PubReader ePub

Purpose
Cetuximab demonstrates improved efficacy outcomes in patients with metastatic colorectal cancer (mCRC) harboring wild-type KRAS exon 2. Resistance to cetuximab is mediated by activating less frequent mutations in the RAS genes beyond KRAS exon 2. We performed extended RASmutational analysis using a high -throughput genotyping platform (OncoMap) and evaluated extended RAS analysis for predicting cetuximab efficacy in patients harboring wild-type KRAS exon 2 tumors following Sanger sequencing.
Materials and Methods
Extended RAS analysis was performed on 227 wild-type KRAS exon 2 mCRC patients who received cetuximab as salvage treatment using OncoMap ver. 4.0. Targeted genes included exon 2, exon 3, and exon 4, both in KRAS and NRAS, and included BRAF exon 15. We assessed efficacy by the new RAS mutation status.
Results
The OncoMap detected 57 additional mutations (25.1%): 25 (11%) in KRAS exon 2 and 32 (14.1%) beyond KRAS exon 2. Survival differences were observed after dividing patients into the wild-type RAS group (n=170) and mutant RAS group (n=57) using OncoMap. Progression-free survival was 4.8 months versus 1.8 months (hazard ratio [HR], 0.44; 95% confidence interval [CI], 0.32 to 0.61), and overall survival was 11.9 months versus 8.4 months (HR, 0.65; 95% CI, 0.47 to 0.88).
Conclusion
Sanger sequencing is not sufficient for selecting candidates for cetuximab treatment. High-throughput extended RAS genotyping is a feasible approach for this purpose and identifies patients who might benefit from cetuximab treatment.

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Metastatik Kolorektal Kanserli Hastaların RAS Mutasyon Durumuna Göre Klinik ve Patolojik Özellikleri
Mehmet SEZEN, Murat ARAZ
Uludağ Üniversitesi Tıp Fakültesi Dergisi.2019; 45(2): 131. CrossRef
Pan-Asian adapted ESMO consensus guidelines for the management of patients with metastatic colorectal cancer: a JSMO–ESMO initiative endorsed by CSCO, KACO, MOS, SSO and TOS
T. Yoshino, D. Arnold, H. Taniguchi, G. Pentheroudakis, K. Yamazaki, R.-H. Xu, T.W. Kim, F. Ismail, I.B. Tan, K.-H. Yeh, A. Grothey, S. Zhang, J.B. Ahn, M.Y. Mastura, D. Chong, L.-T. Chen, S. Kopetz, T. Eguchi-Nakajima, H. Ebi, A. Ohtsu, A. Cervantes, K.
Annals of Oncology.2018; 29(1): 44. CrossRef
Ligand-Independent Epidermal Growth Factor Receptor Overexpression Correlates with Poor Prognosis in Colorectal Cancer
Sumi Yun, Yoonjin Kwak, Soo Kyung Nam, An Na Seo, Heung-Kwon Oh, Duck-Woo Kim, Sung-Bum Kang, Hye Seung Lee
Cancer Research and Treatment.2018; 50(4): 1351. CrossRef
Primary tumor location predicts poor clinical outcome with cetuximab in RAS wild-type metastatic colorectal cancer
Dalyong Kim, Sun Young Kim, Ji Sung Lee, Yong Sang Hong, Jeong Eun Kim, Kyu-pyo Kim, Jihun Kim, Se Jin Jang, Young-Kwang Yoon, Tae Won Kim
BMC Gastroenterology.2017;[Epub] CrossRef

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ZNF488 Enhances the Invasion and Tumorigenesis in Nasopharyngeal Carcinoma Via the Wnt Signaling Pathway Involving Epithelial Mesenchymal Transition: Dan Zong, Li Yin, Qian Zhong, Wen-jie Guo, Jian-hua Xu, Ning Jiang, Zhi-rui Lin, Man-zhi Li, Ping Han, Lin Xu, Xia He, Mu-sheng Zeng; Cancer Res Treat. 2016;48(1):334-344. Published online March 12, 2015; DOI: https://doi.org/10.4143/crt.2014.311

Abstract PDF PubReader ePub

Purpose
The purpose of this study was to investigate the function of Zinc finger protein 488 (ZNF488) in nasopharyngeal carcinoma (NPC). Materials and Methods The endogenous expression of ZNF488 in NPC tissues, normal nasopharyngeal epithelium tissues and NPC cell lines were detected by quantitative reverse transcription polymerase chain reaction. ZNF488 over-expressing and knock-down NPC cell line models were established through retroviral vector pMSCV mediated over-expression and small interfering RNA (siRNA) mediated knock-down. The invasion and migration capacities were evaluated by wound healing and transwell invasion assays in ZNF488 over-expressing and control cell lines. Soft-agar colony formation and a xenograft experiment were performed to study tumorigenic ability in vitro and in vivo. Immunofluorescence and western blotting analysis were used to examine protein changes followed by ZNF488 over-expression. Microarray analysis was performed to explore gene expression profilings, while luciferase reporter assay to evaluate the transcriptive activity of Tcf/Lef.
Results
ZNF488 was over-expressed in NPC tissues compared with normal tissues, especially higher in 5-8F and S18, which are well-established high metastatic NPC clones. Functional studies indicate that over-expression of ZNF488 provokes invasion, whereas knock-down of ZNF488 alleviates invasive capability. Moreover, over-expression of ZNF488 promotes NPC tumor growth both in vitro and in vivo. Our data further show that over-expression of ZNF488 induces epithelial mesenchymal transition (EMT) by activating the WNT/β-catenin signaling pathway. Conclusion Our data strongly suggest that ZNF488 acts as an oncogene, promoting invasion and tumorigenesis by activating the Wnt/β-catenin pathway to induce EMT in NPC.

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Integrating E-cadherin expression levels with TNM staging for enhanced prognostic prediction in colorectal cancer patients
Jae-Ghi Lee, Ilkyu Park, Hannah Lee, Seungyoon Nam, Jisup Kim, Won-Suk Lee, Myunghee Kang, Jung Ho Kim
BMC Cancer.2025;[Epub] CrossRef
Vitiligo non‐responding lesions to narrow band UVB have intriguing cellular and molecular abnormalities that may prevent epidermal repigmentation
Nathaniel B. Goldstein, Andrea Steel, Landon Tomb, Zachary Berk, Junxiao Hu, Velmurugan Balaya, Laura Hoaglin, Kavya Ganuthula, Meet Patel, Erica Mbika, William A. Robinson, Dennis R. Roop, David A. Norris, Stanca A. Birlea
Pigment Cell & Melanoma Research.2024; 37(3): 378. CrossRef
Zinc finger protein 468 up-regulation of TFAM contributes to the malignant growth and cisplatin resistance of breast cancer cells
Zhaoyang Jia, Feng Wang, Gongzhuo Li, Ping Jiang, Yuanxiu Leng, Longzhu Ke, Li Luo, Wei Gao
Cell Division.2024;[Epub] CrossRef
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Caiyan Yin, Jianwei Yu, Gaohua Liu, Jun He, Peng Wu
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NEK2 promotes esophageal squamous cell carcinoma cell proliferation, migration and invasion through the Wnt/β-catenin signaling pathway
Dong Guo, Weinan Yao, Xingyu Du, Jing Dong, Xueyuan Zhang, Wenbin Shen, Shuchai Zhu
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Overexpression of ZNF488 supports pancreatic cancer cell proliferation and tumorigenesis through inhibition of ferroptosis via regulating SCD1-mediated unsaturated fatty acid metabolism
Qifeng Xiao, Zhongmin Lan, Shuisheng Zhang, Hu Ren, Shunda Wang, Peng Wang, Lin Feng, Dan Li, Chengfeng Wang, Xiaofeng Bai, Jianwei Zhang
Biology Direct.2023;[Epub] CrossRef
ZNF488 Promotes the Invasion and Migration of Pancreatic Carcinoma Cells through the Akt/mTOR Pathway
Hongquan Qiu, Liang Zhang, Dongzhi Wang, Yu Zhang, Hongyu Cai, Haiyan Miao, Feihu Chu, Osamah Ibrahim Khalaf
Computational and Mathematical Methods in Medicine.2022; 2022: 1. CrossRef
Carbonic anhydrase IX stratifies patient prognosis and identifies nodal status in animal models of nasopharyngeal carcinoma using a targeted imaging strategy
Wenhui Huang, Kun Wang, Weiyuan Huang, Zicong He, Jingming Zhang, Bin Zhang, Zhiyuan Xiong, Kelly McCabe Gillen, Wenzhe Li, Feng Chen, Xing Yang, Shuixing Zhang, Jie Tian
European Journal of Nuclear Medicine and Molecular Imaging.2022; 49(13): 4427. CrossRef
Identification of novel biomarkers and small-molecule compounds for nasopharyngeal carcinoma with metastasis
Jing-Lin Mi, Meng Xu, Chang Liu, Ren-Sheng Wang
Medicine.2020; 99(32): e21505. CrossRef
Nucleolar and spindle associated protein 1 promotes metastasis of cervical carcinoma cells by activating Wnt/β-catenin signaling
Han Li, Weijing Zhang, Ming Yan, Jiaqi Qiu, Jueming Chen, Xiaoying Sun, Xiangfu Chen, Libing Song, Yanna Zhang
Journal of Experimental & Clinical Cancer Research.2019;[Epub] CrossRef
Wnt/β-Catenin Signaling Pathway-Related Proteins (DKK-3, β-Catenin, and c-MYC) Are Involved in Prognosis of Nasopharyngeal Carcinoma
Qiran Pang, Wenting Hu, Xinglin Zhang, Mingjie Pang
Cancer Biotherapy and Radiopharmaceuticals.2019; 34(7): 436. CrossRef
Long Noncoding RNAs and Messenger RNAs Expression Profiles Potentially Regulated by ZBTB7A in Nasopharyngeal Carcinoma
Fei Liu, Jiazhang Wei, Yanrong Hao, Fengzhu Tang, Wei Jiao, Shenhong Qu, Ning He, Yonglin Cai, Jiao Lan, Yong Yang, Yongli Wang, Min Li, Jingjin Weng, Bing Li, Jinlong Lu, Xing Han
BioMed Research International.2019; 2019: 1. CrossRef
Stable knockdown of ZBTB7A promotes cell proliferation and progression in nasopharyngeal carcinoma
Fei Liu, Fengzhu Tang, Jiao Lan, Wei Jiao, Yongfeng Si, Wensheng Lu, Mingzheng Mo, Bing Li, Jinlong Lu, Jiazhang Wei, Ying Qin, Ruiping Xiao, Benjian Zhang, Yongli Wang, Weiming Xiong
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Sara Franceschi, Francesca Lessi, Paolo Aretini, Valerio Ortenzi, Cristian Scatena, Michele Menicagli, Marco La Ferla, Prospero Civita, Katia Zavaglia, Claudia Scopelliti, Alessandro Apollo, Francesco Giovanni Carbone, Riccardo Vannozzi, Generoso Bevilacq
Oncotarget.2018; 9(35): 24014. CrossRef
Deficiency of pigment epithelium-derived factor in nasopharyngeal carcinoma cells triggers the epithelial–mesenchymal transition and metastasis
Ting Zhang, Ping Yin, Zichen Zhang, Banglao Xu, Di Che, Zhiyu Dai, Chang Dong, Ping Jiang, Honghai Hong, Zhonghan Yang, Ti Zhou, Jianyong Shao, Zumin Xu, Xia Yang, Guoquan Gao
Cell Death & Disease.2017; 8(6): e2838. CrossRef
TIMELESS confers cisplatin resistance in nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway and promoting the epithelial mesenchymal transition
Sai-Lan Liu, Huan-Xin Lin, Chu-Yong Lin, Xiao-Qing Sun, Li-Ping Ye, Fang Qiu, Wen Wen, Xin Hua, Xian-Qiu Wu, Jun Li, Li-Bing Song, Ling Guo
Cancer Letters.2017; 402: 117. CrossRef
Zinc-finger protein 545 is inactivated due to promoter methylation and functions as a tumor suppressor through the Wnt/β-catenin, PI3K/AKT and MAPK/ERK signaling pathways in colorectal cancer
Shili Xiang, Tingxiu Xiang, Qian Xiao, Yunhai Li, Bianfei Shao, Tao Luo
International Journal of Oncology.2017; 51(3): 801. CrossRef
Differences in Zbtb7a expression cause heterogeneous changes in human nasopharyngeal carcinoma CNE3 sublines
Fei Liu, Jiao Lan, Wei Jiao, Xianglan Mo, Yongta Huang, Huilan Ye, Ruiping Xiao, Yongli Wang, Mingzheng Mo, Liwei Shi
Oncology Letters.2017; 14(3): 2669. CrossRef
Mifepristone increases mRNA translation rate, triggers the unfolded protein response, increases autophagic flux, and kills ovarian cancer cells in combination with proteasome or lysosome inhibitors
Lei Zhang, Maria B. Hapon, Alicia A. Goyeneche, Rekha Srinivasan, Carlos D. Gamarra-Luques, Eduardo A. Callegari, Donis D. Drappeau, Erin J. Terpstra, Bo Pan, Jennifer R. Knapp, Jeremy Chien, Xuejun Wang, Kathleen M. Eyster, Carlos M. Telleria
Molecular Oncology.2016; 10(7): 1099. CrossRef
ZNF143 enhances metastasis of gastric cancer by promoting the process of EMT through PI3K/AKT signaling pathway
Song Wei, Linjun Wang, Lei Zhang, Bowen Li, Zheng Li, Qun Zhang, Jiwei Wang, Liang Chen, Guangli Sun, Qing Li, Hao Xu, Diancai Zhang, Zekuan Xu
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Genetic polymorphisms of Wnt/β-catenin pathway genes are associated with the efficacy and toxicities of radiotherapy in patients with nasopharyngeal carcinoma
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Oncotarget.2016; 7(50): 82528. CrossRef
CFTR is a potential marker for nasopharyngeal carcinoma prognosis and metastasis
Ziwei Tu, Qu Chen, Jie Ting Zhang, Xiaohua Jiang, Yunfei Xia, Hsiao Chang Chan
Oncotarget.2016; 7(47): 76955. CrossRef

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Forkhead Transcription Factor FOXO1 Inhibits Angiogenesis in Gastric Cancer in Relation to SIRT1: Sue Youn Kim, Young San Ko, Jinju Park, Yiseul Choi, Jong-Wan Park, Younghoon Kim, Jung-Soo Pyo, Young Bok Yoo, Jae-Seon Lee, Byung Lan Lee; Cancer Res Treat. 2016;48(1):345-354. Published online March 3, 2015; DOI: https://doi.org/10.4143/crt.2014.247

Abstract PDF PubReader ePub

Purpose
We previously reported that forkhead transcription factors of the O class 1 (FOXO1) expression in gastric cancer (GC) was associated with angiogenesis-related molecules. However, there is little experimental evidence for the direct role of FOXO1 in GC. In the present study, we investigated the effect of FOXO1 on the tumorigenesis and angiogenesis in GC and its relationship with SIRT1.
Materials and Methods
Stable GC cell lines (SNU-638 and SNU-601) infected with a lentivirus containing FOXO1 shRNA were established for animal studies as well as cell culture experiments. We used xenograft tumors in nude mice to evaluate the effect of FOXO1 silencing on tumor growth and angiogenesis. In addition, we examined the association between FOXO1 and SIRT1 by immunohistochemical tissue array analysis of 471 human GC specimens and Western blot analysis of xenografted tumor tissues.
Results
In cell culture, FOXO1 silencing enhanced hypoxia inducible factor-1α (HIF-1α) expression and GC cell growth under hypoxic conditions, but not under normoxic conditions. The xenograft study showed that FOXO1 downregulation enhanced tumor growth, microvessel areas, HIF-1α activation and vascular endothelial growth factor (VEGF) expression. In addition, inactivated FOXO1 expression was associated with SIRT1 expression in human GC tissues and xenograft tumor tissues.
Conclusion
Our results indicate that FOXO1 inhibits GC growth and angiogenesis under hypoxic conditions via inactivation of the HIF-1α–VEGF pathway, possibly in association with SIRT1. Thus, development of treatment modalities aiming at this pathway might be useful for treating GC.

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Tumor-derived exosomal miR-1247-3p promotes angiogenesis in bladder cancer by targeting FOXO1
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Yu-Han Chen, Chun-Lan Li, Wen-Jia Chen, Jing Liu, Hua-Tao Wu
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Philippe Icard, Ludovic Fournel, Zherui Wu, Marco Alifano, Hubert Lincet
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Quxie Capsule Inhibits Colon Tumor Growth Partially Through Foxo1-Mediated Apoptosis and Immune Modulation
Dongmei Chen, Yufei Yang, Peiying Yang
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Wei Sun, Bing Wang, Xing-Long Qu, Bi-Qiang Zheng, Wen-Ding Huang, Zheng-Wang Sun, Chun-Meng Wang, Yong Chen
Cells.2019; 9(1): 87. CrossRef
Oncogenic USP22 supports gastric cancer growth and metastasis by activating c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling
Hongxia Liu, Ningning Liu, Yali Zhao, Xiaoshan Zhu, Changsong Wang, Qinqin Liu, Chunfang Gao, Xusheng Zhao, Juntang Li
Aging.2019; 11(21): 9643. CrossRef
FOXO1: Another avenue for treating digestive malignancy?
Feiyu Shi, Tian Li, Zhi Liu, Kai Qu, Chengxin Shi, Yaguang Li, Qian Qin, Liang Cheng, Xin Jin, Tianyu Yu, Wencheng Di, Jianwen Que, Hongping Xia, Junjun She
Seminars in Cancer Biology.2018; 50: 124. CrossRef
Homeostatic interplay between FoxO proteins and ER proteostasis in cancer and other diseases
Matías González-Quiroz, Hery Urra, Celia María Limia, Claudio Hetz
Seminars in Cancer Biology.2018; 50: 42. CrossRef
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Shuai Jiang, Tian Li, Zhi Yang, Wei Hu, Yang Yang
International Journal of Cancer.2018; 143(7): 1560. CrossRef
Sinomenine Induces G1-Phase Cell Cycle Arrest and Apoptosis in Malignant Glioma Cells Via Downregulation of Sirtuin 1 and Induction of p53 Acetylation
Xiaoyan He, Mayinur Maimaiti, Yan Jiao, Xuegang Meng, Hongyan Li
Technology in Cancer Research & Treatment.2018;[Epub] CrossRef
Impact of curcumin on sirtuins: A review
Elham Zendedel, Alexandra E Butler, Stephen L Atkin, Amirhossein Sahebkar
Journal of Cellular Biochemistry.2018; 119(12): 10291. CrossRef
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Peng Zhang, Haifeng Gao, Qing Li, Xinlei Chen, Xifa Wu
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miR-101 suppresses HBV replication and expression by targeting FOXO1 in hepatoma carcinoma cell lines
Yanjing Wang, Hui Tian
Biochemical and Biophysical Research Communications.2017; 487(1): 167. CrossRef
FOXO1 inhibits the invasion and metastasis of hepatocellular carcinoma by reversing ZEB2-induced epithelial-mesenchymal transition
Tianxiu Dong, Yu Zhang, Yaodong Chen, Pengfei Liu, Tingting An, Jiuwei Zhang, Haichao Yang, Wenjing Zhu, Xiuhua Yang
Oncotarget.2017; 8(1): 1703. CrossRef
c-Jun N-terminal kinase activation has a prognostic implication and is negatively associated with FOXO1 activation in gastric cancer
Youngsun Choi, Jinju Park, Yiseul Choi, Young San Ko, Da-Ae Yu, Younghoon Kim, Jung-Soo Pyo, Bo Gun Jang, Min A. Kim, Woo Ho Kim, Byung Lan Lee
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Transcriptional repression of FOXO1 by KLF4 contributes to glioma progression
Guodong Tang, Dingyang Liu, Gelei Xiao, Qing Liu, Jian Yuan
Oncotarget.2016; 7(49): 81757. CrossRef
Loss of FOXO1 promotes gastric tumour growth and metastasis through upregulation of human epidermal growth factor receptor 2/neu expression
Young San Ko, Sung Jin Cho, Jinju Park, Younghoon Kim, Yong Joon Choi, Jung-Soo Pyo, Bo Gun Jang, Jong-Wan Park, Woo Ho Kim, Byung Lan Lee
British Journal of Cancer.2015; 113(8): 1186. CrossRef

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Peptide Nucleic Acid Clamping Versus Direct Sequencing for the Detection of EGFR Gene Mutation in Patients with Non-small Cell Lung Cancer: Seong-Hoon Yoon, Yoo-Duk Choi, In-Jae Oh, Kyu-Sik Kim, Hayoung Choi, Jinsun Chang, Hong-Joon Shin, Cheol-Kyu Park, Young-Chul Kim; Cancer Res Treat. 2015;47(4):661-669. Published online February 23, 2015; DOI: https://doi.org/10.4143/crt.2014.282

Abstract PDF PubReader ePub

Purpose
Direct sequencing (DS) is the standard method for detection of epidermal growth factor receptor (EGFR) gene mutation in non-small cell lung cancer (NSCLC); however, low detection sensitivity is a problem. The aim of this study is to demonstrate higher detection rate of EGFR gene mutation with peptide nucleic acid (PNA) clamping compared with DS. Materials and Methods This is a single arm, prospective study for patients with stage IIIB/IV or relapsed NSCLC. Using tumor DNA from 138 patients, both DS and PNA clamping for EGFR gene in exon 18, 19, 20, and 21 were performed. Discrepant results between the two methods were verified using Cobas and a mutant enrichment based next generation sequencing (NGS). Patients with activating mutations were treated with EGFR tyrosine kinase inhibitor (EGFR-TKI, gefitinib, or erlotinib) as first line treatment.
Results
Of 138 paired test sets, 24 (17.4%) and 45 (32.6%) cases with activating mutations were detected by DS and PNA clamping, respectively. The difference of detection rate between the two methods was 15.2% (95% confidence interval, 8.7% to 17.8%; p < 0.001). Between the two methods, 25 cases showed discrepant results (n=23, PNA+/DS–; n=2, PNA–/DS+). Mutations were confirmed by Cobas or NGS in 22 of 23 PNA+/DS– cases. The response rates to EGFR-TKI were 72.2% in the PNA+/DS+ group and 85.0% in the PNA+/DS– group. Conclusion PNA clamping showed a significantly higher detection rate of EGFR gene mutation compared with DS. Higher sensitivity of PNA clamping was not compromised by the loss of predictive power of response to EGFR-TKI.

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Hayoung Choi, Jae‐Kyeong Lee, Hyung‐Joo Oh, Min‐Seok Kim, Bo Gun Kho, Cheol Kyu Park, In‐Jae Oh, Young‐Chul Kim
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Bronchial brushing cytology is comparable to bronchial biopsy for epidermal growth factor receptor mutation test in non-small cell lung cancer
Joo-Yeon Koo, Nah-Ihm Kim, Taebum Lee, Yoo-Duk Choi
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Insu Kim, Jung Seop Eom, Eun Jung Jo, Jeongha Mok.Ki Uk, Kwangha Lee, Ki Uk Kim, Hye‐Kyung Park, Min Ki Lee, Mi‐Hyun Kim
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Xiao-Dong Ren, Ding-Yuan Liu, Hai-Qin Guo, Liu Wang, Na Zhao, Ning Su, Kun Wei, Sai Ren, Xue-Mei Qu, Xiao-Tian Dai, Qing Huang
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Soo-Jin Kim, Eunhee Kim, Kyung-Taek Rim
Molecular & Cellular Toxicology.2018; 14(2): 221. CrossRef
Feasibility of re‐biopsy and EGFR mutation analysis in patients with non‐small cell lung cancer
Tae‐Ok Kim, In‐Jae Oh, Bo Gun Kho, Ha Young Park, Jin Sun Chang, Cheol‐Kyu Park, Hong‐Joon Shin, Jung‐Hwan Lim, Yong‐Soo Kwon, Yu‐Il Kim, Sung‐Chul Lim, Young‐Chul Kim, Yoo‐Duk Choi
Thoracic Cancer.2018; 9(7): 856. CrossRef
Clinical Activity of Pan-HER Inhibitors Against HER2-Mutant Lung Adenocarcinoma
In-Jae Oh, Jae Young Hur, Cheol-Kyu Park, Young-Chul Kim, Seung Joon Kim, Min Ki Lee, Hee Joung Kim, Kye Young Lee, Jae Cheol Lee, Chang-Min Choi
Clinical Lung Cancer.2018; 19(5): e775. CrossRef
Genetic Biomarkers and Their Applications to Prevent Occupational Diseases: A Literature Review
Kyung-Taek Rim
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Molecular masquerading of rare EGFR L858M/L861R mutations as common L858R/L861Q mutations by PNA clamping assay
Ji Hyung Hong, Seung-Hyun Jung, Min Sung Kim, Sug Hyung Lee, Yeun-Jun Chung
Pathology.2017; 49(4): 453. CrossRef
Mutations of the Epidermal Growth Factor Receptor Gene in Triple-Negative Breast Cancer
Aeri Kim, Min Hye Jang, Soo Jung Lee, Young Kyung Bae
Journal of Breast Cancer.2017; 20(2): 150. CrossRef
Peptide nucleic acids: Advanced tools for biomedical applications
Anjali Gupta, Anuradha Mishra, Nidhi Puri
Journal of Biotechnology.2017; 259: 148. CrossRef
Non-invasive quantification of cell-free DNA mutations in plasma during lung tumor progression in mice
Soo-Jin Kim, Eunhee Kim, Kyung-Taek Rim
Cancer Biomarkers.2017; 20(4): 477. CrossRef
Peptide Nucleic Acid-Based Biosensors for Cancer Diagnosis
Roberta D’Agata, Maria Giuffrida, Giuseppe Spoto
Molecules.2017; 22(11): 1951. CrossRef
Generation of lung cancer cell lines harboring EGFR T790M mutation by CRISPR/Cas9-mediated genome editing
Mi-Young Park, Min Hee Jung, Eun Young Eo, Seokjoong Kim, Sang Hoon Lee, Yeon Joo Lee, Jong Sun Park, Young Jae Cho, Jin Haeng Chung, Cheol Hyeon Kim, Ho Il Yoon, Jae Ho Lee, Choon-Taek Lee
Oncotarget.2017; 8(22): 36331. CrossRef
Application of Peptide Nucleic Acid-based Assays Toward Detection of Somatic Mosaicism
Christopher S Hong, Chunzhang Yang, Zhengping Zhuang
Molecular Therapy - Nucleic Acids.2016; 5: e314. CrossRef
Quantification of epidermal growth factor receptor (EGFR) mutation may be a predictor of EGFR‐tyrosine kinase inhibitor treatment response
Ha Young Park, Hyung Joo Oh, Ki‐Hyun Kim, Tae‐Ok Kim, Cheol‐Kyu Park, Hong‐Jun Shin, Jung‐Hwan Lim, Yong‐Soo Kwon, In‐Jae Oh, Yu‐Il Kim, Sung‐Chul Lim, Young‐Chul Kim, Yoo‐Duk Choi
Thoracic Cancer.2016; 7(6): 639. CrossRef
Association between GWAS-identified lung adenocarcinoma susceptibility loci andEGFRmutations in never-smoking Asian women, and comparison with findings from Western populations
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Human Molecular Genetics.2016; : ddw414. CrossRef

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RASSF1A Suppresses Cell Migration through Inactivation of HDAC6 and Increase of Acetylated alpha-Tubulin: Hae-Yun Jung, Jun Seok Jung, Young Mi Whang, Yeul Hong Kim; Cancer Res Treat. 2013;45(2):134-144. Published online June 30, 2013; DOI: https://doi.org/10.4143/crt.2013.45.2.134

Abstract PDF PubReader ePub

PURPOSE
The RAS association domain family protein 1 (RASSF1) has been implicated in a tumor-suppressive function through the induction of acetylated alpha-tubulin and modulation of cell migration. However, the mechanisms of how RASSF1A is associated with acetylation of alpha-tubulin for controlling cell migration have not yet been elucidated. In this study, we found that RASSF1A regulated cell migration through the regulation of histon deacetylase 6 (HDAC6), which functions as a tubulin deacetylase.
MATERIALS AND METHODS
The cell migration was assessed using wound-healing and transwell assays. The role of RASSF1A on cell migration was examined by immunofluorescence staining, HDAC activity assay and western blot analysis.
RESULTS
Cell migration was inhibited and cell morphology was changed in RASSF1A-transfected H1299 cells, compared with controls, whereas HDAC6 protein expression was not changed by RASSF1A transfection in these cells. However, RASSF1A inhibited deacetylating activity of HDAC6 protein and induced acetylated alpha-tubulin expression. Furthermore, acetylated alpha-tubulin and HDAC6 protein were co-localized in the cytoplasm in RASSF1A-transfected H1299 cells. Conversely, when the endogenous RASSF1A expression in HeLa cells was blocked with RASSF1A siRNA treatment, acetylated alpha-tubulin was co-localized with HDAC6 protein throughout the whole cells, including the nucleus, compared with scramble siRNA-treated HeLa cells. The restoration of RASSF1A by 5-Aza-dC treatment also induced acetylated alpha-tubulin through inhibition of HDAC6 activity that finally resulted in suppressing cell migration in H1299 cells. To further confirm the role of HDAC6 in RASSF1A-mediated cell migration, the HDAC6 expression in H1299 cells was suppressed by using HDAC6 siRNA, and cell motility was found to be decreased through enhanced acetylated alpha-tubulin.
CONCLUSION
The results of this study suggest that the inactivation of HDAC6 by RASSF1A regulates cell migration through increased acetylated alpha-tubulin protein.

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Pathogenic variants of TUBB8 cause oocyte spindle defects by disrupting with EB1/CAKP5 interactions and potential treatment targeting microtubule acetylation through HDAC6 inhibition
Hui Luo, Jianhua Chen, Cao Li, Tian Wu, Siyue Yin, Guangping Yang, Yipin Wang, Zhihan Guo, Saifei Hu, Yanni He, Yingnan Wang, Yao Chen, Youqiang Su, Congxiu Miao, Yun Qian, Ruizhi Feng
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Paxillin/HDAC6 regulates microtubule acetylation to promote directional migration of keratinocytes driven by electric fields
Luojia Liu, Xiaoqiang Liu, Ying Chen, Meng Kong, Jinghong Zhang, Min Jiang, Hongling Zhou, Jinrui Yang, Xu Chen, Ze Zhang, Chao Wu, Xupin Jiang, Jiaping Zhang
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research.2024; 1871(2): 119628. CrossRef
Inhibition of histone deacetylase 6 destabilizes ERK phosphorylation and suppresses cancer proliferation via modulation of the tubulin acetylation-GRP78 interaction
Onsurang Wattanathamsan, Naphat Chantaravisoot, Piriya Wongkongkathep, Sakkarin Kungsukool, Paninee Chetprayoon, Pithi Chanvorachote, Chanida Vinayanuwattikun, Varisa Pongrakhananon
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Inter-relationship of Histone Deacetylase-6 with Tau-cytoskeletal organization and remodeling
Abhishek Ankur Balmik, Subashchandrabose Chinnathambi
European Journal of Cell Biology.2022; 101(2): 151202. CrossRef
HDAC6 inhibitor, ACY1215 suppress the proliferation and induce apoptosis of gallbladder cancer cells and increased the chemotherapy effect of gemcitabine and oxaliplatin
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Autophagic degradation of KAT2A/GCN5 promotes directional migration of vascular smooth muscle cells by reducing TUBA/α-tubulin acetylation
Changhan Ouyang, Jing Mu, Qiulun Lu, Jian Li, Huaiping Zhu, Qilong Wang, Ming-Hui Zou, Zhonglin Xie
Autophagy.2020; 16(10): 1753. CrossRef
RASSF1A Regulates Spindle Organization by Modulating Tubulin Acetylation via SIRT2 and HDAC6 in Mouse Oocytes
Hyuk-Joon Jeon, Jeong Su Oh
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The unraveling of substrate specificity of histone deacetylase 6 domains using acetylome peptide microarrays and peptide libraries
Zsofia Kutil, Lubica Skultetyova, David Rauh, Marat Meleshin, Ivan Snajdr, Zora Novakova, Jana Mikesova, Jiri Pavlicek, Martin Hadzima, Petra Baranova, Barbora Havlinova, Pavel Majer, Mike Schutkowski, Cyril Barinka
The FASEB Journal.2019; 33(3): 4035. CrossRef
Suppressor of hepatocellular carcinoma RASSF1A activates autophagy initiation and maturation
Wenjiao Li, Fei Yue, Yuan Dai, Boyun Shi, Guibin Xu, Xianhan Jiang, Xinke Zhou, Gerd P. Pfeifer, Leyuan Liu
Cell Death & Differentiation.2019; 26(8): 1379. CrossRef
The Role and Function of Ras-association domain family in Cancer: A Review
Mohammad Reza Zinatizadeh, Seyed Ali Momeni, Peyman Kheirandish Zarandi, Ghanbar Mahmoodi Chalbatani, Hassan Dana, Hamid Reza Mirzaei, Mohammad Esmaeil Akbari, Seyed Rouhollah Miri
Genes & Diseases.2019; 6(4): 378. CrossRef
RASSF1A, puppeteer of cellular homeostasis, fights tumorigenesis, and metastasis—an updated review
Fatéméh Dubois, Emmanuel Bergot, Gérard Zalcman, Guénaëlle Levallet
Cell Death & Disease.2019;[Epub] CrossRef
Tumor suppressor C-RASSF proteins
Hiroaki Iwasa, Shakhawoat Hossain, Yutaka Hata
Cellular and Molecular Life Sciences.2018; 75(10): 1773. CrossRef
Dual-functionality of RASSF1A overexpression in A375 cells is mediated by activation of IL-6/STAT3 regulatory loop
Mei Yi, Wei Wang, Shengnan Chen, Ya Peng, Junjun Li, Jing Cai, Ying Zhou, Qian Peng, Yuanyuan Ban, Zhaoyang Zeng, Xiaoling Li, Wei Xiong, Guiyuan Li, Bo Xiang
Molecular Biology Reports.2018; 45(5): 1277. CrossRef
Epigenetic reactivation of RASSF1A by phenethyl isothiocyanate (PEITC) and promotion of apoptosis in LNCaP cells
Sarandeep S.S. Boyanapalli, Wenji Li, Francisco Fuentes, Yue Guo, Christina N. Ramirez, Ximena-Parades Gonzalez, Douglas Pung, Ah-Ng Tony Kong
Pharmacological Research.2016; 114: 175. CrossRef
The Potential of Histone Deacetylase Inhibitors in Breast Cancer Therapy
Namita Chatterjee, Martin Tenniswood
Breast Cancer Management.2015; 4(2): 85. CrossRef
CpG site-specific RASSF1a hypermethylation is associated with occupational PAH exposure and genomic instability
Zhini He, Huawei Duan, Biao Zhang, Miao Li, Liping Chen, Bo Zhang, Xiaonian Zhu, Chen Gao, Jie Li, Xiao Zhang, Jingmaio Zhang, Shan Wang, Xiaowen Zeng, Daochuan Li, Xiumei Xing, Zhengbao Zhang, Lu Ma, Qing Bai, Caixia Liu, Yongmei Xiao, Yuxin Zheng, Wen C
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Microtubule segment stabilization by RASSF1A is required for proper microtubule dynamics and Golgi integrity
Christopher Arnette, Nadia Efimova, Xiaodong Zhu, Geoffrey J. Clark, Irina Kaverina, Erika Holzbaur
Molecular Biology of the Cell.2014; 25(6): 800. CrossRef
RASSF tumor suppressor gene family: Biological functions and regulation
Natalia Volodko, Marilyn Gordon, Mohamed Salla, Haya Abu Ghazaleh, Shairaz Baksh
FEBS Letters.2014; 588(16): 2671. CrossRef
MicroRNA expression profiling in male and female familial breast cancer
R Pinto, S De Summa, K Danza, O Popescu, A Paradiso, L Micale, G Merla, O Palumbo, M Carella, S Tommasi
British Journal of Cancer.2014; 111(12): 2361. CrossRef

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Expression of BamHI-A Rightward Transcripts in Epstein-Barr Virus-Associated Gastric Cancers: Bo-Gun Jang, Eun Ji Jung, Woo Ho Kim; Cancer Res Treat. 2011;43(4):250-254. Published online December 27, 2011; DOI: https://doi.org/10.4143/crt.2011.43.4.250

Abstract PDF PubReader ePub

PURPOSE
About 10% of all gastric cancers (GCs) are Epstein-Barr virus (EBV)-associated. However, the oncogene of EBV in gastric carcinogenesis has not yet been established. In the present study, we investigated the virus-derived transcripts in the EBV-infected GC cell line to explore the viral oncogene of EBV-positive GCs.
MATERIALS AND METHODS
We used the SNU719 cell line, a naturally derived EBV-infected GC cell line. The individual expressed sequence tags from the cDNA libraries of SNU719 were searched against the mRNA subset extracted from the GenBank data base. Sequence reaction was carried out for the EBV-associated clones. Reverse transcription-polymerase chain reaction was performed after cells were partitioned into nuclear and cytoplasmic fractions.
RESULTS
Using bioinformatic tools, we selected 13 EBV-associated clones from cDNA libraries of SNU719. By sequencing analysis, we revealed that they were all associated with RPMS1, one of the BamHI-A rightward transcripts (BART) of EBV. Some BART cDNAs such as RPMS1 and A73 are known to be translated into protein in vitro, and have been shown to have some biochemical functions relevant to tumorigenesis. But, presently, the BART transcripts were expressed only in the nucleus and not in the cytoplasm, arguing against their role as messenger RNAs. Some other BART transcripts expressed in GCs (BARF0, CST, vIL, BARF1, BLLF1, and BcLF1) were also extensively detected in the nucleus.
CONCLUSION
BART transcripts are the predominant viral transcripts expressed in EBV-associated GCs, and they are located only in the nucleus. Therefore, it seems less likely that BART transcripts produce functional proteins to play a role in carcinogenesis of EBV-associated GCs.

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EBV DNA methylation profiles and its application in distinguishing nasopharyngeal carcinoma and nasal NK/T-cell lymphoma
Cao-Li Tang, Xi-Zhao Li, Ting Zhou, Chang-Mi Deng, Cheng-Tao Jiang, Yu-Meng Zhang, Ying Liao, Tong-Min Wang, Yong-Qiao He, Wen-Qiong Xue, Wei-Hua Jia, Xiao-Hui Zheng
Clinical Epigenetics.2024;[Epub] CrossRef
Long non-coding RNAs in Epstein–Barr virus-related cancer
Yitong Liu, Zhizhong Hu, Yang Zhang, Chengkun Wang
Cancer Cell International.2021;[Epub] CrossRef
Epstein–Barr virus-associated gastric cancer: A distinct subtype
Jing Yang, Zhifeng Liu, Bin Zeng, Guangsheng Hu, Runliang Gan
Cancer Letters.2020; 495: 191. CrossRef
Role of BamHI-A Rightward Frame 1 in Epstein–Barr Virus-Associated Epithelial Malignancies
Rancés Blanco, Francisco Aguayo
Biology.2020; 9(12): 461. CrossRef
Epstein-Barr Virus (EBV)-derived BARF1 encodes CD4- and CD8-restricted epitopes as targets for T-cell immunotherapy
MAMTA KALRA, ULRIKE GERDEMANN, JESSICA D. LUU, MINTHRAN C. NGO, ANN M. LEEN, CHRYSTAL U. LOUIS, CLIONA M. ROONEY, STEPHEN GOTTSCHALK
Cytotherapy.2019; 21(2): 212. CrossRef
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Jun-ting Huang, Jian-ning Chen, Li-ping Gong, Yuan-hua Bi, Jing Liang, Lu Zhou, Dan He, Chun-kui Shao
Virology.2019; 529: 144. CrossRef
DNA Methylation Pattern of Early Genes of Epstein Barr Virus Associated With Gastric Carcinoma in Group of Iraqi Patients
Hiba Sabah Jasim
Journal of Pure and Applied Microbiology.2019; 13(1): 441. CrossRef
Conservation and polymorphism of EBV RPMS1 gene in EBV-associated tumors and healthy individuals from endemic and non-endemic nasopharyngeal carcinoma areas in China
Shuo Wu, Wen Liu, Hong Li, Zhenzhen Zhao, Yang Yang, Hua Xiao, Yingying Song, Bing Luo
Virus Research.2018; 250: 75. CrossRef
The Methylation Status and Expression of Epstein-Barr Virus Early Genes BARF1 and BHRF1 in Epstein-Barr Virus-Associated Gastric Carcinomas
Jing Li, Wen Liu, Kui Che, Yan Zhang, Zhenzhen Zhao, Bing Luo
Gastroenterology Research and Practice.2017; 2017: 1. CrossRef
Genetics and Molecular Biology of Epstein-Barr Virus-Encoded BART MicroRNA: A Paradigm for Viral Modulation of Host Immune Response Genes and Genome Stability
David H. Dreyfus
Journal of Immunology Research.2017; 2017: 1. CrossRef
The role of Epstein-Barr virus infection in the pathogenesis of nasopharyngeal carcinoma
Chi Man Tsang, Sai Wah Tsao
Virologica Sinica.2015; 30(2): 107. CrossRef
Distinct Viral and Mutational Spectrum of Endemic Burkitt Lymphoma
Francesco Abate, Maria Raffaella Ambrosio, Lucia Mundo, Maria Antonella Laginestra, Fabio Fuligni, Maura Rossi, Sakellarios Zairis, Sara Gazaneo, Giulia De Falco, Stefano Lazzi, Cristiana Bellan, Bruno Jim Rocca, Teresa Amato, Elena Marasco, Maryam Etebar
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Differences in Gastric Carcinoma Microenvironment Stratify According to EBV Infection Intensity: Implications for Possible Immune Adjuvant Therapy
Michael J. Strong, Guorong Xu, Joseph Coco, Carl Baribault, Dass S. Vinay, Michelle R. Lacey, Amy L. Strong, Teresa A. Lehman, Michael B. Seddon, Zhen Lin, Monica Concha, Melody Baddoo, MaryBeth Ferris, Kenneth F. Swan, Deborah E. Sullivan, Matthew E. Bur
PLoS Pathogens.2013; 9(5): e1003341. CrossRef

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Role of Loss of O⁶-Methylguanine DNA Methyltransferase (MGMT) Expression in Non-Small Cell Lung Carcinomas (NSCLCs): with Reference to the Relationship with p53 Overexpression: Na-Hye Myong; Cancer Res Treat. 2010;42(2):95-100. Published online June 30, 2010; DOI: https://doi.org/10.4143/crt.2010.42.2.95

Abstract PDF PubReader ePub

Purpose

Functional inactivation of the O⁶-methylguanine-DNA methyltransferase (MGMT) gene has been demonstrated as loss of MGMT protein and suggested that it plays an important role in primary human neoplasia, including lung cancer. It has also been reported to be associated with the G : C→A : T transition mutation in the p53 gene of lung cancer. The aims of this study were to investigate the role of MGMT expression loss and its prognostic significance in non-small cell lung carcinomas (NSCLCs), and its correlation with p53 overexpression as well as influence on patient survival.

Materials and Methods

112 surgically resected NSCLC specimens were reviewed by medical records for their clinicopathologic variables. Their tissue microarray blocks were immunostained with anti-human MGMT and p53 primary antibodies. Correlation between MGMT loss and the clinicopathologic prognostic factors, including p53 overexpression and the single or combined actions of MGMT loss and p53 overexpression on patient survival were statistically analyzed by SPSS15.0.

Results

Reduced or absent MGMT expression was found in 48 of 112 NSCLCs (43%), and significantly associated with nodal metastasis and squamous or undifferentiated cell types. Loss of MGMT expression was correlated with p53 overexpression in adenocarcinomas, but not in overall NSCLCs. Its solitary or combined actions with p53 overexpression did not have influence on patient survival.

Conclusion

Loss of MGMT expression is a relatively common event in NSCLCs and significantly associated with nodal metastasis and p53 overexpression, suggesting that it may play a major role in pulmonary carcinogenesis, and also in disease progression of NSCLCs.

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O 6 -Methylguanine-DNA methyltransferase (MGMT): A drugable target in lung cancer?
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Relationship Between the Expression of O6-Methylguanine-DNA Methyltransferase (MGMT) and p53, and the Clinical Response in Metastatic Pancreatic Adenocarcinoma Treated with FOLFIRINOX
Carole Vitellius, Caroline Eymerit-Morin, Dominique Luet, Lionel Fizanne, Fanny Foubert, Sandrine Bertrais, Marie-Christine Rousselet, François-Xavier Caroli-Bosc
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Modest Anti-Cancer Activity of a Bile Acid Acylated Heparin Derivative in a PC14PE6 Induced Orthotopic Lung Cancer Model: Zheng Yun Cui, Min Jae Park, Jeeyun Lee, Jin Seok Ahn, Myung Ju Ahn, Soo Won Seo, Jin Woo Park, Youngro Byun, Keunchil Park; Cancer Res Treat. 2009;41(2):80-86. Published online June 30, 2009; DOI: https://doi.org/10.4143/crt.2009.41.2.80

Abstract PDF PubReader ePub

Purpose

A novel chemically modified heparin derivative, heparin-deoxycholic acid nano-particles, has lower anticoagulant activity, and was recently reported to have significant anti-tumor effects on squamous head and neck cancer cells. Therefore, the aim of this study was to evaluate the anti-tumor effects of heparin-deoxycholic acid nano-particles in a human lung adenocarcinoma cell line.

Materials and Methods

An orthotopic lung cancer model in 16 mice was developed using intra-thoracic injections of 0.5×10⁶ PC14PE6 cells. Ten days after inoculation, the mice were divided into two groups. PBS and Heparin-DOCA particles were injected once a day every 3 days in the tail vein, for a total of 5 injections. The body weight and survival of each mouse were monitored and the tumor size in the lung was measured by SPECT-CT before and after heparin-DOCA nano-particle treatment.

Results

IThe HD particles had no significant cytotoxicity when the PC9 cells were treated in vitro. There was no statistical difference in tumor size, body weight and survival between the HD treated and control groups in vivo. Furthermore, there was no difference in the amount of CD31 between tumor tissues in the two study groups.

Conclusion

HD synthesized with unfractionated heparin had no apparent inhibitory effects on tumor growth in a PC14PE6 cell induced orthotopic lung cancer mouse model. The HD particles did not significantly inhibit tumor-induced angiogenesis at the tumor sites.

Citations

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Improvement of orthotopic lung cancer mouse model via thoracotomy and orotracheal intubation enabling in vivo imaging studies
Geun Ho Im, Moon-Sun Jang, Julius Juhyun Chung, Kyoung-Nam Kim, Jae-Hun Kim, Sun I Kim, Jung Hee Lee
Laboratory Animals.2014; 48(2): 124. CrossRef
The antiangiogenic properties of sulfated β-cyclodextrins in anticancer formulations incorporating 5-fluorouracil
Clare A. Watson, Kara L. Vine, Julie M. Locke, Anna Bezos, Christopher R. Parish, Marie Ranson
Anti-Cancer Drugs.2013; 24(7): 704. CrossRef

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Association of Single Nucleotide Polymorphisms in PIM-1 Gene with the Risk of Korean Lung Cancer: Dae Sik Kim, Jae Sook Sung, Eun Soon Shin, Jeong-Seon Ryu, In Keun Choi, Kyong Hwa Park, Yong Park, Eui Bae Kim, Seh Jong Park, Yeul Hong Kim; Cancer Res Treat. 2008;40(4):190-196. Published online December 31, 2008; DOI: https://doi.org/10.4143/crt.2008.40.4.190

Abstract PDF PubReader ePub

Purpose

The expression of the PIM-1 gene, which is a proto-oncogene that encodes a serine/threonine kinase, is associated with multiple cellular functions such as proliferation, differentiation, apoptosis and tumorigenesis. In particular, several studies have reported that the PIM-1 gene is associated with the development of lymphoma, leukemia and prostate cancer. Therefore, this study was conducted to evaluate the association between the single nucleotide polymorphisms in the PIM-1 gene and the risk of lung cancer occurrence in the Korean population.

Materials and Methods

To evaluate the role of the PIM-1 gene in the development of lung cancer, the genotypes of the PIM-1 gene were determined in 408 lung cancer patients and 410 normal subjects.

Results

We found that the T-C-T-C haplotypes of the PIM-1 gene (-1196 T>C, IVS4 +55 T>C, IVS4 +1416 T>A and +3684 C>A) were associated with an increased risk of lung cancer [adjusted odds ratio (aOR): 3.98; 95% CI: 1.24~12.75, p-value: 0.020]. In particular, these haplotypes showed an increased risk of lung cancer in males (aOR: 5.67; 95% CI: 1.32~24.30, p-value: 0.019) and smokers (aOR: 7.82; 95% CI: 1.75~34.98, p-value: 0.007).

Conclusions

The present results suggest that the T-C-T-C haplotype of the PIM-1 gene could influence the risk of developing smoking-related lung cancer in the Korean population. Additional functional studies with an larger sample sized analysis are warranted to reconfirm our findings.

Citations

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A review on structure-function mechanism and signaling pathway of serine/threonine protein PIM kinases as a therapeutic target
Ajaya Kumar Rout, Budheswar Dehury, Satya Narayan Parida, Sushree Swati Rout, Rajkumar Jena, Neha Kaushik, Nagendra Kumar Kaushik, Sukanta Kumar Pradhan, Chita Ranjan Sahoo, Ashok Kumar Singh, Meenakshi Arya, Bijay Kumar Behera
International Journal of Biological Macromolecules.2024; 270: 132030. CrossRef
Impact of Pim1 mutations on the survival outcomes of patients with breast cancer: Insights from a clinical study
Syed Sultan Beevi, Kavitha Anbrasu, Vinod Kumar Verma, Nagesh Kishan Panchal, Krishna Kiran Kannepalli, Raghu Ram Pillarisetti, Sailaja Madigubba, Jyotsana Dwivedi, Neha Damodar, Radhika Chowdary Darapuneni
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Therapeutic targeting of PIM KINASE signaling in cancer therapy: Structural and clinical prospects
Aanchal Rathi, Dhiraj Kumar, Gulam Mustafa Hasan, Mohammad Mahfuzul Haque, Md Imtaiyaz Hassan
Biochimica et Biophysica Acta (BBA) - General Subjects.2021; 1865(11): 129995. CrossRef
Loss of PIM1 correlates with progression and prognosis of salivary adenoid cystic carcinoma (SACC)
Jiajie Xu, Xin Zhu, Qingling Li, Chao Chen, Zhenying Guo, Zhuo Tan, Chuanming Zheng, Minghua Ge
Cancer Cell International.2018;[Epub] CrossRef
PIM Kinase as an Executional Target in Cancer
Xinning Zhang, Mengqiu Song, Joydeb Kumar Kundu, Mee-Hyun Lee, Zhen-Zhen Liu
Journal of Cancer Prevention.2018; 23(3): 109. CrossRef
HistoneH3 demethylase JMJD2A promotes growth of liver cancer cells through up-regulating miR372
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Oncotarget.2017; 8(30): 49093. CrossRef
Expressions of osteopontin (OPN), ανβ3 and Pim-1 associated with poor prognosis in non-small cell lung cancer (NSCLC)
Yi Jin, Da-yue Tong, Lu-ying Tang, Jian-ning Chen, Jing Zhou, Zhi-ying Feng, Chun-kui Shao
Chinese Journal of Cancer Research.2012; 24(2): 103. CrossRef
Overexpression of Osteopontin, αvβ3 and Pim-1 Associated with Prognostically Important Clinicopathologic Variables in Non-Small Cell Lung Cancer
Yi Jin, Da-yue Tong, Jian-ning Chen, Zhi-ying Feng, Jian-yong Yang, Chun-kui Shao, Jia-ping Li, Rossella Rota
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No Association between PIK3CA Polymorphism and Lung Cancer Risk in the Korean Population
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Clinical Significance of Vascular Endothelial Growth Factors (VEGF)-C and -D in Resected Non-Small Cell Lung Cancer: Yoon Ho Ko, Chan-Kwon Jung, Myung-Ah Lee, Jae Ho Byun, Jin Hyoung Kang, Kyo Young Lee, Keon Hyun Jo, Young Pil Wang, Young Seon Hong; Cancer Res Treat. 2008;40(3):133-140. Published online September 30, 2008; DOI: https://doi.org/10.4143/crt.2008.40.3.133

Abstract PDF PubReader ePub

Purpose

Lymphatic spread of tumor is an important prognostic factor for patients with non-small cell lung carcinoma (NSCLC). Vascular endothelial growth factor-C (VEGF-C) and VEGF-D play important roles in lymphangiogenesis via the VEGF receptor 3 (VEGFR-3). We sought to determine whether VEGF-C, VEGF-D and VEGFR-3 are involved in the clinical outcomes of patients with resected NSCLC.

Materials and Methods

Using immunohistochemical staining, we investigated the protein expressions of VEGF-C, VEGF-D and VEGFR-3 in the tissue array specimens from patients who underwent resection for NSCLC. The immunoreactivity for p53 was also examined. The clinicopathological implications of these molecules were statistically analyzed.

Results

Analysis of a total of 118 specimens showed that VEGF-C, VEGF-D and their co-expression were significantly associated with more advanced regional lymph node metastasis (p=0.019, p=0.044 and p=0.026, respectively, N2 versus N0 and N1). A VEGFR-3 expression had a strong correlation with peritumoral lymphatic invasion (p=0.047). On the multivariate analysis for survival and recurrence, pathologic N2 lymph node metastasis was the only independent prognostic factor, but none of the investigated molecules showed any statistical correlation with recurrence and survival.

Conclusions

The present study revealed that high expressions of VEGF-C and VEGF-D were strongly associated with more advanced regional lymph node metastasis in patients with resected NSCLC.

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Advances in lymphatic metastasis of non-small cell lung cancer
Xiaofei Zhang, Li Ma, Man Xue, Yanning Sun, Zhaoxia Wang
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Prediction of VEGF and EGFR Expression in Peripheral Lung Cancer Based on the Radiomics Model of Spectral CT Enhanced Images
Linhua Wu, Jian Li, Xiaowei Ruan, Jialiang Ren, Xuejun Ping, Bing Chen
International Journal of General Medicine.2022; Volume 15: 6725. CrossRef
Lymphangiogenesis in Gastric Cancer regulated through Akt/mTOR-VEGF-C/VEGF-D axis
Hongxia Chen, Runnian Guan, Yupeng Lei, Jianyong Chen, Qi Ge, Xiaoshen Zhang, Ruoxu Dou, Hongyuan Chen, Hao Liu, Xiaolong Qi, Xiaodong Zhou, Changyan Chen
BMC Cancer.2015;[Epub] CrossRef
Prognostic Impact of Elevation of Vascular Endothelial Growth Factor Family Expression in Patients with Non-small Cell lung Cancer: an Updated Meta-analysis
Chun-Long Zheng, Chen Qiu, Mei-Xiao Shen, Xiao Qu, Tie-Hong Zhang, Ji-Hong Zhang, Jia-Jun Du
Asian Pacific Journal of Cancer Prevention.2015; 16(5): 1881. CrossRef
Lymphangiogenic Markers and Their Impact on Nodal Metastasis and Survival in Non-Small Cell Lung Cancer - A Structured Review with Meta-Analysis
Thomas K. Kilvaer, Erna-Elise Paulsen, Sigurd M. Hald, Tom Wilsgaard, Roy M. Bremnes, Lill-Tove Busund, Tom Donnem, Xin-Yuan Guan
PLOS ONE.2015; 10(8): e0132481. CrossRef
A Gene Signature Combining the Tissue Expression of Three Angiogenic Factors is a Prognostic Marker in Early-stage Non-small Cell Lung Cancer
Elena Sanmartín, Rafael Sirera, Marta Usó, Ana Blasco, Sandra Gallach, Santiago Figueroa, Nieves Martínez, Cristina Hernando, Antonio Honguero, Miguel Martorell, Ricardo Guijarro, Rafael Rosell, Eloisa Jantus-Lewintre, Carlos Camps
Annals of Surgical Oncology.2014; 21(2): 612. CrossRef
VEGF-C in non-small cell lung cancer: Meta-analysis
Hao Jiang, Wei Shao, Wei Zhao
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High density of peritumoral lymphatic vessels measured by D2-40/podoplanin and LYVE-1 expression in gastric cancer patients: an excellent prognostic indicator or a false friend?
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Multiplexed analysis of angiogenesis and lymphangiogenesis factors predicts outcome for non-small cell lung cancer patients
Valsamo K. Anagnostou, Dina G. Tiniakos, Marianthi Fotinou, Apostolos Achimastos, Konstantinos N. Syrigos
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JUNG YEON KIM, BYUNG-NOE BAE, JI EUN KWON, HYUN-JUNG KIM, KYEONGMEE PARK
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Supplementation with a-Tocopherol or ß-Carotene Reduces Serum Concentrations of Vascular Endothelial Growth Factor-D, but Not -A or -C, in Male Smokers
Alison M. Mondul, Helen C. Rager, William Kopp, Jarmo Virtamo, Demetrius Albanes
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The Bone Morphogenesis Protein-2 (BMP-2) is Associated with Progression to Metastatic Disease in Gastric Cancer: Yong Park, Jee Won Kim, Dae Sik Kim, Eui Bae Kim, Se Jong Park, Jin Yong Park, Woo Suk Choi, Jong Gyu Song, Hee Yun Seo, Sang Cheul Oh, Byung Soo Kim, Jong Jae Park, Yeul Hong Kim, Jun Suk Kim; Cancer Res Treat. 2008;40(3):127-132. Published online September 30, 2008; DOI: https://doi.org/10.4143/crt.2008.40.3.127

Abstract PDF PubReader ePub

Purpose

Bone Morphogenetic Proteins (BMPs) are members of the TGF-β superfamily and it has been demonstrated that BMPs enhance migration, invasion and metastasis. The purpose of this study was to identify the association between the serum BMP-2 level and the progression status of gastric cancer.

Materials and Methods

Fifty-five patients with metastatic gastric cancer (metastatic disease group), six patients with early gastric cancer without lymph node metastasis (the EGC group), and ten healthy control subjects were enrolled in this study. The serum BMP-2 level was quantified by use of a commercially available ELISA kit. In EGC group patients and patients with metastatic disease, whole blood was obtained before endoscopic mucosal resection and before the commencement of a scheduled cycle of systemic chemotherapy, respectively.

Results

No significant difference in the mean serum BMP-2 levels was observed between the control subjects and the EGC group patients (87.95 pg/ml for the control subjects and 84.50 pg/ml for the EGC group, p=1.0). However, the metastatic disease group patients had a significantly higher level of serum BMP (179.61 pg/ml) than the control subjects and EGC group patients (87.95 pg/ml for the control subjects and 84.50 pg/ml for the EGC group, p<0.0001). Moreover, the mean serum BMP-2 level from patients with a bone metastasis was significantly higher than the mean serum BMP-2 level from patients without a bone metastasis (204.73 pg/ml versus 173.33 pg/ml, p=0.021).

Conclusions

BMP-2 seems to have a role in progression to metastatic disease in gastric cancer, especially in the late stage of tumorigenesis, including invasion and metastasis. BMP-2 may facilitate bone metastasis in gastric cancer. To confirm these findings, further studies are required with tissue specimens and the use of a cancer cell line.

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Review Articles

Improving Conventional or Low Dose Metronomic Chemotherapy with Targeted Antiangiogenic Drugs: Robert S. Kerbel; Cancer Res Treat. 2007;39(4):150-159. Published online December 31, 2007; DOI: https://doi.org/10.4143/crt.2007.39.4.150

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One of the most significant developments in medical oncology practice has been the approval of various antiangiogenic drugs for the treatment of a number of different malignancies. These drugs include bevacizumab (Avastin®), the anti-VEGF monoclonal antibody. Thus far, bevacizumab appears to induce clinical benefit in patients who have advanced metastatic disease only or primarily when it is combined with conventional chemotherapy. The reasons for the chemo-enhancing effects of bevacizumab are unknown, and this is a subject that we have been actively studying along with additional ways that antiangiogenic drugs may be combined with chemotherapy. In this respect, we have focused much of our effort on metronomic low dose chemotherapy. We have been studying the hypothesis that some chemotherapy drugs at maximum tolerated doses or other cytotoxic- like drugs such as acute "vascular disrupting agents" (VDAs) can cause an acute mobilization of proangiogenic cells from the bone marrow which home to and colonize the treated tumors, thus accelerating their recovery. These cells include endothelial progenitor cells. This systemic process can be largely blocked by a targeted antiangiogenic drug, e.g. anti-VEGFR-2 antibodies. In addition, metronomic chemotherapy, i.e., close regular administration of chemotherapy drugs at low non-toxic doses with no breaks, over prolonged periods of time not only prevents the acute CEP bone marrow response, but can even target the cells. This potential antiangiogenic effect of metronomic chemotherapy can also be boosted by combination with a targeted antiangiogenic agent. Treatment combinations of metronomic chemotherapy and an antiangiogenic drug have moved into phase II clinical trial testing with particularly encouraging results thus far reported in metastatic breast and recurrent ovarian cancer. Oral chemotherapy drugs such as cyclophosphamide (CTX), methotrexate are the main chemotherapeutics used for such trials. Oral 5-FU prodrugs such as UFT would also appear to be highly suitable based on long term adjuvant therapy studies in patients. Recent preclinical results using metronomic cyclophosphamide and metronomic UFT in models of advanced metastatic breast cancer suggest that this type of combination might be particularly promising for metronomic chemotherapy in this indication, particularly when combined with a targeted antiangiogenic drug.

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Tumor Angiogenesis: Initiation and Targeting - Therapeutic Targeting of an FGF-Binding Protein, an Angiogenic Switch Molecule, and Indicator of Early Stages of Gastrointestinal Adenocarcinomas -: Elena Tassi, Anton Wellstein; Cancer Res Treat. 2006;38(4):189-197. Published online December 31, 2006; DOI: https://doi.org/10.4143/crt.2006.38.4.189

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Tumor angiogenesis has been related to the initiation as well as progression toward more aggressive behavior of human tumors. In particular, the activity of angiogenic factors is crucial for tumor progression. We previously characterized a secreted fibroblast growth factor-binding protein (FGF-BP) as a chaperone molecule, which binds to various FGFs, enhances FGF-mediated biochemical and biologic events and importantly is a crucial rate-limiting factor for tumor-dependent angiogenesis. We generated monoclonal antibodies that target FGF-BP protein and used them as a tool to evaluate frequency and pattern of FGF-BP expression during the malignant progression of pancreas and colorectal carcinoma in archival tissue samples. We found that FGF-BP is dramatically upregulated during the initiation of colorectal and pancreatic adenocarcinoma. Crucial genetic events underlying the initiation and progression of colorectal and pancreatic adenocarcinoma with a particular focus on the modulation of angiogenesis and antiangiogenic therapies are discussed. We propose that the upregulation of the secreted FGF-BP protein during early phases of pancreas and colon cancer could make this protein a possible serum marker indicating the presence of high-risk premalignant lesions. Furthermore, the biological activity of FGF-BP is neutralized by monoclonal antibodies suggesting the potential for antibody-based therapeutic targeting.

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