Cancer Research and Treatment

Original Articles

Gastrointestinal cancer

Analysis of Plasma Circulating Tumor DNA in Borderline Resectable Pancreatic Cancer Treated with Neoadjuvant Modified FOLFIRINOX: Clinical Relevance of DNA Damage Repair Gene Alteration Detection: Dong-Hoon Lim, Hyunseok Yoon, Kyu-pyo Kim, Baek-Yeol Ryoo, Sang Soo Lee, Do Hyun Park, Tae Jun Song, Dae Wook Hwang, Jae Hoon Lee, Ki Byung Song, Song Cheol Kim, Seung-Mo Hong, Jaewon Hyung, Changhoon Yoo; Cancer Res Treat. 2023;55(4):1313-1320. Published online May 4, 2023; DOI: https://doi.org/10.4143/crt.2023.452

Abstract PDF Supplementary Material PubReader ePub

Purpose
There are no reliable biomarkers to guide treatment for patients with borderline resectable pancreatic cancer (BRPC) in the neoadjuvant setting. We used plasma circulating tumor DNA (ctDNA) sequencing to search biomarkers for patients with BRPC receiving neoadjuvant mFOLFIRINOX in our phase 2 clinical trial (NCT02749136).
Materials and Methods
Among the 44 patients enrolled in the trial, patients with plasma ctDNA sequencing at baseline or post-operation were included in this analysis. Plasma cell-free DNA isolation and sequencing were performed using the Guardant 360 assay. Detection of genomic alterations, including DNA damage repair (DDR) genes, were examined for correlations with survival.
Results
Among the 44 patients, 28 patients had ctDNA sequencing data qualified for the analysis and were included in this study. Among the 25 patients with baseline plasma ctDNA data, 10 patients (40%) had alterations of DDR genes detected at baseline, inclu-ding ATM, BRCA1, BRCA2 and MLH1, and showed significantly better progression-free survival than those without such DDR gene alterations detected (median, 26.6 vs. 13.5 months; log-rank p=0.004). Patients with somatic KRAS mutations detected at baseline (n=6) had significantly worse overall survival (median, 8.5 months vs. not applicable; log-rank p=0.003) than those without. Among 13 patients with post-operative plasma ctDNA data, eight patients (61.5%) had detectable somatic alterations.
Conclusion
Detection of DDR gene mutations from plasma ctDNA at baseline was associated with better survival outcomes of pati-ents with borderline resectable pancreatic ductal adenocarcinoma treated with neoadjuvant mFOLFIRINOX and may be a prognostic biomarker.

Citations

Citations to this article as recorded by

A Practical Approach to Interpreting Circulating Tumor DNA in the Management of Gastrointestinal Cancers
Zexi Allan, David S Liu, Margaret M Lee, Jeanne Tie, Nicholas J Clemons
Clinical Chemistry.2024; 70(1): 49. CrossRef
High somatic mutations in circulating tumor DNA predict response of metastatic pancreatic ductal adenocarcinoma to first-line nab-paclitaxel plus S-1: prospective study
Lei Huang, Yao Lv, Shasha Guan, Huan Yan, Lu Han, Zhikuan Wang, Quanli Han, Guanghai Dai, Yan Shi
Journal of Translational Medicine.2024;[Epub] CrossRef
Decoding the Dynamics of Circulating Tumor DNA in Liquid Biopsies
Khadija Turabi, Kelsey Klute, Prakash Radhakrishnan
Cancers.2024; 16(13): 2432. CrossRef
Building on the clinical applicability of ctDNA analysis in non-metastatic pancreatic ductal adenocarcinoma
Ibone Labiano, Ana E. Huerta, Maria Alsina, Hugo Arasanz, Natalia Castro, Saioa Mendaza, Arturo Lecumberri, Iranzu Gonzalez-Borja, David Guerrero-Setas, Ana Patiño-Garcia, Gorka Alkorta-Aranburu, Irene Hernández-Garcia, Virginia Arrazubi, Elena Mata, Davi
Scientific Reports.2024;[Epub] CrossRef
Liquid biopsy analysis of lipometabolic exosomes in pancreatic cancer
Wei Guo, Peiyao Ying, Ruiyang Ma, Zuoqian Jing, Gang Ma, Jin Long, Guichen Li, Zhe Liu
Cytokine & Growth Factor Reviews.2023; 73: 69. CrossRef

3,673 View
257 Download
4 Web of Science
5 Crossref

Gynecologic cancer

Genomic Correlates of Unfavorable Outcome in Locally Advanced Cervical Cancer Treated with Neoadjuvant Chemoradiation: Yuchun Wei, Chuqing Wei, Liang Chen, Ning Liu, Qiuxiang Ou, Jiani C. Yin, Jiaohui Pang, Zhenhao Fang, Xue Wu, Xiaonan Wang, Dianbin Mu, Yang Shao, Jinming Yu, Shuanghu Yuan; Cancer Res Treat. 2022;54(4):1209-1218. Published online January 17, 2022; DOI: https://doi.org/10.4143/crt.2021.963

Abstract PDF Supplementary Material PubReader ePub

Purpose
Neoadjuvant therapy modality can increase the operability rate and mitigate pathological risks in locally advanced cervical cancer, but treatment response varies widely. It remains unclear whether genetic alterations correlate with the response to neoadjuvant therapy and disease-free survival (DFS) in locally advanced cervical cancer.
Materials and Methods
A total of 62 locally advanced cervical cancer (stage IB-IIA) patients who received neoadjuvant chemoradiation plus radical hysterectomy were retrospectively analyzed. Patients’ tumor biopsy samples were comprehensively profiled using targeted next generation sequencing. Pathologic response to neoadjuvant treatment and DFS were evaluated against the association with genomic traits.
Results
Genetic alterations of PIK3CA were most frequent (37%), comparable to that of Caucasian populations from The Cancer Genome Atlas. The mutation frequency of genes including TERT, POLD1, NOS2, and FGFR3 was significantly higher in Chinese patients whereas RPTOR, EGFR, and TP53 were underrepresented in comparison to Caucasians. Germline mutations were identified in 21% (13/62) of the cohort and more than half (57%) had mutations in DNA damage repair genes, including BRCA1/2, TP53 and PALB2. Importantly, high tumor mutation burden, TP53 polymorphism (rs1042522), and KEAP1 mutations were found to be associated with poor pathologic response to neoadjuvant chemoradiation treatment. KEAP1 mutations, PIK3CA-SOX2 co-amplification, TERC copy number gain, and TYMS polymorphism correlated with an increased risk of disease relapse.
Conclusion
We report the genomic profile of locally advanced cervical cancer patients and the distinction between Asian and Caucasian cohorts. Our findings highlight genomic traits associated with unfavorable neoadjuvant chemoradiation response and a higher risk of early disease recurrence.

Citations

Citations to this article as recorded by

Comprehensive characterization of PKHD1 mutation in human colon cancer
Lu Han, Fangming Gong, Xuxiaochen Wu, Wanxiangfu Tang, Hua Bao, Yue Wang, Daizhenru Wang, Yulan Sun, Peng Li
Cancer Medicine.2024;[Epub] CrossRef
PBRM1 presents a potential ctDNA marker to monitor response to neoadjuvant chemotherapy in cervical cancer
Wenhan Li, Yuhui Huang, Man Xiao, Jing Zhao, Shi Du, Zehua Wang, Sha Hu, Lu Yang, Jing Cai
iScience.2024; 27(3): 109160. CrossRef
Comprehensive genomic profiling of pulmonary spindle cell carcinoma using tissue and plasma samples: insights from a real‐world cohort analysis
Yi Sun, Shilei Qin, Song Wang, Jiaohui Pang, Qiuxiang Ou, Weiquan Liang, Hai Zhong
The Journal of Pathology: Clinical Research.2024;[Epub] CrossRef
PD-1 inhibitor plus concurrent chemoradiotherapy for high-risk locally advanced cervical cancer
Cong Wang, Lijun Liu, Xia Li, Jia Lei, Yiqian Li, Zhibo Shen, Huirong Shi, Yan Cheng
Future Oncology.2024; 20(20): 1415. CrossRef
A biomarker exploration in small-cell lung cancer for brain metastases risk and prophylactic cranial irradiation therapy efficacy
Li Li, Ning Liu, Tao Zhou, Xueting Qin, Xiaoyu Song, Song Wang, Jiaohui Pang, Qiuxiang Ou, Yong Wang, Dexian Zhang, Jiaran Li, Fuhao Xu, Shuming Shi, Jinming Yu, Shuanghu Yuan
Lung Cancer.2024; 196: 107959. CrossRef
Prospects of POLD1 in Human Cancers: A Review
Michał Gola, Przemysław Stefaniak, Janusz Godlewski, Barbara Jereczek-Fossa, Anna Starzyńska
Cancers.2023; 15(6): 1905. CrossRef
Copy-number-gain of telomerase reverse transcriptase (hTERT) is associated with an unfavorable prognosis in esophageal adenocarcinoma
Su Ir Lyu, Felix C. Popp, Adrian Georg Simon, Anne Maria Schultheis, Thomas Zander, Caroline Fretter, Wolfgang Schröder, Christiane J. Bruns, Thomas Schmidt, Alexander Quaas, Karl Knipper
Scientific Reports.2023;[Epub] CrossRef

7,060 View
170 Download
7 Web of Science
7 Crossref

Gastrointestinal cancer

Inhibition of WEE1 Potentiates Sensitivity to PARP Inhibitor in Biliary Tract Cancer: Hye-Rim Seo, Ah-Rong Nam, Ju-Hee Bang, Kyoung-Seok Oh, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh; Cancer Res Treat. 2022;54(2):541-553. Published online August 6, 2021; DOI: https://doi.org/10.4143/crt.2021.473

Abstract PDF PubReader ePub

Purpose
Up to 20% of patients with biliary tract cancer (BTC) have alterations in DNA damage response (DDR) genes, including homologous recombination (HR) genes. Therefore, the DDR pathway could be a promising target for new drug development in BTC. We aim to investigate the anti-tumor effects using poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors in BTC.
Materials and Methods
We used 10 BTC cell lines to evaluate an anti-tumor effect of olaparib (a PARP inhibitor) and AZD1775 (a WEE1 inhibitor) in in vitro. Additionally, we established SNU869 xenograft model for in vivo experiments.
Results
In this study, we observed a modest anti-proliferative effect of olaparib. DNA double-strand break (DSB) and apoptosis were increased by olaparib in BTC cells. However, olaparib-induced DNA DSB was repaired through the HR pathway, and G2 arrest was induced to secure the time for repair. As AZD1775 typically regulates the G2/M checkpoint, we combined olaparib with AZD1775 to abrogate G2 arrest. We observed that AZD1775 downregulated p-CDK1, a G2/M cell cycle checkpoint protein, and induced early mitotic entry. AZD1775 also decreased CtIP and RAD51 expression and disrupted HR repair. In xenograft model, olaparib plus AZD1775 treatment reduced tumor growth more potently than did monotherapy with either drug.
Conclusion
This is the first study to suggest that olaparib combined with AZD1775 can induce synergistic anti-tumor effects against BTC. Combination therapy that blocks dual PARP and WEE1 has the potential to be further clinically developed for BTC patients.

Citations

Citations to this article as recorded by

Current and Future Therapeutic Targets for Directed Molecular Therapies in Cholangiocarcinoma
Philipp Heumann, Andreas Albert, Karsten Gülow, Denis Tümen, Martina Müller, Arne Kandulski
Cancers.2024; 16(9): 1690. CrossRef
Combined strategies with PARP inhibitors for the treatment of BRCA wide type cancer
Yijun Xie, Di Xiao, Duo Li, Mei Peng, Wei Peng, Huaxin Duan, Xiaoping Yang
Frontiers in Oncology.2024;[Epub] CrossRef
Update on Combination Strategies of PARP Inhibitors
Zhuoqun Lin, Lingfang Wang, Ziyu Xing, Fenfen Wang, Xiaodong Cheng
Cancer Control.2024;[Epub] CrossRef
The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer
Deqian Xie, Bowen Jiang, Shijin Wang, Qifei Wang, Guangzhen Wu
Frontiers in Cell and Developmental Biology.2023;[Epub] CrossRef
DNA Damage Response Inhibitors in Cholangiocarcinoma: Current Progress and Perspectives
Öykü Gönül Geyik, Giulia Anichini, Engin Ulukaya, Fabio Marra, Chiara Raggi
Cells.2022; 11(9): 1463. CrossRef
Targeted Therapy of HPV Positive and Negative Tonsillar Squamous Cell Carcinoma Cell Lines Reveals Synergy between CDK4/6, PI3K and Sometimes FGFR Inhibitors, but Rarely between PARP and WEE1 Inhibitors
Ourania N. Kostopoulou, Mark Zupancic, Mariona Pont, Emma Papin, Monika Lukoseviciute, Borja Agirre Mikelarena, Stefan Holzhauser, Tina Dalianis
Viruses.2022; 14(7): 1372. CrossRef
Targeted Therapy with PI3K, PARP, and WEE1 Inhibitors and Radiotherapy in HPV Positive and Negative Tonsillar Squamous Cell Carcinoma Cell Lines Reveals Synergy while Effects with APR-246 Are Limited
Karin Byskata, Monika Lukoseviciute, Filippo Tuti, Mark Zupancic, Ourania N. Kostopoulou, Stefan Holzhauser, Tina Dalianis
Cancers.2022; 15(1): 93. CrossRef

6,842 View
225 Download
10 Web of Science
7 Crossref

General

Pan-cancer Analysis of Tumor Mutational Burden and Homologous Recombination DNA Damage Repair Using Targeted Next-Generation Sequencing: Hai-Yun Wang, Ling Deng, Ying-Qing Li, Xiao Zhang, Ya-Kang Long, Xu Zhang, Yan-Fen Feng, Yuan He, Tao Tang, Xin-Hua Yang, Fang Wang; Cancer Res Treat. 2021;53(4):973-982. Published online February 18, 2021; DOI: https://doi.org/10.4143/crt.2020.798

Abstract PDF Supplementary Material PubReader ePub

Purpose
Current variability in methods for tumor mutational burden (TMB) estimation and reporting demonstrates the urgent need for a homogeneous TMB assessment approach. Here, we compared TMB distributions in different cancer types using two customized targeted panels commonly used in clinical practice.
Materials and Methods
TMB spectra of 295- and 1021-gene panels in multiple cancer types were compared using targeted next-generation sequencing (NGS). The TMB distributions across a diverse cohort of 2,332 cancer cases were then investigated for their associations with clinical features. Treatment response data were collected for 222 patients who received immune-checkpoint inhibitors (ICIs) and their homologous recombination DNA damage repair (HR-DDR) and programmed death-ligand 1 (PD-L1) expression were additionally assessed and compared with the TMB and response rate.
Results
The median TMB between gene panels was similar despite a wide range in TMB values. The highest TMB was 8 and 10 in patients with squamous cell carcinoma and esophageal carcinoma according to the classification of histopathology and cancer types, respectively. Twenty-three out of 103 patients (22.3%) were HR-DDR‒positive and could benefit from ICI therapy; out of those 23 patients, seven patients had high TMB (p=0.004). Additionally, PD-L1 expression was not associated with TMB or treatment response among patients receiving ICIs.
Conclusion
Targeted NGS assays demonstrated the ability to evaluate TMB in pan-cancer samples as a tool to predict response to ICIs. In addition, TMB integrated with HR-DDR‒positive status could be a significant biomarker for predicting ICI response in patients.

Citations

Citations to this article as recorded by

Comprehensive molecular findings in primary malignant melanoma of the esophagus: A multicenter study
Ling Deng, Hai‐Yun Wang, Chun‐Fang Hu, Xiao‐Yun Liu, Kuntai Jiang, Juan‐Juan Yong, Xiao‐Yan Wu, Kai‐Hua Guo, Fang Wang
Pigment Cell & Melanoma Research.2024; 37(3): 363. CrossRef
Genomic Features of Homologous Recombination Deficiency in Breast Cancer: Impact on Testing and Immunotherapy
Umer Ali, Sunitha Vungarala, Venkataswarup Tiriveedhi
Genes.2024; 15(2): 162. CrossRef
Biomarkers to predict efficacy of immune checkpoint inhibitors in colorectal cancer patients: a systematic review and meta-analysis
Hang Yu, Qingquan Liu, Keting Wu, Shuang Tang
Clinical and Experimental Medicine.2024;[Epub] CrossRef
Clinical significance of genetic profiling based on different anatomic sites in patients with mucosal melanoma who received or did not receive immune checkpoint inhibitors
Hai-Yun Wang, Ye Liu, Ling Deng, Kuntai Jiang, Xin-Hua Yang, Xiao-Yan Wu, Kai-Hua Guo, Fang Wang
Cancer Cell International.2023;[Epub] CrossRef
Homologous recombination repair gene mutations as a predictive biomarker for immunotherapy in patients with advanced melanoma
Zhixuan You, Meng Lv, Xuanyu He, Yingqin Pan, Junfeng Ge, Xue Hu, Yating Zheng, Mengli Huang, Chengzhi Zhou, Changxuan You
Frontiers in Immunology.2022;[Epub] CrossRef
The role of DNA damage repair (DDR) system in response to immune checkpoint inhibitor (ICI) therapy
Congqi Shi, Kaiyu Qin, Anqi Lin, Aimin Jiang, Quan Cheng, Zaoqu Liu, Jian Zhang, Peng Luo
Journal of Experimental & Clinical Cancer Research.2022;[Epub] CrossRef
Maximizing Small Biopsy Patient Samples: Unified RNA-Seq Platform Assessment of over 120,000 Patient Biopsies
P. Sean Walsh, Yangyang Hao, Jie Ding, Jianghan Qu, Jonathan Wilde, Ruochen Jiang, Richard T. Kloos, Jing Huang, Giulia C. Kennedy
Journal of Personalized Medicine.2022; 13(1): 24. CrossRef

7,473 View
221 Download
7 Web of Science
7 Crossref

Inhibition of ATR Increases the Sensitivity to WEE1 Inhibitor in Biliary Tract Cancer: Ah-Rong Nam, Mei-Hua Jin, Ju-Hee Bang, Kyoung-Seok Oh, Hye-Rim Seo, Do-Youn Oh, Yung-Jue Bang; Cancer Res Treat. 2020;52(3):945-956. Published online April 17, 2020; DOI: https://doi.org/10.4143/crt.2020.080

Abstract PDF Supplementary Material PubReader ePub

Purpose
Currently, the DNA damage response (DDR) pathway represents a key target for new cancer drug development. Advanced biliary tract cancer (BTC) has a poor prognosis because of the lack of efficacious treatment options. Although DNA repair pathway alterations have been reported in many patients with BTC, little is known regarding the effects of DDR-targeted agents against BTC.
Materials and Methods
In this study, nine BTC cell lines were exposed to the WEE1 inhibitor (AZD1775). In vitro, MTT assay, colony-forming assay, cell cycle analysis, phospho-histone H3 staining assay, Transwell migration assay, and western blot were performed. Then, to enhance the antitumor effect of AZD1775, the combination treatment of WEE1 inhibitor and ataxia telangiectasia mutated and Rad3 related (ATR) inhibitor (AZD6738) was conducted using MTT assay and comet assay. Finally, HuCCT-1 and SNU2670 xenograft models were established to confirm the anti-tumor effect of AZD1775 alone. Furthermore, the combination treatment was also evaluated in SNU2670 xenograft models.
Results
AZD1775 blocked the phosphorylation of CDC2 and CDC25C in all cell lines, but significantly increased apoptosis and S phase arrest in sensitive cells. However, increased p-ATR and phosphorylated ataxia telangiectasia mutated levels were observed in less sensitive cells. In addition, in vitro and in vivo data illustrated that AZD1775 combined with AZD6738 exerted more potent anti-tumor effects than either drug alone. Although WEE1 inhibition has promising anti-tumor effects in some BTC cells, the addition of ATR inhibitors could enhance its efficacy.
Conclusion
Taken together, this study supports further clinical development of DDR-targeted strategies as monotherapy or combination regimens for BTC.

Citations

Citations to this article as recorded by

Current and Future Therapeutic Targets for Directed Molecular Therapies in Cholangiocarcinoma
Philipp Heumann, Andreas Albert, Karsten Gülow, Denis Tümen, Martina Müller, Arne Kandulski
Cancers.2024; 16(9): 1690. CrossRef
Inhibition of the ATR-DNAPKcs-RB axis drives G1/S-phase transition and sensitizes triple-negative breast cancer (TNBC) to DNA holliday junctions
Yue-miao Hu, Xue-cun Liu, Lei Hu, Zhi-wen Dong, Hong-ying Yao, Ying-jie Wang, Wen-jing Zhao, Yu-ke Xiang, Yi Liu, Hong-bo Wang, Qi-kun Yin
Biochemical Pharmacology.2024; 225: 116310. CrossRef
Combination of S-1 and the oral ATR inhibitor ceralasertib is effective against pancreatic cancer cells
Yoshihito Morimoto, Kimihiko Takada, Ami Nakano, Osamu Takeuchi, Kazuhiro Watanabe, Masayoshi Hirohara, Yutaka Masuda
Cancer Chemotherapy and Pharmacology.2024; 94(6): 763. CrossRef
Immunomodulatory effects of trastuzumab deruxtecan through the cGAS-STING pathway in gastric cancer cells
Kyoung-Seok Oh, Ah-Rong Nam, Ju-Hee Bang, Yoojin Jeong, Sea Young Choo, Hyo Jung Kim, Su In Lee, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh
Cell Communication and Signaling.2024;[Epub] CrossRef
Targeting replication stress in cancer therapy
Alexandre André B. A. da Costa, Dipanjan Chowdhury, Geoffrey I. Shapiro, Alan D. D’Andrea, Panagiotis A. Konstantinopoulos
Nature Reviews Drug Discovery.2023; 22(1): 38. CrossRef
Combined Inhibition of Smoothened and the DNA Damage Checkpoint WEE1 Exerts Antitumor Activity in Cholangiocarcinoma
Giulia Anichini, Chiara Raggi, Mirella Pastore, Laura Carrassa, Luisa Maresca, Enrica Crivaro, Tiziano Lottini, Lea Duwe, Jesper B. Andersen, Lorenzo Tofani, Luca Di Tommaso, Jesus M. Banales, Annarosa Arcangeli, Fabio Marra, Barbara Stecca
Molecular Cancer Therapeutics.2023; 22(3): 343. CrossRef
Inhibiting WEE1 Augments the Antitumor Efficacy of Cisplatin in Urothelial Carcinoma by Enhancing the DNA Damage Process
Yu-Li Su, Ling-Yi Xiao, Shih-Yu Huang, Chia-Che Wu, Li-Chung Chang, Yi-Hua Chen, Hao-Lun Luo, Chun-Chieh Huang, Ting-Ting Liu, Jei-Ming Peng
Cells.2023; 12(11): 1471. CrossRef
The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer
Deqian Xie, Bowen Jiang, Shijin Wang, Qifei Wang, Guangzhen Wu
Frontiers in Cell and Developmental Biology.2023;[Epub] CrossRef
Enrichment of Wee1/CDC2 and NF-κB Signaling Pathway Constituents Mutually Contributes to CDDP Resistance in Human Osteosarcoma
Zhengbo Hu, Lugen Li, Wenxing Lan, Xiao Wei, Xiangyuan Wen, Penghuan Wu, Xianliao Zhang, Xinhua Xi, Yufa Li, Liqi Wu, Wenhu Li, Xiaohong Liao
Cancer Research and Treatment.2022; 54(1): 277. CrossRef
ATR inhibitor AZD6738 increases the sensitivity of colorectal cancer cells to 5‑fluorouracil by inhibiting repair of DNA damage
Takuya Suzuki, Takahisa Hirokawa, Anri Maeda, Shinnosuke Harata, Kaori Watanabe, Takeshi Yanagita, Hajime Ushigome, Nozomi Nakai, Yuzo Maeda, Kazuyoshi Shiga, Ryo Ogawa, Akira Mitsui, Masahiro Kimura, Yoichi Matsuo, Hiroki Takahashi, Shuji Takiguchi
Oncology Reports.2022;[Epub] CrossRef
Inhibition of WEE1 Potentiates Sensitivity to PARP Inhibitor in Biliary Tract Cancer
Hye-Rim Seo, Ah-Rong Nam, Ju-Hee Bang, Kyoung-Seok Oh, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh
Cancer Research and Treatment.2022; 54(2): 541. CrossRef
DNA Damage Response Inhibitors in Cholangiocarcinoma: Current Progress and Perspectives
Öykü Gönül Geyik, Giulia Anichini, Engin Ulukaya, Fabio Marra, Chiara Raggi
Cells.2022; 11(9): 1463. CrossRef
Multiple-low-dose therapy: effective killing of high-grade serous ovarian cancer cells with ATR and CHK1 inhibitors
Anya Golder, Louisa Nelson, Anthony Tighe, Bethany Barnes, Camilla Coulson-Gilmer, Robert D Morgan, Joanne C McGrail, Stephen S Taylor
NAR Cancer.2022;[Epub] CrossRef
Differential Effects of Combined ATR/WEE1 Inhibition in Cancer Cells
Gro Elise Rødland, Sissel Hauge, Grete Hasvold, Lilli T. E. Bay, Tine T. H. Raabe, Mrinal Joel, Randi G. Syljuåsen
Cancers.2021; 13(15): 3790. CrossRef
Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation
Jacqueline Nathansen, Felix Meyer, Luise Müller, Marc Schmitz, Kerstin Borgmann, Anna Dubrovska
Cancers.2021; 13(19): 4818. CrossRef
The Role of the Hedgehog Pathway in Cholangiocarcinoma
Giulia Anichini, Laura Carrassa, Barbara Stecca, Fabio Marra, Chiara Raggi
Cancers.2021; 13(19): 4774. CrossRef
Targeting P53 as a Future Strategy to Overcome Gemcitabine Resistance in Biliary Tract Cancers
Chiao-En Wu, Yi-Ru Pan, Chun-Nan Yeh, John Lunec
Biomolecules.2020; 10(11): 1474. CrossRef

8,931 View
264 Download
18 Web of Science
17 Crossref

Therapeutic Co-targeting of WEE1 and ATM Downregulates PD-L1 Expression in Pancreatic Cancer: Mei Hua Jin, Ah-Rong Nam, Ji Eun Park, Ju-Hee Bang, Yung-Jue Bang, Do-Youn Oh; Cancer Res Treat. 2020;52(1):149-166. Published online June 25, 2019; DOI: https://doi.org/10.4143/crt.2019.183

Abstract PDF Supplementary Material PubReader ePub

Purpose
Pancreatic cancer (PC) is one of the most lethal cancers worldwide, but there are currently no effective treatments. The DNA damage response (DDR) is under investigation for the development of novel anti-cancer drugs. Since DNA repair pathway alterations have been found frequently in PC, the purpose of this study was to test the DDR-targeting strategy in PC using WEE1 and ATM inhibitors.
Materials and Methods
We performed in vitro experiments using a total of ten human PC cell lines to evaluate antitumor effect of AZD1775 (WEE1 inhibitor) alone or combination with AZD0156 (ATM inhibitor). We established Capan-1–mouse model for in vivo experiments to confirm our findings.
Results
In our research, we found that WEE1 inhibitor (AZD1775) as single agent showed anti-tumor effects in PC cells, however, targeting WEE1 upregulated p-ATM level. Here, we observed that co-targeting of WEE1 and ATM acted synergistically to reduce cell proliferation and migration, and to induce DNA damage in vitro. Notably, inhibition of WEE1 or WEE1/ATM downregulated programmed cell death ligand 1 expression by blocking glycogen synthase kinase-3β serine 9 phosphorylation and decrease of CMTM6 expression. In Capan-1 mouse xenograft model, AZD1775 plus AZD0156 (ATM inhibitor) treatment reduced tumor growth and downregulated tumor expression of programmed cell death ligand 1, CMTM6, CD163, and CXCR2, all of which contribute to tumor immune evasion.
Conclusion
Dual blockade of WEE1 and ATM might be a potential therapeutic strategy for PC. Taken toget

Citations

Citations to this article as recorded by

The Killer’s Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer
Marisabel Mecca, Simona Picerno, Salvatore Cortellino
International Journal of Molecular Sciences.2024; 25(5): 2750. CrossRef
The molecular crosstalk between innate immunity and DNA damage repair/response: Interactions and effects in cancers
Sahar Omidvar, Vahid Vahedian, Zahra Sourani, Davood Yari, Mehrdad Asadi, Negin Jafari, Lida Khodavirdilou, Molood Bagherieh, Moein Shirzad, Vahid Hosseini
Pathology - Research and Practice.2024; 260: 155405. CrossRef
Progress of ATM inhibitors: opportunities and challenges
Shan Du, Qi Liang, Jianyou Shi
European Journal of Medicinal Chemistry.2024; : 116781. CrossRef
A prognostic risk model for ovarian cancer based on gene expression profiles from gene expression omnibus database
Wei Fan, Xiaoyun Chen, Ruiping Li, Rongfang Zheng, Yunyun Wang, Yuzhen Guo
Biochemical Genetics.2023; 61(1): 138. CrossRef
PGD2 displays distinct effects in diffuse large B-cell lymphoma depending on different concentrations
Shunfeng Hu, Tiange Lu, Juanjuan Shang, Yiqing Cai, Mengfei Ding, Xiangxiang Zhou, Xin Wang
Cell Death Discovery.2023;[Epub] CrossRef
The Landscape and Therapeutic Targeting of BRCA1, BRCA2 and Other DNA Damage Response Genes in Pancreatic Cancer
Ioannis A. Voutsadakis, Antonia Digklia
Current Issues in Molecular Biology.2023; 45(3): 2105. CrossRef
Bosutinib high density lipoprotein nanoformulation has potent tumour radiosensitisation effects
Pouya Dehghankelishadi, Parisa Badiee, Michelle F. Maritz, Nicole Dmochowska, Benjamin Thierry
Journal of Nanobiotechnology.2023;[Epub] CrossRef
Could Inhibiting the DNA Damage Repair Checkpoint Rescue Immune-Checkpoint-Inhibitor-Resistant Endometrial Cancer?
Yinuo Li, Xiangyu Wang, Xin Hou, Xiangyi Ma
Journal of Clinical Medicine.2023; 12(8): 3014. CrossRef
The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer
Deqian Xie, Bowen Jiang, Shijin Wang, Qifei Wang, Guangzhen Wu
Frontiers in Cell and Developmental Biology.2023;[Epub] CrossRef
The DNA Damage Response and Inflammation in Cancer
Vanessa Klapp, Beatriz Álvarez-Abril, Giuseppe Leuzzi, Guido Kroemer, Alberto Ciccia, Lorenzo Galluzzi
Cancer Discovery.2023; 13(7): 1521. CrossRef
CMTM6, a potential immunotherapy target
Jie Liang, Shaohua Li, Wei Li, Wei Rao, Shuo Xu, Haining Meng, Fengqi Zhu, Dongchang Zhai, Mengli Cui, Dan Xu, Jinzhen Cai, Bei Zhang
Journal of Cancer Research and Clinical Oncology.2022; 148(1): 47. CrossRef
Loss of CMTM6 promotes DNA damage-induced cellular senescence and antitumor immunity
Hanfeng Wang, Yang Fan, Weihao Chen, Zheng Lv, Shengpan Wu, Yundong Xuan, Chenfeng Wang, Yongliang Lu, Tao Guo, Donglai Shen, Fan Zhang, Qingbo Huang, Yu Gao, Hongzhao Li, Xin Ma, Baojun Wang, Yan Huang, Xu Zhang
OncoImmunology.2022;[Epub] CrossRef
Cell cycle checkpoints and beyond: Exploiting the ATR/CHK1/WEE1 pathway for the treatment of PARP inhibitor–resistant cancer
Nitasha Gupta, Tzu-Ting Huang, Sachi Horibata, Jung-Min Lee
Pharmacological Research.2022; 178: 106162. CrossRef
DNA damage response inhibition‐based combination therapies in cancer treatment: Recent advances and future directions
Tianen Chen, Suparat Tongpeng, Ziyi Lu, Win Topatana, Sarun Juengpanich, Shijie Li, Jiahao Hu, Jiasheng Cao, Cheeshin Lee, Yitong Tian, Mingyu Chen, Xiujun Cai
Aging and Cancer.2022; 3(1): 44. CrossRef
The clinical and prognostic significance of CMTM6/PD-L1 in oncology
Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Homa Darmani
Clinical and Translational Oncology.2022; 24(8): 1478. CrossRef
Targeting oncogene and non-oncogene addiction to inflame the tumour microenvironment
Giulia Petroni, Aitziber Buqué, Lisa M. Coussens, Lorenzo Galluzzi
Nature Reviews Drug Discovery.2022; 21(6): 440. CrossRef
CMTM6 as a master regulator of PD-L1
Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Homa Darmani
Cancer Immunology, Immunotherapy.2022; 71(10): 2325. CrossRef
Targeting protein kinases benefits cancer immunotherapy
Zhengkun Zhang, Lang Bu, Junhang Luo, Jianping Guo
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer.2022; 1877(4): 188738. CrossRef
CMTM6 and CMTM4 as two novel regulators of PD-L1 modulate the tumor microenvironment
Tong Zhang, Haixiang Yu, Xiangpeng Dai, Xiaoling Zhang
Frontiers in Immunology.2022;[Epub] CrossRef
The role of DNA damage repair (DDR) system in response to immune checkpoint inhibitor (ICI) therapy
Congqi Shi, Kaiyu Qin, Anqi Lin, Aimin Jiang, Quan Cheng, Zaoqu Liu, Jian Zhang, Peng Luo
Journal of Experimental & Clinical Cancer Research.2022;[Epub] CrossRef
CMTM6 as a candidate risk gene for cervical cancer: Comprehensive bioinformatics study
Xiaoting Huang, Wei Liu, Chunshan Liu, Jijie Hu, Baiyao Wang, Anbang Ren, Xiaona Huang, Yawei Yuan, Jinquan Liu, Mingyi Li
Frontiers in Molecular Biosciences.2022;[Epub] CrossRef
DNA damaging agents and DNA repair: From carcinogenesis to cancer therapy
Larissa Costa de Almeida, Felipe Antunes Calil, João Agostinho Machado-Neto, Leticia Veras Costa-Lotufo
Cancer Genetics.2021; 252-253: 6. CrossRef
Immunomodulation by targeted anticancer agents
Giulia Petroni, Aitziber Buqué, Laurence Zitvogel, Guido Kroemer, Lorenzo Galluzzi
Cancer Cell.2021; 39(3): 310. CrossRef
Targeting WEE1 by adavosertib inhibits the malignant phenotypes of hepatocellular carcinoma
Jian Chen, Xing Jia, Zequn Li, Wenfeng Song, Cheng Jin, Mengqiao Zhou, Haiyang Xie, Shusen Zheng, Penghong Song
Biochemical Pharmacology.2021; 188: 114494. CrossRef
WEE1 inhibition reverses trastuzumab resistance in HER2-positive cancers
Mei-Hua Jin, Ah-Rong Nam, Ju-Hee Bang, Kyoung-Seok Oh, Hye-Rim Seo, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh
Gastric Cancer.2021; 24(5): 1003. CrossRef
ATR inhibition amplifies antitumor effects of olaparib in biliary tract cancer
Ah-Rong Nam, Jeesun Yoon, Mei-Hua Jin, Ju-Hee Bang, Kyoung-Seok Oh, Hye-Rim Seo, Jae-Min Kim, Tae-Yong Kim, Do-Youn Oh
Cancer Letters.2021; 516: 38. CrossRef
Development of Immunotherapy Combination Strategies in Cancer
Timothy A. Yap, Eileen E. Parkes, Weiyi Peng, Justin T. Moyers, Michael A. Curran, Hussein A. Tawbi
Cancer Discovery.2021; 11(6): 1368. CrossRef
Therapeutic resistance in pancreatic ductal adenocarcinoma: Current challenges and future opportunities
Aditi Jain, Vikas Bhardwaj
World Journal of Gastroenterology.2021; 27(39): 6527. CrossRef
A steroidal saponin isolated from Allium chinense simultaneously induces apoptosis and autophagy by modulating the PI3K/Akt/mTOR signaling pathway in human gastric adenocarcinoma
Jingwen Xu, Mingmei Zhang, Xiaoying Lin, Yihai Wang, Xiangjiu He
Steroids.2020; : 108672. CrossRef

11,746 View
503 Download
33 Web of Science
29 Crossref

Therapeutic Targeting of the DNA Damage Response Using an ATR Inhibitor in Biliary Tract Cancer: Ah-Rong Nam, Mei Hua Jin, Ji Eun Park, Ju-Hee Bang, Do-Youn Oh, Yung-Jue Bang; Cancer Res Treat. 2019;51(3):1167-1179. Published online December 3, 2018; DOI: https://doi.org/10.4143/crt.2018.526

Abstract PDF PubReader ePub

Purpose
The DNA damage response (DDR) is a multi-complex network of signaling pathways involved in DNA damage repair, cell cycle checkpoints, and apoptosis. In the case of biliary tract cancer (BTC), the strategy of DDR targeting has not been evaluated, even though many patients have DNA repair pathway alterations. The purpose of this study was to test the DDR-targeting strategy in BTC using an ataxia-telangiectasia and Rad3-related (ATR) inhibitor.
Materials and Methods
A total of nine human BTC cell lines were used for evaluating anti-tumor effect of AZD6738 (ATR inhibitor) alone or combination with cytotoxic chemotherapeutic agents through MTT assay, colony-forming assays, cell cycle analyses, and comet assays. We established SNU478-mouse model for in vivo experiments to confirm our findings.
Results
Among nine human BTC cell lines, SNU478 and SNU869 were the most sensitive to AZD6738, and showed low expression of both ataxia-telangiectasia mutated (ATM) and p53. AZD6738 blocked p-Chk1 and p-glycoprotein and increased γH2AX, a marker of DNA damage, in sensitive cells. AZD6738 significantly increased apoptosis, G2/M arrest and p21, and decreased CDC2. Combinations of AZD6738 and cytotoxic chemotherapeutic agents exerted synergistic effects in colony-forming assays, cell cycle analyses, and comet assays. In our mouse models, AZD6738 monotherapy decreased tumor growth and the combination with cisplatin showed more potent effects on growth inhibition, decreased Ki-67, and increased terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling than monotherapy with each drug.
Conclusion
In BTC, DDR targeting strategy using ATR inhibitor demonstrated promising antitumor activity alone or in combination with cytotoxic chemotherapeutic agents. This supports further clinical development of DDR targeting strategy in BTC.

Citations

Citations to this article as recorded by

Ataxia telangiectasia and Rad3-related (ATR) inhibition by VE-822 potently reversed 5-flourouracil resistance in colorectal cancer cells through targeting DNA damage response
Ainaz Mihanfar, Faezeh Asghari, Maryam Majidinia
Molecular Biology Reports.2024;[Epub] CrossRef
Combined strategies with PARP inhibitors for the treatment of BRCA wide type cancer
Yijun Xie, Di Xiao, Duo Li, Mei Peng, Wei Peng, Huaxin Duan, Xiaoping Yang
Frontiers in Oncology.2024;[Epub] CrossRef
AZD6738 promotes the tumor suppressive effects of trifluridine in colorectal cancer cells
Shinnosuke Harata, Takuya Suzuki, Hiroki Takahashi, Takahisa Hirokawa, Akira Kato, Kaori Watanabe, Takeshi Yanagita, Hajime Ushigome, Kazuyoshi Shiga, Ryo Ogawa, Akira Mitsui, Masahiro Kimura, Yoichi Matsuo, Shuji Takiguchi
Oncology Reports.2023;[Epub] CrossRef
Therapeutic Targeting of DNA Replication Stress in Cancer
Long Gu, Robert J. Hickey, Linda H. Malkas
Genes.2023; 14(7): 1346. CrossRef
CRISPR screens guide the way for PARP and ATR inhibitor biomarker discovery
Emily M. Schleicher, George‐Lucian Moldovan
The FEBS Journal.2022; 289(24): 7854. CrossRef
Inhibition of WEE1 Potentiates Sensitivity to PARP Inhibitor in Biliary Tract Cancer
Hye-Rim Seo, Ah-Rong Nam, Ju-Hee Bang, Kyoung-Seok Oh, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh
Cancer Research and Treatment.2022; 54(2): 541. CrossRef
DNA Damage Response Inhibitors in Cholangiocarcinoma: Current Progress and Perspectives
Öykü Gönül Geyik, Giulia Anichini, Engin Ulukaya, Fabio Marra, Chiara Raggi
Cells.2022; 11(9): 1463. CrossRef
Aging and biliary tract cancers: Epidemiology, molecular biology, and clinical practice
Xiaoling Weng, Xiaoling Song, Rong Shao, Fatao Liu, Yingbin Liu
Aging and Cancer.2022; 3(2): 95. CrossRef
AZD6738 Inhibits fibrotic response of conjunctival fibroblasts by regulating checkpoint kinase 1/P53 and PI3K/AKT pathways
Longxiang Huang, Qin Ye, Chunlin Lan, Xiaohui Wang, Yihua Zhu
Frontiers in Pharmacology.2022;[Epub] CrossRef
AZD6738 decreases intraocular pressure and inhibits fibrotic response in trabecular meshwork through CHK1/P53 pathway
Longxiang Huang, Zhenni Wei, Xiaohui Wang, Chunlin Lan, Yihua Zhu, Qin Ye
Biochemical Pharmacology.2022; 206: 115340. CrossRef
Synergism of AZD6738, an ATR Inhibitor, in Combination with Belotecan, a Camptothecin Analogue, in Chemotherapy-Resistant Ovarian Cancer
Jin Hur, Mithun Ghosh, Tae Heon Kim, Nahee Park, Kamal Pandey, Young Bin Cho, Sa Deok Hong, Nar Bahadur Katuwal, Minsil Kang, Hee Jung An, Yong Wha Moon
International Journal of Molecular Sciences.2021; 22(3): 1223. CrossRef
ATR inhibition amplifies antitumor effects of olaparib in biliary tract cancer
Ah-Rong Nam, Jeesun Yoon, Mei-Hua Jin, Ju-Hee Bang, Kyoung-Seok Oh, Hye-Rim Seo, Jae-Min Kim, Tae-Yong Kim, Do-Youn Oh
Cancer Letters.2021; 516: 38. CrossRef
Targeting Cellular DNA Damage Responses in Cancer: An In Vitro-Calibrated Agent-Based Model Simulating Monolayer and Spheroid Treatment Responses to ATR-Inhibiting Drugs
Sara Hamis, James Yates, Mark A. J. Chaplain, Gibin G. Powathil
Bulletin of Mathematical Biology.2021;[Epub] CrossRef
The Role of the Hedgehog Pathway in Cholangiocarcinoma
Giulia Anichini, Laura Carrassa, Barbara Stecca, Fabio Marra, Chiara Raggi
Cancers.2021; 13(19): 4774. CrossRef
Targeting the DNA damage response: PARP inhibitors and new perspectives in the landscape of cancer treatment
Sofia Genta, Federica Martorana, Anastasios Stathis, Ilaria Colombo
Critical Reviews in Oncology/Hematology.2021; 168: 103539. CrossRef
Inhibition of ATR Increases the Sensitivity to WEE1 Inhibitor in Biliary Tract Cancer
Ah-Rong Nam, Mei-Hua Jin, Ju-Hee Bang, Kyoung-Seok Oh, Hye-Rim Seo, Do-Youn Oh, Yung-Jue Bang
Cancer Research and Treatment.2020; 52(3): 945. CrossRef
Drug resistance in cancer: mechanisms and tackling strategies
Tanweer Haider, Vikas Pandey, Nagma Banjare, Prem N. Gupta, Vandana Soni
Pharmacological Reports.2020; 72(5): 1125. CrossRef
Targeting P53 as a Future Strategy to Overcome Gemcitabine Resistance in Biliary Tract Cancers
Chiao-En Wu, Yi-Ru Pan, Chun-Nan Yeh, John Lunec
Biomolecules.2020; 10(11): 1474. CrossRef
ATM Inhibitor Suppresses Gemcitabine-Resistant BTC Growth in a Polymerase θ Deficiency-Dependent Manner
Yi-Ru Pan, Chiao-En Wu, Chun-Nan Yeh
Biomolecules.2020; 10(11): 1529. CrossRef
The Cancer Stem Cell Inhibitor Napabucasin (BBI608) Shows General Cytotoxicity in Biliary Tract Cancer Cells and Reduces Cancer Stem Cell Characteristics
Marlena Beyreis, Martin Gaisberger, Martin Jakab, Daniel Neureiter, Katharina Helm, Markus Ritter, Tobias Kiesslich, Christian Mayr
Cancers.2019; 11(3): 276. CrossRef
Inhibition of Wee1 sensitizes AML cells to ATR inhibitor VE-822-induced DNA damage and apoptosis
Wenxiu Qi, Xiaohao Xu, Manying Wang, Xiangyan Li, Chaonan Wang, Liping Sun, Daqing Zhao, Liwei Sun
Biochemical Pharmacology.2019; 164: 273. CrossRef

9,311 View
334 Download
21 Web of Science
21 Crossref

Disulfiram, a Re-positioned Aldehyde Dehydrogenase Inhibitor, Enhances Radiosensitivity of Human Glioblastoma Cells In Vitro: Hyeon Kang Koh, Soo Yeon Seo, Jin Ho Kim, Hak Jae Kim, Eui Kyu Chie, Seung-Ki Kim, Il Han Kim; Cancer Res Treat. 2019;51(2):696-705. Published online August 13, 2018; DOI: https://doi.org/10.4143/crt.2018.249

Abstract PDF PubReader ePub

Purpose
Glioblastoma, the most common brain tumor in adults, has poor prognosis. The purpose of this study was to determine the effect of disulfiram (DSF), an aldehyde dehydrogenase inhibitor, on in vitro radiosensitivity of glioblastoma cells with different methylation status of O⁶-methylguanine-DNA methyltransferase (MGMT) promoter and the underlying mechanism of such effect.
Materials and Methods
Five human glioblastoma cells (U138MG, T98G, U251MG, U87MG, and U373MG) and one normal human astrocyte (NHA) cell were cultured and treated with DSF or 6MV X-rays (0, 2, 4, 6, and 8 Gy). For combined treatment, cells were treated with DSF before irradiation. Surviving fractions fit from cell survival based on colony forming ability. Apoptosis, DNA damage repair, and cell cycle distributionwere assayed bywestern blot for cleaved caspase-3, γH2AX staining, and flow cytometry, respectively.
Results
DSF induced radiosensitization in most of the glioblastoma cells, especially, in the cells with radioresistance as wildtype unmethylated promoter (MGMT-wt), but did not in normal NHA cell. DSF augmented or induced cleavage of caspase-3 in all cells after irradiation. DSF inhibited repair of radiation-induced DNA damage in MGMT-wt cells, but not in cells with methylated MGMT promoter. DSF abrogated radiation-induced G2/M arrest in T98G and U251MG cells.
Conclusion
Radiosensitivity of glioblastoma cells were preferentially enhanced by pre-irradiation DSF treatment compared to normal cell, especially radioresistant cells such as MGMT-wt cells. Induction of apoptosis or inhibition of DNA damage repair may underlie DSF-induced radiosensitization. Clinical benefit of combining DSF with radiotherapy should be investigated in the future.

Citations

Citations to this article as recorded by

The role of KDM4A‐mediated histone methylation on temozolomide resistance in glioma cells through the HUWE1/ROCK2 axis
Xi‐Xi Li, Jia‐Kun Xu, Wei‐Jie Su, Hong‐Lin Wu, Kun Zhao, Chang‐Ming Zhang, Xiang‐Kun Chen, Li‐Xuan Yang
The Kaohsiung Journal of Medical Sciences.2024; 40(2): 161. CrossRef
Glioblastoma Therapy: Past, Present and Future
Elena Obrador, Paz Moreno-Murciano, María Oriol-Caballo, Rafael López-Blanch, Begoña Pineda, Julia Gutiérrez-Arroyo, Alba Loras, Luis Gonzalez-Bonet, Conrado Martinez-Cadenas, José Estrela, María Marqués-Torrejón
International Journal of Molecular Sciences.2024; 25(5): 2529. CrossRef
Exploring Disulfiram’s Anticancer Potential: PLGA Nano-Carriers for Prolonged Drug Delivery and Potential Improved Therapeutic Efficacy
Ibrahim Dumbuya, Ana Maria Pereira, Ibrahim Tolaymat, Adnan Al Dalaty, Basel Arafat, Matt Webster, Barbara Pierscionek, Mouhamad Khoder, Mohammad Najlah
Nanomaterials.2024; 14(13): 1133. CrossRef
Targeting Retinaldehyde Dehydrogenases to Enhance Temozolomide Therapy in Glioblastoma
Rafael Jiménez, Andrada Constantinescu, Muhube Yazir, Paula Alfonso-Triguero, Raquel Pequerul, Xavier Parés, Mileidys Pérez-Alea, Ana Paula Candiota, Jaume Farrés, Julia Lorenzo
International Journal of Molecular Sciences.2024; 25(21): 11512. CrossRef
Clinical, pharmacological, and formulation evaluation of disulfiram in the treatment of glioblastoma - a systematic literature review
Beáta-Mária Benkő, Dimitrios A. Lamprou, Anna Sebestyén, Romána Zelkó, István Sebe
Expert Opinion on Drug Delivery.2023; 20(4): 541. CrossRef
Effect of Disulfiram and Copper Plus Chemotherapy vs Chemotherapy Alone on Survival in Patients With Recurrent Glioblastoma
Katja Werlenius, Sara Kinhult, Tora Skeidsvoll Solheim, Henriette Magelssen, David Löfgren, Munila Mudaisi, Sofia Hylin, Jiri Bartek, Michael Strandéus, Magnus Lindskog, Havyan Bahroz Rashid, Louise Carstam, Sasha Gulati, Ole Solheim, Jiri Bartek, Øyvind
JAMA Network Open.2023; 6(3): e234149. CrossRef
Disulfiram/Copper induces antitumor activity against gastric cancer via the ROS/MAPK and NPL4 pathways
Yao Liu, Xin Guan, Meiling Wang, Naixue Wang, Yutong Chen, Baolei Li, Zhuxuan Xu, Fangwei Fu, Cheng Du, Zhendong Zheng
Bioengineered.2022; 13(3): 6579. CrossRef
Disulfiram in glioma: Literature review of drug repurposing
Shiyu Zhong, Shengyu Liu, Xin Shi, Xudong Zhang, Kunhang Li, Guojun Liu, Lishuai Li, Shanwei Tao, Bowen Zheng, Weichen Sheng, Ziyin Ye, Qichen Xing, Qingqing Zhai, Lijie Ren, Ying Wu, Yijun Bao
Frontiers in Pharmacology.2022;[Epub] CrossRef
Multimodal targeting of glioma with functionalized nanoparticles
Hany E. Marei
Cancer Cell International.2022;[Epub] CrossRef
Formulation Comprising Arsenic Trioxide and Dimercaprol Enhances Radiosensitivity of Pancreatic Cancer Xenografts
Renyan Tang, Jianmin Zhu, Ying Liu, Ning Wu, Jinbin Han
Technology in Cancer Research & Treatment.2021;[Epub] CrossRef
Antioxidant and Antiproliferative Activity of Finasteride against Glioblastoma Cells
Hyeon Ji Kim, Tae-Jun Kim, Yu Gyung Kim, Chaeeun Seong, Jin-Hwa Cho, Wanil Kim, Kyung-Ha Lee, Do-Yeon Kim
Pharmaceutics.2021; 13(9): 1410. CrossRef
Disulfiram Sensitizes a Therapeutic-Resistant Glioblastoma to the TGF-β Receptor Inhibitor
Chan-Chuan Liu, Cheng-Lin Wu, Meng-Xuan Lin, Chun-I Sze, Po-Wu Gean
International Journal of Molecular Sciences.2021; 22(19): 10496. CrossRef
Repurposing Disulfiram for Targeting of Glioblastoma Stem Cells: An In Vitro Study
Lisa Zirjacks, Nicolai Stransky, Lukas Klumpp, Lukas Prause, Franziska Eckert, Daniel Zips, Sabine Schleicher, Rupert Handgretinger, Stephan M. Huber, Katrin Ganser
Biomolecules.2021; 11(11): 1561. CrossRef
The combination of disulfiram and copper for cancer treatment
Hong Li, Jingyu Wang, Chunfu Wu, Lihui Wang, Zhe-Sheng Chen, Wei Cui
Drug Discovery Today.2020; 25(6): 1099. CrossRef
Radiosensitizing high-Z metal nanoparticles for enhanced radiotherapy of glioblastoma multiforme
Jinyeong Choi, Gaeun Kim, Su Bin Cho, Hyung-Jun Im
Journal of Nanobiotechnology.2020;[Epub] CrossRef
Disulfiram as a Therapeutic Agent for Metastatic Malignant Melanoma—Old Myth or New Logos?
Francisco Meraz-Torres, Sarah Plöger, Claus Garbe, Heike Niessner, Tobias Sinnberg
Cancers.2020; 12(12): 3538. CrossRef
Repurposing Disulfiram as An Anti-Cancer Agent: Updated Review on Literature and Patents
Elmira Ekinci, Sagar Rohondia, Raheel Khan, Qingping P. Dou
Recent Patents on Anti-Cancer Drug Discovery.2019; 14(2): 113. CrossRef

9,244 View
297 Download
20 Web of Science
17 Crossref

CCR6 Is a Predicting Biomarker of Radiosensitivity and Potential Target of Radiosensitization in Rectal Cancer: Hui Chang, Jia-wang Wei, Ya-lan Tao, Pei-rong Ding, Yun-fei Xia, Yuan-hong Gao, Wei-wei Xiao; Cancer Res Treat. 2018;50(4):1203-1213. Published online December 21, 2017; DOI: https://doi.org/10.4143/crt.2017.538

Abstract PDF Supplementary Material PubReader ePub

Purpose
This study aimed to explore the functions and mechanisms of C-C motif chemokine receptor 6 (CCR6), a gene associated with progression and metastasis of colorectal cancer (CRC), in radiosensitivity of rectal cancer (RC).
Materials and Methods
RNA sequencing and immunohistochemical analysis on CCR6 expression were performed in pretreatment tissues of RC patients exhibiting different therapeutic effects of radiotherapy. Colonogenic survival assay was conducted in different CRC cell lines to assess their radiosensitivity. And the impact of CCR6 expression on radiosensitivity was validated through RNA interference. The DNA damage repair (DDR) abilities of cell lines with different CCR6 expression were evaluated through immunofluorescence-based γH2AX quantification.
Results
The CCR6 mRNA level was higher in patients without pathologic complete remission (pCR) than in those with pCR (fold changed, 2.11; p=0.004). High-level expression of CCR6 protein was more common in the bad responders than in the good responders (76.3% vs. 37.5%, p < 0.001). The CRC cell lines with higher CCR6 expression (LoVo and sw480) appeared to be more radioresistant, compared with the sw620 cell line which had lower CCR6 expression. CCR6 knockdown made the LoVo cells more sensitive to ionizing radiation (sensitization enhancement ratio, 1.738; p < 0.001), and decreased their DDR efficiency.
Conclusion
CCR6 might affect the RC radiosensitivity through DDR process. These findings supported CCR6 as a predicting biomarker of radiosensitivity and a potential target of radiosensitization for RC patients.

Citations

Citations to this article as recorded by

Mechanisms of radioresistance and the underlying signaling pathways in colorectal cancer cells
Josiane W. Tessmann, Murilo R. Rocha, Jose A. Morgado‐Díaz
Journal of Cellular Biochemistry.2023; 124(1): 31. CrossRef
Nuclear Factor Erythroid 2-Related Factor 2/Kelch-Like ECH-Associated Protein 1 as a Predictor of Prognosis and Radiotherapy Resistance in Patients With Locally Advanced Rectal Cancer: A Prospective Analysis
Ji Min Park, Shin Kim, Sung Uk Bae, Sang Jun Byun, Incheol Seo, Hye Won Lee
Journal of Korean Medical Science.2023;[Epub] CrossRef
Radiotherapy resistance: identifying universal biomarkers for various human cancers
Irina Larionova, Militsa Rakina, Elena Ivanyuk, Yulia Trushchuk, Alena Chernyshova, Evgeny Denisov
Journal of Cancer Research and Clinical Oncology.2022; 148(5): 1015. CrossRef
Predicting response to neoadjuvant chemoradiotherapy in rectal cancer: from biomarkers to tumor models
Moying Li, Qiyun Xiao, Nachiyappan Venkatachalam, Ralf-Dieter Hofheinz, Marlon R. Veldwijk, Carsten Herskind, Matthias P. Ebert, Tianzuo Zhan
Therapeutic Advances in Medical Oncology.2022;[Epub] CrossRef
131I-C19 Iodide Radioisotope and Synthetic I-C19 Compounds as K-Ras4B–PDE6δ Inhibitors: A Novel Approach against Colorectal Cancer—Biological Characterization, Biokinetics and Dosimetry
Pedro Cruz-Nova, Blanca Ocampo-García, Dayan Andrea Carrión-Estrada, Paola Briseño-Diaz, Guillermina Ferro-Flores, Nallely Jiménez-Mancilla, José Correa-Basurto, Martiniano Bello, Libia Vega-Loyo, María del Rocío Thompson-Bonilla, Rosaura Hernández-Rivas,
Molecules.2022; 27(17): 5446. CrossRef
Regulation of pancreatic cancer therapy resistance by chemokines
Shailendra K. Gautam, Soumi Basu, Abhijit Aithal, Nidhi V. Dwivedi, Mansi Gulati, Maneesh Jain
Seminars in Cancer Biology.2022; 86: 69. CrossRef
Biomarkers for Predicting the Response to Radiation-Based Neoadjuvant Therapy in Rectal Cancer
Yuhong Chen, Biao Yang, Mingyang Chen, Zhaojun Li, Zhengyin Liao
Frontiers in Bioscience-Landmark.2022;[Epub] CrossRef
Cancer Stem Cell Biomarkers Predictive of Radiotherapy Response in Rectal Cancer: A Systematic Review
Marzia Mare, Lorenzo Colarossi, Veronica Veschi, Alice Turdo, Dario Giuffrida, Lorenzo Memeo, Giorgio Stassi, Cristina Colarossi
Genes.2021; 12(10): 1502. CrossRef
ceRNA Networks: The Backbone Role in Neoadjuvant Chemoradiotherapy Resistance/Sensitivity of Locally Advanced Rectal Cancer
Lin He, Hao Chang, Yuhong Qi, Bing Zhang, Qiuju Shao
Technology in Cancer Research & Treatment.2021;[Epub] CrossRef
Antitumor and Anti-Metastatic Effects of Citral-Loaded Nanostructured Lipid Carrier in 4T1-Induced Breast Cancer Mouse Model
Noraini Nordin, Swee Keong Yeap, Heshu Sulaiman Rahman, Nur Rizi Zamberi, Nurul Elyani Mohamad, Nadiah Abu, Mas Jaffri Masarudin, Rasedee Abdullah, Noorjahan Banu Alitheen
Molecules.2020; 25(11): 2670. CrossRef
Andrographolide enhanced radiosensitivity by downregulating glycolysis via the inhibition of the PI3K-Akt-mTOR signaling pathway in HCT116 colorectal cancer cells
Xiaofei Li, Ruifang Tian, Lan Liu, Lihui Wang, Dong He, Ke Cao, John K. Ma, Chenghui Huang
Journal of International Medical Research.2020;[Epub] CrossRef
Exploring the radiosensitizing potential of AZD8931: a pilot study on the human LoVo colorectal cancer cell line
Cinzia Antognelli, Isabella Palumbo, Simonetta Piattoni, Monica Calzuola, Beatrice Del Papa, Vincenzo N. Talesa, Cynthia Aristei
International Journal of Radiation Biology.2020; 96(11): 1504. CrossRef
The expression of long noncoding RNA CRCAL‐3 in colorectal cancer and its impacts on cell proliferation and migration
Hui Chang, Guan‐Nan Wang, Ya‐Lan Tao
Journal of Cellular Biochemistry.2019; 120(9): 15369. CrossRef
Pleiotropic Immune Functions of Chemokine Receptor 6 in Health and Disease
Ranmali Ranasinghe, Rajaraman Eri
Medicines.2018; 5(3): 69. CrossRef
Autophagy-regulating microRNAs: potential targets for improving radiotherapy
Hongbin Li, Xiaodong Jin, Bing Chen, Ping Li, Qiang Li
Journal of Cancer Research and Clinical Oncology.2018; 144(9): 1623. CrossRef

9,875 View
220 Download
15 Web of Science
15 Crossref

Interactome Analysis Reveals that Heterochromatin Protein 1γ (HP1γ) Is Associated with the DNA Damage Response Pathway: Hongtae Kim, Jae Duk Choi, Byung-Gyu Kim, Ho Chul Kang, Jong-Soo Lee; Cancer Res Treat. 2016;48(1):322-333. Published online March 6, 2015; DOI: https://doi.org/10.4143/crt.2014.294

Abstract PDF Supplementary Material PubReader ePub

Purpose
Heterochromatin protein 1γ (HP1γ) interacts with chromosomes by binding to lysine 9-methylated histone H3 or DNA/RNA. HP1γ is involved in various biological processes. The purpose of this study is to gain an understanding of how HP1γ functions in these processes by identifying HP1γ-binding proteins using mass spectrometry.
Materials and Methods
We performed affinity purification of HP1γ-binding proteins using G1/S phase or prometaphase HEK293T cell lysates that transiently express mock or FLAG-HP1γ. Coomassie staining was performed for HP1γ-binding complexes, using cell lysates prepared by affinity chromatography FLAG-agarose beads, and the bands were digested and then analyzed using a mass spectrometry.
Results
We identified 99 HP1γ-binding proteins with diverse cellular functions, including spliceosome, regulation of the actin cytoskeleton, tight junction, pathogenic Escherichia coli infection, mammalian target of rapamycin signaling pathway, nucleotide excision repair, DNA replication, homologous recombination, and mismatch repair.
Conclusion
Our results suggested that HP1γ is functionally active in DNA damage response via proteinprotein interaction.

Citations

Citations to this article as recorded by

Inhibition of annexin A7 suppresses senescence‐associated heterochromatin foci formation and senescence through the AMPK/mTOR pathway in human dermal fibroblasts
Nan Li, Xiaomeng Yan, Xiaoling Cui, Congyao Zhao, Zhaomin Lin, Junying Miao
Journal of Cellular Biochemistry.2023; 124(10): 1603. CrossRef
Clinicopathological significance of CBX3 in colorectal cancer: An intensive expression study based on formalin‐fixed and paraffin‐embedded tissues
Hai Wang, Wenyue Zhao, Jiandong Wang, Zhiyuan Zhang
Pathology International.2022; 72(2): 107. CrossRef
Discovery, expression, cellular localization, and molecular properties of a novel, alternative spliced HP1γ isoform, lacking the chromoshadow domain
Angela Mathison, Thiago Milech De Assuncao, Nikita R. Dsouza, Monique Williams, Michael T. Zimmermann, Raul Urrutia, Gwen Lomberk, Albert Jeltsch
PLOS ONE.2020; 15(2): e0217452. CrossRef
CBX3 Promotes Gastric Cancer Progression and Affects Factors Related to Immunotherapeutic Responses

Hexin Lin, Jiabian Lian, Lu Xia, Guoxian Guan, Jun You
Cancer Management and Research.2020; Volume 12: 10113. CrossRef
Cbx3 inhibits vascular smooth muscle cell proliferation, migration, and neointima formation
Cheng Zhang, Dan Chen, Eithne Margaret Maguire, Shiping He, Jiangyong Chen, Weiwei An, Mei Yang, Tayyab Adeel Afzal, Le Anh Luong, Li Zhang, Han Lei, Qingchen Wu, Qingzhong Xiao
Cardiovascular Research.2018; 114(3): 443. CrossRef

11,591 View
103 Download
6 Web of Science
5 Crossref

Activation of ATM-dependent DNA Damage Signal Pathway by a Histone Deacetylase Inhibitor, Trichostatin A: Jong-Soo Lee; Cancer Res Treat. 2007;39(3):125-130. Published online September 30, 2007; DOI: https://doi.org/10.4143/crt.2007.39.3.125

Abstract PDF PubReader ePub

Purpose

Ataxia-telangiectasia mutated (ATM) kinase regulates diverse cellular DNA damage responses, including genome surveillance, cell growth, and gene expression. While the role of histone acetylation/deacetylation in gene expression is well established, little is known as to whether this modification can activate an ATM-dependent signal pathway, and whether this modification can thereby be implicated in an ATM-mediated DNA damage response.

Materials and Methods

Formation of H2AXγ foci was examined in HeLa and U₂OS cells following treatment with a histone deacetylase inhibitor, Trichostatin A (TSA). We determine an ATM-dependency of the TSA-induced DNA damage signal pathway using isogenic A-T (ATM^-) and control (ATM⁺) cells. We monitored the phosphorylation of ATM, an ATM-downstream effector kinase, Chk2, and H2AXγ to detect the activation of the ATM-de pendent DNA damage signal pathway.

Results

Exposure of cells to TSA results in the formation of H2AXγ foci in HeLa and U₂OS cells. The TSA-induced formation of H2AXγ foci occurs in an ATM-dependent manner. TSA induces phosphorylation of serine 1981 of ATM, accumulation of phosphorylated H2AX and Chk2, and formation of H2AX foci, in a manner analogous to genotoxic DNA damage.

Conclusion

In this work, we show that TSA induces a DNA damage signaling pathway in an ATM-dependent manner. These results suggest that ATM can respond to altered histone acetylation induced by the histone deacetylase inhibitor, TSA.

Citations

Citations to this article as recorded by

Making gene editing accessible in resource limited environments: recommendations to guide a first-time user
Shivani Goolab, Janine Scholefield
Frontiers in Genome Editing.2024;[Epub] CrossRef
Increased DNA damage in full-grown oocytes is correlated with diminished autophagy activation
Fei Sun, Nourhan Nashat Ali, Daniela Londoño-Vásquez, Constantine A. Simintiras, Huanyu Qiao, M. Sofia Ortega, Yuksel Agca, Masashi Takahashi, Rocío M. Rivera, Andrew M. Kelleher, Peter Sutovsky, Amanda L. Patterson, Ahmed Z. Balboula
Nature Communications.2024;[Epub] CrossRef
Modulating CRISPR/Cas9 genome-editing activity by small molecules
Siwei Chen, Deng Chen, Bin Liu, Hidde J. Haisma
Drug Discovery Today.2022; 27(4): 951. CrossRef
Genetic variations in ATM and H2AX loci contribute to risk of hematological abnormalities in individuals exposed to BTEX chemicals
Samaneh Jafari Roshan, Yaser Mansoori, Seyed Reza Hosseini, Davood Sabour, Abdolreza Daraei
Journal of Clinical Laboratory Analysis.2022;[Epub] CrossRef
TSA Promotes CRISPR/Cas9 Editing Efficiency and Expression of Cell Division-Related Genes from Plant Protoplasts
Seung Hee Choi, Myoung Hui Lee, Da Mon Jin, Su Ji Ju, Woo Seok Ahn, Eun Yee Jie, Ji Min Lee, Jiyoung Lee, Cha Young Kim, Suk Weon Kim
International Journal of Molecular Sciences.2021; 22(15): 7817. CrossRef
Targeting repair pathways with small molecules increases precise genome editing in pluripotent stem cells
Stephan Riesenberg, Tomislav Maricic
Nature Communications.2018;[Epub] CrossRef
CCR6 Is a Predicting Biomarker of Radiosensitivity and Potential Target of Radiosensitization in Rectal Cancer
Hui Chang, Jia-wang Wei, Ya-lan Tao, Pei-rong Ding, Yun-fei Xia, Yuan-hong Gao, Wei-wei Xiao
Cancer Research and Treatment.2018; 50(4): 1203. CrossRef
CBP/p300 acetyltransferases regulate the expression of NKG2D ligands on tumor cells
M Sauer, M Schuldner, N Hoffmann, A Cetintas, K S Reiners, O Shatnyeva, M Hallek, H P Hansen, S Gasser, E P von Strandmann
Oncogene.2017; 36(7): 933. CrossRef
Myelodysplasia-associated mutations in serine/arginine-rich splicing factor SRSF2 lead to alternative splicing of CDC25C
Lindsey Skrdlant, Jeremy M. Stark, Ren-Jang Lin
BMC Molecular Biology.2016;[Epub] CrossRef
Loss of H3K9me3 Correlates with ATM Activation and Histone H2AX Phosphorylation Deficiencies in Hutchinson-Gilford Progeria Syndrome
Haoyue Zhang, Linlin Sun, Kun Wang, Di Wu, Mason Trappio, Celeste Witting, Kan Cao, Michael Shing-Yan Huen
PLOS ONE.2016; 11(12): e0167454. CrossRef
Survival of primary, but not of cancer cells after combined Plk1-HDAC inhibition
Lisa Lange, Peter Hemmerich, Birgit Spänkuch
Oncotarget.2015; 6(28): 25801. CrossRef
A Small-Molecule Probe of the Histone Methyltransferase G9a Induces Cellular Senescence in Pancreatic Adenocarcinoma
Yuan Yuan, Qiu Wang, Joshiawa Paulk, Stefan Kubicek, Melissa M. Kemp, Drew J. Adams, Alykhan F. Shamji, Bridget K. Wagner, Stuart L. Schreiber
ACS Chemical Biology.2012; 7(7): 1152. CrossRef
Development of a High-Content High-Throughput Screening Assay for the Discovery of ATM Signaling Inhibitors
Catherine Bardelle, Joanna Boros
SLAS Discovery.2012; 17(7): 912. CrossRef
The MRN complex in double‐strand break repair and telomere maintenance
Brandon J. Lamarche, Nicole I. Orazio, Matthew D. Weitzman
FEBS Letters.2010; 584(17): 3682. CrossRef
ATM modulates transcription in response to histone deacetylase inhibition as part of its DNA damage response
Eun Ryoung Jang, Jae Duk Choi, Mi Ae Park, Gajin Jeong, Hyeseong Cho, Jong-Soo Lee
Experimental and Molecular Medicine.2010; 42(3): 195. CrossRef
Modulating Polo-Like Kinase 1 as a Means for Cancer Chemoprevention
Travis L. Schmit, Mark C. Ledesma, Nihal Ahmad
Pharmaceutical Research.2010; 27(6): 989. CrossRef

9,426 View
75 Download
16 Crossref

Review Article

p63 and p73 in Tumor Suppression and Promotion: Frank D. McKeon; Cancer Res Treat. 2004;36(1):6-12. Published online February 29, 2004; DOI: https://doi.org/10.4143/crt.2004.36.1.6

Abstract PDF PubReader ePub

The recent discovery of two genes, termed p63 and p73, encoding transcription factors highly homologous to p53 presents unexpected challenges and opportunities for the understanding and treatment of cancers. The questions raised are many but center on determining whether these new genes possess novel tumor suppressor functions, cooperate with p53, or impart oncogenic effects. At present there is considerable discord in the field concerning these concepts with some favoring a tumor suppressor role for the p53 family members and others an oncogenic influence. In support of a tumor suppressor role is the ability of p73 and p63 isoforms to transactivate p53 target genes and the large body of work linking p73, and to some extent p63, in apoptotic events in response to cellular stresses generally considered the purview of p53. More recently, p73 has been implicated in cell death following T cell activation, the response of cancers to chemotherapy, and finally, along with p63, to the function of p53 itself. Opposing this view is the fact that the p73 and p63 genes are rarely mutated in cancers and the stark absence of tumors in the p73 null mouse. Moreover, the high expression of dominant negative (dn) versions of the p73 and p63 proteins supports an anti-p53 function and therefore possibly an oncogenic effect. Indeed, the p63 gene is located in a region of chromosome three amplified in squamous cell carcinomas and the number of reports of dn-p63 overexpression in these diseases is increasing. This review will examine both sides of these arguments in an attempt to decipher common themes and to identify opportunities these genes represent for understanding tumorigenesis.

Citations

Citations to this article as recorded by

p53 amyloid pathology is correlated with higher cancer grade irrespective of the mutant or wild-type form
Shinjinee Sengupta, Namrata Singh, Ajoy Paul, Debalina Datta, Debdeep Chatterjee, Semanti Mukherjee, Laxmikant Gadhe, Jyoti Devi, Yeshwanth Mahesh, Mohit Kumar Jolly, Samir K. Maji
Journal of Cell Science.2023;[Epub] CrossRef
Genome-Wide Identification of Autophagy Prognostic Signature in Pancreatic Cancer
Jianfa Yu, Qi Lang, Chongli Zhong, Shuang Wang, Yu Tian
Dose-Response.2021; 19(2): 155932582110232. CrossRef
A Newly Defined Pyroptosis-Related Gene Signature for the Prognosis of Bladder Cancer
Weikang Chen, Wenhao Zhang, Tao Zhou, Jian Cai, Zhixian Yu, Zhigang Wu
International Journal of General Medicine.2021; Volume 14: 8109. CrossRef
ΔNp63 to TAp63 expression ratio as a potential molecular marker for cervical cancer prognosis
Sunyoung Park, Suji Lee, Jungho Kim, Geehyuk Kim, Kwang Hwa Park, Tae Ue Kim, Dawn Chung, Hyeyoung Lee, Hiromu Suzuki
PLOS ONE.2019; 14(4): e0214867. CrossRef
Identification of a novel microRNA-mRNA regulatory biomodule in human prostate cancer
Yanqiong Zhang, Funeng Jiang, Huichan He, Jianheng Ye, Xia Mao, Qiuyan Guo, Shu-lin Wu, Weide Zhong, Chin-Lee Wu, Na Lin
Cell Death & Disease.2018;[Epub] CrossRef
p53 family members — important messengers in cell death signaling in photodynamic therapy of cancer?
Pilar Acedo, Joanna Zawacka-Pankau
Photochemical & Photobiological Sciences.2015; 14(8): 1389. CrossRef

10,296 View
81 Download
6 Crossref

First
Prev
Page of 1
Next
Last

Search