Cancer Research and Treatment

Original Articles

Genitourinary cancer

Physical Activity and Bladder Cancer Risk: Findings of the Japan Collaborative Cohort Study: Hang An, Keyang Liu, Kokoro Shirai, Ryo Kawasaki, Akiko Tamakoshi, Hiroyasu Iso; Cancer Res Treat. 2024;56(2):616-623. Published online October 6, 2023; DOI: https://doi.org/10.4143/crt.2023.962

Abstract PDF Supplementary Material PubReader ePub: Purpose
The association of physical activity with the risk of bladder cancer remains inconsistent among Asian populations. We aimed to examine the association in a large Japanese cohort.
Materials and Methods
In a population-based prospective cohort study, a total of 50,374 Japanese adults aged 40-79 years without a history of cancer or cardiovascular disease who had information on physical activity from self-administrated questionnaires were used for analysis. We performed Cox proportional hazard models to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for incident bladder cancer after adjusting for several potential confounders.
Results
During the median 17.5 years of follow-up, 153 incident bladder cancers (116 men and 37 women) were identified. After the multivariable adjustment, HRs (95% CI) of bladder cancer concerning those with recreational sports participation of 1-2 hr/wk, 3-4 hr/wk, and 5 hr/wk and more were 0.67 (0.38-1.20), 0.79 (0.36-1.74), and 0.28 (0.09-0.89), respectively (p for trend=0.017). Compared with mostly sitting at the workplace, occupational physical activity of standing and walking were associated with a lower risk of bladder cancer (HR, 0.53 [95% CI, 0.32 to 0.85]). Hours of daily walking were not associated with the risk. The lower risk of bladder cancer was more evident for recreational sports (HR, 0.33 [95% CI, 0.10 to 1.00]), and for occupational standing and walking activity at work (HR, 0.57 [95% CI, 0.33 to 0.98]) among men.
Conclusion
Recreational sports participation and occupational physical activity were inversely associated with the risk of bladder cancer among Japanese, especially in men.

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General

Perspectives on Professional Burnout and Occupational Stress among Medical Oncologists: A Cross-sectional Survey by Korean Society for Medical Oncology (KSMO): Yun-Gyoo Lee, Chi Hoon Maeng, Do Yeun Kim, Bong-Seog Kim; Cancer Res Treat. 2020;52(4):1002-1009. Published online July 10, 2020; DOI: https://doi.org/10.4143/crt.2020.190

Abstract PDF PubReader ePub

Purpose
This study aimed to investigate the prevalence and risk factors of burnout and occupational stress among medical oncologists in Korea.
Methods
A survey was conducted of medical oncologists who were members of Korean Society for Medical Oncology (KSMO) using the Korean Occupational Stress Scale, the validated Maslach Burnout Inventory (MBI) and supplemental questions about work and lifestyle factors.
Results
Among 220 active KSMO members, 111 responses were collected. The median age was 42 years (range, 32 to 63 years). Two-thirds of responders worked 6 days per week and half of them worked a total of 60-80 hours per week. Each medical oncologist treated a median of 90-120 patients per week in outpatient clinics and 20-30 patients per week in patient practices. MBI subscales indicated a high level of emotional exhaustion in 74%, a high level of depersonalization in 86%, and a low level of personal accomplishment in 65%: 68% had professional burnout according to high emotional exhaustion and high depersonalization scores. The risk of burnout was higher for medical oncologists aged from 30-39 than 40-49 years, and unmarried than married. Considering personal accomplishment, females had a higher risk of burnout. The median score of occupational stress was 63 (range, 43 to 88). Having night-duty call was the strongest risk factor on more stress. A higher stress score was associated with a higher prevalence of burnout.
Conclusion
Burnout and occupational stress are quite common amongst Korean medical oncologists. Achieving a healthy work-life balance, ensuring balanced workload distribution, and engaging in proper stress relief solutions are necessary.

Citations

Citations to this article as recorded by

Job stress and burnout affecting the mental health of Korean medical faculty members: constructing causality among latent variables
Ji-Hyun Seo, Hwa-ok Bae
Korean Journal of Medical Education.2024; 36(1): 27. CrossRef
Pilotstudie zu beruflicher Gratifikation und Gesundheit
I. Böckelmann, I. Zavgorodnii, O. Litovchenko, M. Krasnoselskyi, B. Thielmann
Zentralblatt für Arbeitsmedizin, Arbeitsschutz und Ergonomie.2024; 74(3): 118. CrossRef
Associations among the workplace violence, burnout, depressive symptoms, suicidality, and turnover intention in training physicians: a network analysis of nationwide survey
Je-Yeon Yun, Sun Jung Myung, Kyung Sik Kim
Scientific Reports.2023;[Epub] CrossRef
Work-Related Stress, Health Status, and Status of Health Apps Use in Korean Adult Workers
Won Ju Hwang, Minjeong Kim
International Journal of Environmental Research and Public Health.2022; 19(6): 3197. CrossRef

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Invasion-Metastasis by Hepatocyte Growth Factor/c-Met Signaling Concomitant with Induction of Urokinase Plasminogen Activator in Human Pancreatic Cancer: Role as Therapeutic Target: Kyung Hee Lee, Myung Soo Hyun, Jae Ryong Kim; Cancer Res Treat. 2003;35(3):207-212. Published online June 30, 2003; DOI: https://doi.org/10.4143/crt.2003.35.3.207

Abstract PDF

PURPOSE
Increased expression of the hepatocytes growth factor (HGF) receptor (c-Met) and urokinase type plasminogen activator (uPA) correlate with the development and metastasis of cancers. However, the mechanisms by which HGF/c-Met signaling mediate cancer progression and metastasis are unclear. Therefore, we investigated the roles of HGF/c-Met in tumor progression and metastasis in pancreatic cancer cell lines, L3.6PL and IMIN-PC2. MATERIALS AND METHODS: To see the functional c-Met protein, we were performed immunoprecipitation for functional c-Met protein. And also performed western bolot analysis and gel zymography for the functional uPA protein. To see the inhibition effects of uPAR monoclonal antibody on invasiveness of two pancreatic cancer cell lines, we were carried out standard two chamber invasion assay. RESULTS: At first, we observed the HGF-mediated c-Met phosphorylation and cell growth. c-Met phosphorylation was increased in the HGF-treated cells in a dose dependent manner. HGF resulted in increments of cell growth and ERK phosphorylation. HGF treatment increased the uPA expression and the uPA activity. A monoclonal antibody 3936, specific to uPAR receptor, inhibited HGF- mediated tumor cell invasion in a dose dependent manner.
CONCLUSION
These results suggest that functional c- Met and HGF/c-Met signaling up-regulate the activity of uPA and result in increments of invasion-metastasis in the pancreatic cancer cells.

Citations

Citations to this article as recorded by

PP2A complex disruptor SET prompts widespread hypertranscription of growth-essential genes in the pancreatic cancer cells
He Xu, Di Wu, Mingming Xiao, Yubin Lei, Yalan Lei, Xianjun Yu, Si Shi
Science Advances.2024;[Epub] CrossRef
Reactive oxygen species regulate the generation of urokinase plasminogen activator in human hepatoma cells via MAPK pathways after treatment with hepatocyte growth factor
Kyung Hee Lee, Jae-Ryong Kim
Experimental and Molecular Medicine.2009; 41(3): 180. CrossRef
Reactive oxygen species regulate urokinase plasminogen activator expression and cell invasion via mitogen-activated protein kinase pathways after treatment with hepatocyte growth factor in stomach cancer cells
Kyung Hee Lee, Sang Woon Kim, Jae-Ryong Kim
Journal of Experimental & Clinical Cancer Research.2009;[Epub] CrossRef
Cellular Mechanisms of Hepatocyte Growth Factor-Mediated Urokinase Plasminogen Activator Secretion by MAPK Signaling in Hepatocellular Carcinoma
Kyung Hee Lee, Eun Young Choi, Myung Soo Hyun, Jong Ryul Eun, Byung Ik Jang, Tae Nyeun Kim, Heon Ju Lee, Dong Shik Lee, Sung Su Yun, Hong Jīn Kim, Jung Hye Kim, Jae-Ryong Kim
Tumori Journal.2008; 94(4): 523. CrossRef
Association of Extracellular Cleavage of E-Cadherin Mediated by MMP-7 with HGF-Induced in vitro Invasion in Human Stomach Cancer Cells
K.H. Lee, E.Y. Choi, M.S. Hyun, B.I. Jang, T.N. Kim, S.W. Kim, S.K. Song, J.H. Kim, J.-R. Kim
European Surgical Research.2007; 39(4): 208. CrossRef
Hepatocyte Growth Factor/c-Met Signaling in Regulating Urokinase Plasminogen Activator in Human Stomach Cancer: A Potential Therapeutic Target for Human Stomach Cancer
Kyung Hee Lee, Eun Young Choi, Myung Soo Hyun, Byung Ik Jang, Tae Nyeun Kim, Sang Woon Kim, Sun Kyo Song, Jung Hye Kim, Jae-Ryong Kim
The Korean Journal of Internal Medicine.2006; 21(1): 20. CrossRef
Expression of E-Cadherin and uPA and their Association with the Prognosis of Pancreatic Cancer
Sang Joon Shin, Kyeong Ok Kim, Min Kyoung Kim, Kyung Hee Lee, Myung Soo Hyun, Keuk Jun Kim, Joon Hyuk Choi, Hong Seok Song
Japanese Journal of Clinical Oncology.2005; 35(6): 342. CrossRef

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Clinical Relevance of Urokinase-type Plasminogen Activator ( uPA ) , uPA Receptor , Plasminogen Activator Inhibitor-1 Co-expression from Tissue and Serum of Breast Cancer as Targets of Biotherapy: Sun Young Rha, Joon Oh Park, Soo Jung Gong, Se Ho Park, Nae Choon Yoo, Woo Ick Yang, Jae Kyung Roh, Jin Sik Min, Kyong Sik Lee, Byung Soo Kim, Hyun Cheol Chung; J Korean Cancer Assoc. 1999;31(2):256-266.

Abstract PDF: PURPOSE
We measured and compared the uPA, plasminogen activator inhibitor-1 (PAI-1) and uPA receptor (uPAR) levels in breast cancer tissues and blood of the patients to evaluate their clinical relevance for biotherapy.
MATERIALS AND METHODS
uPA, PAI-1 (Monozyme, Netherland), uPAR (American Diagnostics, USA) levels were measured by ELISA assay in 192 breast cancer tissues, in 18 normal breast tissues and in 163 blood from breast cancer patients. RESULTS: There was a tendency of uPA increment from ductal carcinoma in situ while increment of PAI-1 and uPAR occurred from Ti. With the progression of cancer, uPA, PAI-1, uPAR tended to decrease; however, the uPA/uPAR, uPA/PAI-1 ratios remained unchanged. There was a correlation of uPA expression between normal and cancer tissues ( r(2)= 0.49). Correlation of uPA and PAI-1 was found in normal tissue and stage I cancer tissue while correlation of uPAR and PAI-1 was found with cancer progression. Between cancer tissue and blood significant correlations were found in uPA, PAI-1, uPAR levels.
CONCLUSION
uPA, PAI-1, uPAR levels in cancer tissue elevated from the early stage maintaining correlative expressions with cancer progression. A positive correlation between cancer tissue and blood level suggested the applicability of the levels of uPA, PAI-1 or uPAR for detecting patients for biotherapy.

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Clinical Significance of Urokinase-type Plasminogen Activator (uPA) Expression from Serum and Tissue of Gastric Cancer Patients: Hyun Cheol Chung, Joon Oh Park, Hyun Ja Kwon, Tae Soo Kim, Hei Cheol Chung, Soo Jung Gong, Hwa Young Lee, Sun Young Rha, Nae Choon Yoo, Joo Hang Kim, Jae Kyung Roh, Sung Hoon Noh, Jin Sik Min, Byung Soo Kim; J Korean Cancer Assoc. 1997;29(5):765-773.

Abstract PDF: PURPOSE
We measured the gastric cancer tissue uPA and plasminogen activator inhibitor-1 (PAI-1) levels and compared them to those of the peripheral and portal blood levels to evaluate the correlation.
MATERIALS AND METHODS
Tissue uPA and PAI-1 levels were measured by ELISA assay (Monozyme, Netherland) in paired 85 normal and cancer tissues resected from gastric cancer patients. In 50 patients, blood uPA and PAI-1 levels were measured from pre- operative peripheral and portal blood, post-operative portal blood.
RESULTS
Gastric cancer tissue uPA and PAI-1 levels increased from the early stage. The elevated cancer-to-normal ratios of the uPA and PAI-1 were constant from stage I to IV. There were correlations of uPA between normal and cancer tissues (r2=0.38) and between peripheral and pre-resection portal blood level (r2=0.64). There were no correlations between tissue PAI-1 level and blood PAI-1 levels. However, there were correlations in PAI- 1/uPA ratio between cancer tissue and peripheral blood (r2=0.25), peripheral blood and pre- resection portal blood (r2=0.60).
CONCLUSION
Even if the cancer tissue levels of uPA and PAI-1 increased from the early stage of gastric cancer, only blood uPA level correlated with tissue uPA level. A modest correlation found in PAI-1/uPA ratio between cancer tissue and blood suggests applicability of blood PAI-1/uPA ratio in predicting tissue uPA, PAI-1 expression.

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Expression of Urokinase - type Plasminogen Activator a New Biologic Marker of the Invasion and Metastasis in Gastric Cancer: Sung Hoon Noh, Jae Yong Cho, Sun Young Rha, Hyun Cheol Chung, Joon Oh Park, Chong In Lee, Nae Choon Yoo, Joo Hang Kim, Jae Kyung Roh, Jin Sup Choi, Jin Sik Min, Byung Soo Kim; J Korean Cancer Assoc. 1996;28(2):198-207.

Abstract PDF: Mortality in gastric cancer is related to invasion and metastasis. Evidence has accumulated that invasion and rnetastasis in solid tumors require the action of tumor associated proteases, which promotes the dissolution of the surrounding tumor matrix and the basement membrane. The serine protease urokinase-type plasminogen activator(uPA), which is elevated in solid tumors, appears to play a key role in these processes. We used enzymelinked immunoabsorbent assays(ELISA) to test uPA antigen expression in tissue extracts of normal and cancer tissue of 160 gastric cancer patients. uPA level was significantly higher in cancerous tissue than normal gastric tissue(9.4 vs 5.3 ng/mg protein cytosol: p<0.001). When the uPA level was correlated to other prognostic parameters, uPA positivity is associated with grade of anaplasia(p=0.005). Univariate analysis showed that a uPA positivity is significantly associated with short. disease-free survival(p=0.005). Multivariate analysis with known prognostic parameters revealed that the uPA positivity was an independent prognostic parameter for short disease-free survival. These data indicate that uPA is a potentially important prognostic factor in gastric cancer. Consequently, we suggest that modulation of uPA is needed to prevent invasion and metastasis in gastric cancer patients.

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