Biochemical Failure in Prostate Cancer

2012 ◽  
pp. 807-811
Author(s):  
Tian Zhang ◽  
Andrew Z. Wang
Keyword(s):  
Prostate Cancer ◽  
Biochemical Failure

660: Altered MUC-1 (EMA) Protein Expression Studied by Tissue Microarray Predicts Biochemical Failure after Radical Prostatectomy in Prostate Cancer

2007 ◽  
Vol 177 (4S) ◽  
pp. 222-222
Author(s):  
Mireia Musquera ◽  
Maria J. Ribal ◽  
Yolanda Arce ◽  
Humberto Villavicencio ◽  
Fernando Algaba ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Radical Prostatectomy ◽  
Protein Expression ◽  
Tissue Microarray ◽  
Biochemical Failure

Docetaxel, estramustine, and short-term androgen withdrawal for patients with biochemical failure after definitive local therapy for prostate cancer

2001 ◽  
Vol 28 (4M) ◽  
pp. 32-39 ◽  
Author(s):  
Mary-Ellen Taplin ◽  
Glenn J. Bubley ◽  
Barur Rajeshkumar ◽  
Todd Shuster ◽  
Yoo-Joung Ko ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Local Therapy ◽  
Biochemical Failure ◽  
Short Term ◽  
Androgen Withdrawal

scholarly journals ATM Kinase Inhibition Preferentially Sensitises PTEN-Deficient Prostate Tumour Cells to Ionising Radiation

Cancers ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 79
Author(s):  
Conor Hanna ◽  
Victoria L. Dunne ◽  
Steven M. Walker ◽  
Karl T. Butterworth ◽  
Nuala McCabe ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cellular Response ◽  
Advanced Prostate Cancer ◽  
Combined Treatment ◽  
Locally Advanced ◽  
Biochemical Failure ◽  
Ionising Radiation ◽  
Effective Treatment Option ◽  
Normal Prostate ◽  
Minimal Toxicity

Radical radiotherapy, often in combination with hormone ablation, is a safe and effective treatment option for localised or locally-advanced prostate cancer. However, up to 30% of patients with locally advanced PCa will go on to develop biochemical failure, within 5 years, following initial radiotherapy. Improving radiotherapy response is clinically important since patients exhibiting biochemical failure develop castrate-resistant metastatic disease for which there is no curative therapy and median survival is 8–18 months. The aim of this research was to determine if loss of PTEN (highly prevalent in advanced prostate cancer) is a novel therapeutic target in the treatment of advanced prostate cancer. Previous work has demonstrated PTEN-deficient cells are sensitised to inhibitors of ATM, a key regulator in the response to DSBs. Here, we have shown the role of PTEN in cellular response to IR was both complex and context-dependent. Secondly, we have confirmed ATM inhibition in PTEN-depleted cell models, enhances ionising radiation-induced cell killing with minimal toxicity to normal prostate RWPE-1 cells. Furthermore, combined treatment significantly inhibited PTEN-deficient tumour growth compared to PTEN-expressing counterparts, with minimal toxicity observed. We have further shown PTEN loss is accompanied by increased endogenous levels of ROS and DNA damage. Taken together, these findings provide pre-clinical data for future clinical evaluation of ATM inhibitors as a neoadjuvant/adjuvant in combination with radiation therapy in prostate cancer patients harbouring PTEN mutations.

scholarly journals Time Interval to Biochemical Failure as a Surrogate End Point in Locally Advanced Prostate Cancer: Analysis of Randomized Trial NRG/RTOG 9202

2019 ◽  
Vol 37 (3) ◽  
pp. 213-221 ◽  
Author(s):  
James J. Dignam ◽  
Daniel A. Hamstra ◽  
Herbert Lepor ◽  
David Grignon ◽  
Harmar Brereton ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Randomized Trial ◽  
Locally Advanced ◽  
Biochemical Failure ◽  
Mediating Effect ◽  
Time Interval ◽  
Short Term ◽  
End Points ◽  
End Point

Background In prostate cancer, end points that reliably portend prognosis and treatment benefit (surrogate end points) can accelerate therapy development. Although surrogate end point candidates have been evaluated in the context of radiotherapy and short-term androgen deprivation (AD), potential surrogates under long-term (24 month) AD, a proven therapy in high-risk localized disease, have not been investigated. Materials and Methods In the NRG/RTOG 9202 randomized trial (N = 1,520) of short-term AD (4 months) versus long-term AD (LTAD; 28 months), the time interval free of biochemical failure (IBF) was evaluated in relation to clinical end points of prostate cancer–specific survival (PCSS) and overall survival (OS). Survival modeling and landmark analysis methods were applied to evaluate LTAD benefit on IBF and clinical end points, association between IBF and clinical end points, and the mediating effect of IBF on LTAD clinical end point benefits. Results LTAD was superior to short-term AD for both biochemical failure (BF) and the clinical end points. Men remaining free of BF for 3 years had relative risk reductions of 39% for OS and 73% for PCSS. Accounting for 3-year IBF status reduced the LTAD OS benefit from 12% (hazard ratio [HR], 0.88; 95% CI, 0.79 to 0.98) to 6% (HR, 0.94; 95% CI, 0.83 to 1.07). For PCSS, the LTAD benefit was reduced from 30% (HR, 0.70; 95% CI, 0.52 to 0.82) to 6% (HR, 0.94; 95% CI, 0.72 to 1.22). Among men with BF, by 3 years, 50% of subsequent deaths were attributed to prostate cancer, compared with 19% among men free of BF through 3 years. Conclusion The IBF satisfied surrogacy criteria and identified the benefit of LTAD on disease-specific survival and OS. The IBF may serve as a valid end point in clinical trials and may also aid in risk monitoring after initial treatment.

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