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Biomedical subjects

Michael Cher

Publications and source records attributed to Michael Cher.

3 recordsLinked to original sources

Understanding randomized controlled trial generalizability through an embedded molecular diagnostics trial.

BACKGROUND: Issues with randomized controlled trial generalizability are well described, but whether these issues result from differences in patient treatment across contexts remains unknown. We studied treatment of patients with high-risk prostate cancer after radical prostatectomy inside and outside a randomized controlled trial evaluating the impact of a genomic classifier on post-radical prostatectomy treatment decision making (Genomics in Michigan Impacting Observation of Radiation [G-MINOR]; ClinicalTrials.gov identifier NCT02783950). METHODS: G-MINOR enrolled 338 patients; propensity score-matched eligible but unenrolled patient cohorts (pretrial and trial contemporary) from the Michigan Urological Surgery Improvement Collaborative (MUSIC), in which the trial was embedded, were compared for rates and time to secondary treatment (adjuvant or salvage therapy) after prostatectomy. RESULTS: Among 338 patients in the G-MINOR cohort, 69 (31 adjuvant, 38 salvage) received secondary treatment compared with 266 (183 adjuvant, 83 salvage) and 104 (60 adjuvant, 44 salvage) in the 1014 contemporary and 338 pretrial-matched MUSIC cohorts. Time to secondary treatment was much shorter in the MUSIC cohort across all comparisons. For example, matching G-MINOR to synchronous MUSIC patients demonstrated 84% vs 74% estimated 2-year treatment-free survival for trial and real-world patients, respectively (P&#x2009;<&#x2009;.001). CONCLUSIONS: Controlling for key clinicopathologic factors, patients in the G-MINOR randomized controlled trial and MUSIC cohorts were treated differently, even after stratifying by genomic risk. These findings suggest that challenges in randomized controlled trial generalizability extend beyond the representativeness of trial participants. Differences in management may also explain why divergent patient outcomes are observed in randomized controlled trials vs real-world settings.

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Tissue inhibitor of metalloproteinase-3 induces apoptosis in prostate cancer cells and confers increased sensitivity to paclitaxel.

Prostate cancer is the most common cancer and the second leading cause of cancer-related death in American men. To investigate the possible usefulness of tissue inhibitor of metalloproteinase-3 (TIMP-3) in prostate cancer gene therapy, we used an adenovirus expressing TIMP-3 to assess its role as an apoptosis trigger in highly metastatic prostate cancer cell lines PC-3 and DU-145. We showed that TIMP-3 alone induced apoptotic cell death which was triggered by mitochondrion-mediated caspase-3 activation. In combination treatment, we found that adenovirus-mediated expression of TIMP-3 greatly sensitised prostate cancer cells to chemotherapeutic drug paclitaxel, indicating a superadditive or synergistic effect of TIMP-3 and cytostatic treatment on prostate cancer cell death. The proper combination of adenovirus-mediated expression of TIMP-3 with conventional chemotherapeutic drug(s) could have potential benefits in treating highly metastatic prostate cancer.

Antineoplastic Agents, Phytogenic↗

Allelic loss at 16q23.2 is associated with good prognosis in high grade prostate cancer.

PURPOSE: Loss of heterozygosity (LOH) at 16q23.2 is an early and frequent event in prostate cancer. LOH is thought to be involved in tumor development and progression mainly through inactivation of tumor suppressor genes. However, it has been demonstrated that LOH at 16q23.2 is an independent marker of good prognosis in breast cancer. In the present study, we evaluated the clinical relevance of 16q23.2 LOH in prostate cancer, together with other LOH frequently associated with this disease. EXPERIMENTAL DESIGN: Tumoral and normal DNA were extracted from 61 radical prostatectomies, including 30 pT2 tumors with low Gleason score 5,6 (group 1), and 31 pT3 high grade (G8-9) tumors (group 2). Median follow-up after surgery was 42 months. Three patients reccured in group 1, and 20 in group 2. LOH analysis was performed using highly informative microsatellites markers, at 16q23.2, and at other chromosome loci frequently deleted in prostate cancer: 7q31, 8p22, 12p13, 13q14, and 18q21. RESULTS: LOH at 16q23.2 is associated with low stage low grade tumors and lower preoperative PSA, while LOH at 8p22 is more frequent in high stage high grade prostate cancer. In group 2, 16q23.2 LOH was the only predictor of disease-free survival in univariate and multivariate analysis, and the cumulative LOH rate was not higher in patients non-deleted for 16q23.2. CONCLUSION: These results emphasize the interest of 16q23.2 as an independent prognostic factor in high-grade prostate cancer, and suggest that this chromosomal region may contain a gene involved in tumor progression.

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