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Walter M. Stadler

Researcher at University of Chicago

Publications -  513
Citations -  37554

Walter M. Stadler is an academic researcher from University of Chicago. The author has contributed to research in topics: Cancer & Prostate cancer. The author has an hindex of 88, co-authored 494 publications receiving 34323 citations. Previous affiliations of Walter M. Stadler include Cleveland Clinic & Northwestern University.

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A Phase II study of oxaliplatin in urothelial cancer.

TL;DR: In this article, a double-arm two-stage Phase II trial was conducted to assess the antitumor activity of oxaliplatin, a third generation platinum derivative with a 1,2-diaminocyclohexane (DACH) carrier ligand, in patients with metastatic transitional cell carcinoma of the bladder.
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857 randomized phase iii trial of sorafenib in advanced renal cell carcinoma (rcc): impact of crossover on survival

TL;DR: The lower HR observed after censoring placebo patients crossed over to sorafenib suggests a continued beneficial effect of sorafinib, the first novel, oral approved treatment for advanced RCC in more than a decade.
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Study of cohort-specific consent and patient control in phase I cancer trials.

TL;DR: A clinical trial design that uses an interactive informed consent process in which patient-subjects can choose to become directly involved in decisions of dose escalation may reduce the magnitude of many of the commonly recognized ethical dilemmas associated with this form of clinical research.
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Phase II trial of sunitinib in bevacizumab-refractory metastatic renal cell carcinoma (mRCC): Updated results and analysis of circulating biomarkers

TL;DR: This study evaluated the safety and activity of sunitinib in mRCC patients previously treated with the VEGF-neutralizing antibody, bevacizumab, and levels of angiogenic biomarkers, including plasma VEGf and soluble VEGFR-3, were assessed for predictive significance with clinical response.
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Alterations of the 9p21 and 9q33 chromosomal bands in clinical bladder cancer specimens by fluorescence in situ hybridization.

TL;DR: The proposition that chromosome 9 losses occur early in bladder oncogenesis and before p53 alterations or development of aneusomy is strengthened, as the observed homozygous deletions strengthen the hypotheses that CDKN2 and DBCCR1 are important tumor suppressor genes.