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Keith T. Schmidt

Researcher at National Institutes of Health

Publications -  21
Citations -  259

Keith T. Schmidt is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Prostate cancer & Cancer. The author has an hindex of 5, co-authored 17 publications receiving 138 citations.

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Precision Oncology Medicine: The Clinical Relevance of Patient-Specific Biomarkers Used to Optimize Cancer Treatment.

TL;DR: Clinical trials are assessing novel diagnostic tools with a combination of different targeted therapeutics while also examining tumor biomarkers that were previously unexplored in a variety of cancer histologies, further shifting the 1 gene–1 drug paradigm toward a more comprehensive, multigene approach.
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Resistance to second-generation androgen receptor antagonists in prostate cancer.

TL;DR: The use of second-generation androgen receptor antagonists (SG-ARAs) has greatly impacted the treatment of metastatic prostate cancer, providing tolerable and efficacious alternatives to chemotherapy as mentioned in this paper.
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Whole-exome sequencing reveals germline-mutated small cell lung cancer subtype with favorable response to DNA repair-targeted therapies.

TL;DR: In this article, the extent of inherited susceptibility to small cell lung cancer (SCLC), the most lethal type of lung cancer, was assessed by sequenced germline exomes of 87 patients (77 SCLC and 10 extrapulmonary small cell) and found 42 deleterious variants in 35 cancer-predisposition genes among 43.7% of patients.
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Reviewing the role of healthy volunteer studies in drug development

TL;DR: The use of HVs in the clinical development of oncology drugs is more limited but is nonetheless useful for evaluating clinical pharmacology and establishing an appropriate starting dose for studies in cancer patients.
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The potential role of curcumin in prostate cancer: the importance of optimizing pharmacokinetics in clinical studies

TL;DR: Curcumin was shown to down-regulate AR expression, limit AR binding to the androgen response element of the prostate specific antigen (PSA) gene, and reduce the expression of PSA in LNCaP cells.