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Analysis of BRCA2 Copy Number Loss and Genomic Instability in Circulating Tumor Cells from Patients with Metastatic Castration-resistant Prostate Cancer
BRCA2 alterations predict for a response to poly-ADP-ribose polymerase inhibition in metastatic castration-resistant prostate cancer (mCRPC). However, detection is hindered by insufficient tumor tissue and low sensitivity of cell-free DNA for detecting copy number loss. To evaluate the BRCA2 loss detection using single-cell, shallow whole-genome sequencing (sWGS) of circulating tumor cells (CTCs) in patients with mCRPC.
Optimizing the future: how mathematical models inform treatment schedules for cancer
Highlights For decades, mathematical models have influenced how we schedule chemotherapeutics: the most notable example stems from the Norton–Simon hypothesis which led to the advent of dose-dense scheduling to improve disease-free and overall survival. Newer mathematical models have leveraged game theory and ecological principles to propose adaptive therapy scheduling, with the aim of stabilizing a patient's disease and preventing the growth of surviving resistant cell populations.
Clinical Utility of the Nuclear-localized AR-V7 Biomarker in Circulating Tumor Cells in Improving Physician Treatment Choice in Castration-resistant Prostate Cancer
To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect. Fig. 1 CONSORT and treatment diagrams. (A) CONSORT diagram outlining samples used for propensity score and risk score generation and subset analyzed. (B) Flow diagram illustrating cohort treatment and AR-V7 testing history. The scoring criteria for AR-V7 positivity were prespecified, and the AR-V7 results were not released to physicians.
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