Frequent CHD1 deletions in prostate cancers of African American men is associated with rapid disease progression.

We analyzed genomic data from the prostate cancer of African- and European American men to identify differences contributing to racial disparity of outcome. We also performed FISH-based studies of Chromodomain helicase DNA-binding protein 1 (CHD1) loss on prostate cancer tissue microarrays. We created CHD1-deficient prostate cancer cell lines for genomic, drug sensitivity and functional homologous recombination (HR) activity analysis.

Reprogramming of the FOXA1 cistrome in treatment-emergent neuroendocrine prostate cancer.

Lineage plasticity, the ability of a cell to alter its identity, is an increasingly common mechanism of adaptive resistance to targeted therapy in cancer. An archetypal example is the development of neuroendocrine prostate cancer (NEPC) after treatment of prostate adenocarcinoma (PRAD) with inhibitors of androgen signaling. NEPC is an aggressive variant of prostate cancer that aberrantly expresses genes characteristic of neuroendocrine (NE) tissues and no longer depends on androgens.

Plasma cell-free DNA variant analysis compared with methylated DNA analysis in renal cell carcinoma.

Purpose: Plasma cell-free DNA (cfDNA) variant analysis is commonly used in many cancer subtypes. Cell-free methylated DNA immunoprecipitation sequencing (cfMeDIP-seq) has shown high sensitivity for cancer detection. To date, studies have not compared the sensitivity of both methods in a single cancer subtype.

Expression QTL-based analyses reveal candidate causal genes and loci across five tumor types.

The majority of trait-associated loci discovered through genome-wide association studies are located outside of known protein coding regions. Consequently, it is difficult to ascertain the mechanism underlying these variants and to pinpoint the causal alleles. Expression quantitative trait loci (eQTLs) provide an organizing principle to address both of these issues.