Integrative genomic profiling of human prostate cancer

By Barry S. Taylor, Nikolaus Schultz, H. Hieronymus, A. Gopalan, Yonghong Xiao, B. Carver, V. Arora, Poorvi Kaushik, Ethan G. Cerami, B. Reva and 16 more. Cancer Cell, 2010

3,651 citations recorded by the source corpus.

SUMMARY Annotation of prostate cancer genomes provides a foundation for discoveries that can impact disease understanding and treatment. Concordant assessment of DNA copy number, mRNA expression, and focused exon resequencing in 218 prostate cancer tumors identified the nuclear receptor coactivator NCOA2 as an oncogene in ~11 percent of tumors. Additionally, the androgen-driven TMPRSS2-ERG fusion was associated with a previously unrecognized, prostate-specific deletion at chromosome 3p14 that implicates FOXP1, RYBP and SHQ1 as potential cooperative tumor suppressors. DNA copy-number data from primary tumors revealed that copy-number alterations robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score. The genomic and clinical outcome data from these patients is now made available as a public resource.

Subfields: Cancer Research, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/e8cfd5b41662252a09402dbd3f5c992aa72a74d3

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Citations in the corpus

Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer. (2011, methodology): “Our preclinical data predict that single-agent PI3K pathway inhibitor therapy will most likely result in disease stabilization rather than tumor regression, particularly in PTEN null tumors that represent 40%of primary cancers and 70%ofmetastases (Taylor et al., 2010).”
Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis. (2012, methodology): “To this end, we analyzed Lats1 and Lats2 expression in a cohort of 132 clinically localized prostate cancer, 18 metastatic prostate cancer, and 29 benign adjacent prostate tissues (Taylor et al. 2010).”
Integrative clinical genomics of advanced prostate cancer (2015, positive): “Multiple studies have identified recurrent somatic mutations, copy number alterations, and oncogenic structural DNA rearrangements (chromoplexy) in primary prostate cancer (Baca et al., 2013; Barbieri et al., 2012; Berger et al., 2011; Cooper et al., 2015; Pflueger et al., 2011; Taylor et al., 2010;”
Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs (2011, positive): “PTEN and ceRNA Coexpression Analysis and Genomic Status Assessment Coexpression in prostate cancer was evaluated using GEO super-series GSE21032 (Taylor et al., 2010).”
Genetics and biology of prostate cancer (2018, background): “Primary prostate tumors and mCRPC exhibit markedly increased genome-wide copy number alterations yet show only modestly increased mutations (Taylor et al. 2010; Grasso et al. 2012; Hieronymus and Sawyers 2012; The Cancer Genome Atlas Research Network 2015).”
miRTarBase update 2014: an information resource for experimentally validated miRNA-target interactions (2013, background): “Supplementary Data are available at NAR Online, including [54–69].”