Integrative genomic and proteomic analysis of prostate cancer reveals signatures of metastatic progression.

By S. Varambally, Jianjun Yu, B. Laxman, Daniel R. Rhodes, R. Mehra, S. Tomlins, R. Shah, U. Chandran, F. Monzon, M. Becich and 5 more. Cancer Cell, 2005

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Molecular profiling of cancer at the transcript level has become routine. Large-scale analysis of proteomic alterations during cancer progression has been a more daunting task. Here, we employed high-throughput immunoblotting in order to interrogate tissue extracts derived from prostate cancer. We identified 64 proteins that were altered in prostate cancer relative to benign prostate and 156 additional proteins that were altered in metastatic disease. An integrative analysis of this compendium of proteomic alterations and transcriptomic data was performed, revealing only 48%-64% concordance between protein and transcript levels. Importantly, differential proteomic alterations between metastatic and clinically localized prostate cancer that mapped concordantly to gene transcripts served as predictors of clinical outcome in prostate cancer as well as other solid tumors.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine, Spectroscopy

View Paper: https://www.semanticscholar.org/paper/d708dc957348a0cdf4aa4323041f7c2725b43696

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Citations in the corpus

Discovery and Validation of a Prostate Cancer Genomic Classifier that Predicts Early Metastasis Following Radical Prostatectomy (2013, background): “The performance of GC was compared to that of previously published gene signatures [11–13,15,16,18–24,28–30] and individual genomic markers associated with prostate cancer progression including CHGA [43], DAB2IP [44], GOLPH2 [45], PAP [46], ETV1 and ERG [47], KI-67 [48], PSA [49], PSCA [50], PSMA [5”
Androgen Receptor Regulates a Distinct Transcription Program in Androgen-Independent Prostate Cancer (2009, methodology): “To identify genes that might account for the androgen-independent growth of abl compared with LNCaP, we examined gene expression profiles of abl cells in the absence of DHT and LNCaP cells in the absence and presence of DHT treatment for 4 hr (Figure S1B) using Affymetrix U133 plus 2.0 expression ar”
A Novel Androgen Receptor Splice Variant Is Upregulated during Prostate Cancer Progression and Promotes Androgen-depletion-resistant Growth (2009, result): “metastatic PCAs in previous gene profiling studies (19, 37, 38).”
The androgen receptor fuels prostate cancer by regulating central metabolism and biosynthesis (2011, result): “…2 (CAMKK2, Figure 3A) as consistently over- expressed in prostate cancer in nine independent clinical gene expression studies (Rhodes et al, 2004; Varambally et al, 2005), showing a similar pattern to the established prostate cancer marker AMACR (Jiang et al, 2001, 2002) (Figure…”