Elucidating altered transcriptional programs Skype cam bitches names

Of the 150 genes that were upregulated in untreated PC compared to CRPC, and downregulated with castration in PC xenografts, 16 core genes consistently re-emerged with castration resistance: PECI; TNFSF10; ABHD12; XRCC3; MAD1L1; SEC61A1; GFM1; TSPAN13; STIL; TRMT12; EIF2B5; TM4SF1; NDUFB11; SLC26A2; AGR2; NT5DC3.

CRPC is often studied in vitro using cell lines derived from metastatic cancer cells (Wang et al., 2009; Yu et al., 2010; Massie et al., 2011), and previous authors have suggested PC cells in culture have different gene expression signatures than primary tumors (Yu et al., 2009; Long et al., 2014).

Of thousands of targets for the androgen receptor (AR), the authors elucidated a subset of 16 core genes that were consistently downregulated with castration and re-emerged with castration resistance.

These 16 AR binding sites were distinct from those observed in cells in culture.

Gene expression signatures in these tumors were compared to tumors from intact mice.

The core genes were downregulated in castration-sensitive tumors compared to tumors from intact animals, and upregulated in castration-resistant tumors (Sharma et al., 2013).

The Prostate Cancer Foundation-Movember Foundation Reproducibility Initiative (PCFMFRI) seeks to address growing concerns about reproducibility in scientific research by conducting replications of recent papers in the field of prostate cancer.

All references to Figures are in reference to the original study.Sharma and colleagues showed that genome-wide binding targets of the AR in tumor tissue differed from those in cultured cells.Expression patterns of the 16 core AR target genes were distinct from those observed in cells in culture, suggesting cellular context can have dramatic effects on downstream transcriptional regulation of AR binding sites. 7C, expression levels of the 16 core genes were analyzed in xenograft tumor tissues that were determined to be either castration-sensitive or castration-resistant.In order to replicate this key finding, we will also compare expression patterns of the core gene set in both castration-sensitive and castration-resistant tumors to the genetic signature of these genes in cultured LNCa P cells with or without androgen exposure in vitro in Protocols 1 and 3.A large number of studies have investigated genome-wide profiling of AR binding (Bolton et al., 2007; Jia et al., 2008; Wang et al., 2009; Yu et al., 2010).

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