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Integrative analyses of multi-omics data to uncover potential mechanisms of transcriptional dysregulation in Prostate Cancer (PCa)

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Session Information

Cancer genomics research over past decades have shown that genetic mutations trigger and encourage the growth and spread of many cancer types. However, Prostate cancer (PCa) is characterized by lower mutation rates & higher rates of recurrent genomic rearrangements. Majority of cases show upregulation of transcription factor genes (ETS family genes ERG & ETV1 upregulation in >50% of samples). Master transcription factor such as Androgen receptor (AR) play pivotal role in the normal development of the prostate gland. Aberrant signaling of AR is the root of many facets of PCa etiology, metastatic castration-resistant prostate cancer (mCRPC) inclusive. Since transcriptional dysregulation is one of the hallmarks of prostate cancer and 2D genomics data does not provide clarity on multiple gene and enhancer coordination involved in regulation, we hypothesize that the changes in the 3-dimensional genomic organization can critically determine the aberrant transcriptional regulation in PCa. Therefore, we focus on TF complexes such as RNA POLII and transcription factors (AR & FOXA1) and their chromatin interactions in three prostate cancer specific and one normal prostate cell lines LNCaP, VCaP, DU145, RWPE-1 (benign cells) and integrate them with multi-omics data (ChIP-Seq, RNA-Seq, aCGH, WGS) to deduce various conclusions regarding PCa transcription dysregulation.



Khyati Chandratre








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