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k/vol1/fastq/ERR116/098/ERR11635198/ERR11635198_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR116/021/ERR11635321/ERR11635321_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR116/030/ERR11635330/ERR11635330_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR116/028/ERR11635328/ERR11635328_2.fastq.gzprimaryOK200GenomicsIndian Biological Data CentreKumar Sandeep, Durgavati Yadav, Monu Deshwal, Dibyabhaba Pradhan and Prabhjot Singh, All India Institute of Medical Sciences, New Delhihttps://www.ebi.ac.uk/ena/browser/view/PRJEB63609IBDCThe standard treatment for prostate cancer is androgen deprivation therapy. However, ADT invariably leads to the development of castration-resistant PCa. Development of mCRPC involves number of molecular mechanisms. Progression to CRPC represents accumulation of resistance strategies deployed by cells against castration. In this study, we wish to understand differences in genetic landscape of the normal and tumor cells in the metastatic prostate cancer, and their correlation with development of mCRPC. We have tried to elucidating germline and tumor mutational landscape in mPCa and study important tumor mutations in cell free DNA and their correlation with development of CRPC.ENAfalseSomatic Variations in naïve Prostate cancer and Castration resistant Prostate CancerClinico genetic prognostic signature for development of metastatic Castration Resistant Prostate Cancer2025-08-282025-06-20PRJEB63609