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prostate cancer genomic sequencing

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https://www.readbyqxmd.com/read/28623072/commentary-on-integrative-clinical-genomics-of-advanced-prostate-cancer-robinson-d-van-allen-em-wu-ym-schultz-n-lonigro-rj-mosquera-jm-montgomery-b-taplin-me-pritchard-cc-attard-g-beltran-h-abida-w-bradley-rk-vinson-j-cao-x-vats-p-kunju-lp-hussain-m-feng-fy
#1
Stephen J Freedland, William J Aronson
Toward development of a precision medicine framework for metastatic, castration-resistant prostate cancer (mCRPC), we established a multi-institutional clinical sequencing infrastructure to conduct prospective whole-exome and transcriptome sequencing of bone or soft tissue tumor biopsies from a cohort of 150 mCRPC affected individuals. Aberrations of AR, ETS genes, TP53, and PTEN were frequent (40%-60% of cases), with TP53 and AR alterations enriched in mCRPC compared to primary prostate cancer. We identified new genomic alterations in PIK3CA/B, R-spondin, BRAF/RAF1, APC, β-catenin, and ZBTB16/PLZF...
June 13, 2017: Urologic Oncology
https://www.readbyqxmd.com/read/28618396/vitamin-d-receptor-binding-site-variants-affect-prostate-cancer-progression
#2
Victor C Lin, Shu-Pin Huang, Huei-Ju Ting, Wen-Lung Ma, Chia-Cheng Yu, Chao-Yuan Huang, Hsin-Ling Yin, Tsung-Yi Huang, Cheng-Hsueh Lee, Ta-Yuan Chang, Te-Ling Lu, Bo-Ying Bao
Vitamin D is an important modulator of cellular proliferation through the vitamin D receptor (VDR) that binds to DNA in the regulatory sequences of target genes. We hypothesized that single nucleotide polymorphisms (SNPs) in VDR-binding sites might affect target gene expression and influence the progression of prostate cancer. Using a genome-wide prediction database, 62 SNPs in VDR-binding sites were selected for genotyping in 515 prostate cancer patients and the findings were replicated in an independent cohort of 411 patients...
May 26, 2017: Oncotarget
https://www.readbyqxmd.com/read/28614298/erf-mutations-reveal-a-balance-of-ets-factors-controlling-prostate-oncogenesis
#3
Rohit Bose, Wouter R Karthaus, Joshua Armenia, Wassim Abida, Phillip J Iaquinta, Zeda Zhang, John Wongvipat, Elizabeth V Wasmuth, Neel Shah, Patrick S Sullivan, Michael G Doran, Ping Wang, Anna Patruno, Yilin Zhao, Deyou Zheng, Nikolaus Schultz, Charles L Sawyers
Half of all prostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expression of the normally silent E26 transformation-specific (ETS) transcription factor ERG in prostate cells. Recent genomic landscape studies of such cancers have reported recurrent point mutations and focal deletions of another ETS member, the ETS2 repressor factor ERF. Here we show these ERF mutations cause decreased protein stability and mostly occur in tumours without ERG upregulation. ERF loss recapitulates the morphological and phenotypic features of ERG gain in normal mouse prostate cells, including expansion of the androgen receptor transcriptional repertoire, and ERF has tumour suppressor activity in the same genetic background of Pten loss that yields oncogenic activity by ERG...
June 14, 2017: Nature
https://www.readbyqxmd.com/read/28611215/genome-wide-crispr-screen-identifies-hnrnpl-as-a-prostate-cancer-dependency-regulating-rna-splicing
#4
Teng Fei, Yiwen Chen, Tengfei Xiao, Wei Li, Laura Cato, Peng Zhang, Maura B Cotter, Michaela Bowden, Rosina T Lis, Shuang G Zhao, Qiu Wu, Felix Y Feng, Massimo Loda, Housheng Hansen He, X Shirley Liu, Myles Brown
Alternative RNA splicing plays an important role in cancer. To determine which factors involved in RNA processing are essential in prostate cancer, we performed a genome-wide CRISPR/Cas9 knockout screen to identify the genes that are required for prostate cancer growth. Functional annotation defined a set of essential spliceosome and RNA binding protein (RBP) genes, including most notably heterogeneous nuclear ribonucleoprotein L (HNRNPL). We defined the HNRNPL-bound RNA landscape by RNA immunoprecipitation coupled with next-generation sequencing and linked these RBP-RNA interactions to changes in RNA processing...
June 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28573914/treatment-strategies-for-dna-repair-deficient-prostate-cancer
#5
Benjamin A Teply, Emmanuel S Antonarakis
Common recurrent genetic alterations have been identified in prostate cancer through comprehensive sequencing efforts, and the prevalence of mutations in DNA repair pathway genes in patients with advanced and metastatic disease approaches 20-25%. Identification of these underlying DNA repair defects may present unique treatment opportunities for patients, both in terms of standard-of-care treatments and selected investigational agents. Areas covered: We review our current understanding of the genomic landscape of prostate cancer, with special attention to alterations in DNA repair pathway genes in metastatic castration-resistant disease...
June 12, 2017: Expert Review of Clinical Pharmacology
https://www.readbyqxmd.com/read/28540598/parp-inhibitors-in-prostate-cancer
#6
REVIEW
Praveen Ramakrishnan Geethakumari, Matthew J Schiewer, Karen E Knudsen, Wm Kevin Kelly
The genomic landscape of metastatic prostate cancer (mPCa) reveals that up to 90% of patients harbor actionable mutations and >20% have somatic DNA repair gene defects (DRD). This provides the therapeutic rationale of PARP inhibition (PARPi) to achieve "synthetic lethality" in treating this fatal disease. Clinical trials with PARP inhibitors have shown significant response rates up to 88% for PCa patients having DRD like BRCA1/2 or ATM mutations. The FDA has awarded "breakthrough designation" to develop the PARPi olaparib in treating this subset of metastatic PCa patients...
June 2017: Current Treatment Options in Oncology
https://www.readbyqxmd.com/read/28515055/exome-sequencing-of-african-american-prostate-cancer-reveals-loss-of-function-erf-mutations
#7
Franklin W Huang, Juan Miguel Mosquera, Andrea Garofalo, Coyin Oh, Maria Baco, Ali Amin-Mansour, Bokang Rabasha, Samira Bahl, Stephanie A Mullane, Brian D Robinson, Saud Aldubayan, Francesca Khani, Beerinder Karir, Eejung Kim, Jeremy Chimene-Weiss, Matan Hofree, Alessandro Romanel, Joseph R Osborne, Jong Wook Kim, Gissou Azabdaftari, Anna Woloszynska-Read, Karen Sfanos, Angelo M De Marzo, Francesca Demichelis, Stacey Gabriel, Eliezer M Van Allen, Jill Mesirov, Pablo Tamayo, Mark A Rubin, Isaac J Powell, Levi A Garraway
African-American men have the highest incidence and mortality from prostate cancer. Whether a biological basis exists for this disparity remains unclear. Exome sequencing (n=102) and targeted validation (n = 90) of localized primary hormone-naïve prostate cancer in African-American men identified several gene mutations not previously observed in this context, including recurrent loss-of-function mutations in ERF, an ETS transcriptional repressor, in 5% of cases. Analysis of existing prostate cancer cohorts revealed ERF deletions in 3% of primary prostate cancers and mutations or deletions in ERF in 3-5% of lethal castration-resistant prostate cancers...
May 17, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28504904/application-of-panel-based-tests-for-inherited-risk-of-cancer
#8
Payal D Shah, Katherine L Nathanson
Next-generation or massively parallel sequencing has transformed the landscape of genetic testing for cancer susceptibility. Panel-based genetic tests evaluate multiple genes simultaneously and rapidly. Because these tests are frequently offered in clinical settings, understanding their clinical validity and utility is critical. When evaluating the inherited risk of breast and ovarian cancers, panel-based tests provide incremental benefit compared with BRCA1/2 genetic testing. For inherited risk of other cancers, such as colon cancer and pheochromocytoma-paraganglioma, the clinical utility and yield of panel-based testing are higher; in fact, simultaneous evaluation of multiple genes has been the historical standard for these diseases...
May 15, 2017: Annual Review of Genomics and Human Genetics
https://www.readbyqxmd.com/read/28487881/whole-genome-sequencing-identifies-homozygous-brca2-deletion-guiding-treatment-in-dedifferentiated-prostate-cancer
#9
Karin Purshouse, Anna Schuh, Benjamin P Fairfax, Sam Knight, Pavlos Antoniou, Helene Dreau, Niko Popitsch, Kevin Gatter, Ian Roberts, Lisa Browning, Zoe Traill, David Kerr, Clare Verrill, Mark Tuthill, Jenny C Taylor, Andrew Protheroe
Whole-genome sequencing (WGS) has transformed the understanding of the genetic drivers of cancer and is increasingly being used in cancer medicine to identify personalized therapies. Here we describe a case in which the application of WGS identified a tumoral BRCA2 deletion in a patient with aggressive dedifferentiated prostate cancer that was repeat-biopsied after disease progression. This would not have been detected by standard BRCA testing, and it led to additional treatment with a maintenance poly ADP ribose polymerase (PARP) inhibitor following platinum-based chemotherapy...
May 2017: Cold Spring Harbor Molecular Case Studies
https://www.readbyqxmd.com/read/28483704/genome-wide-analysis-of-ar-binding-and-comparison-with-transcript-expression-in-primary-human-fetal-prostate-fibroblasts-and-cancer-associated-fibroblasts
#10
REVIEW
Claire Nash, Nadia Boufaied, Ian G Mills, Omar E Franco, Simon W Hayward, Axel A Thomson
The androgen receptor (AR) is a transcription factor, and key regulator of prostate development and cancer, which has discrete functions in stromal versus epithelial cells. AR expressed in mesenchyme is necessary and sufficient for prostate development while loss of stromal AR is predictive of prostate cancer progression. Many studies have characterized genome-wide binding of AR in prostate tumour cells but none have used primary mesenchyme or stroma. We applied ChIPseq to identify genomic AR binding sites in primary human fetal prostate fibroblasts and patient derived cancer associated fibroblasts, as well as the WPMY1 cell line overexpressing AR...
May 5, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28467780/novel-transcription-induced-fusion-rnas-in-prostate-cancer
#11
Sen Zhao, Marthe Løvf, Kristina Totland Carm, Anne Cathrine Bakken, Andreas M Hoff, Rolf I Skotheim
Prostate cancer is a clinically and pathologically heterogeneous disease with a broad spectrum of molecular abnormalities in the genome and transcriptome. One key feature is the involvement of chromosomal rearrangements creating fusion genes. Recent RNA-sequencing technology has uncovered that fusions which are not caused by chromosomal rearrangements, but rather meditated at transcription level, are common in both healthy and diseased cells. Such fusion transcripts have been proven highly associated with prostate cancer development and progression...
April 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28460430/metabolic-heterogeneity-signature-of-primary-treatment-na%C3%A3-ve-prostate-cancer
#12
Dong Lin, Susan L Ettinger, Sifeng Qu, Hui Xue, Noushin Nabavi, Stephen Yiu Chuen Choi, Robert H Bell, Fan Mo, Anne M Haegert, Peter W Gout, Neil Fleshner, Martin E Gleave, Michael Pollak, Colin C Collins, Yuzhuo Wang
To avoid over- or under-treatment of primary prostate tumours, there is a critical need for molecular signatures to discriminate indolent from aggressive, lethal disease. Reprogrammed energy metabolism is an important hallmark of cancer, and abnormal metabolic characteristics of cancers have been implicated as potential diagnostic/prognostic signatures. While genomic and transcriptomic heterogeneity of prostate cancer is well documented and associated with tumour progression, less is known about metabolic heterogeneity of the disease...
April 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28459452/targeting-genomic-rearrangements-in-tumor-cells-through-cas9-mediated-insertion-of-a-suicide-gene
#13
Zhang-Hui Chen, Yan P Yu, Ze-Hua Zuo, Joel B Nelson, George K Michalopoulos, Satdatshan Monga, Silvia Liu, George Tseng, Jian-Hua Luo
Specifically targeting genomic rearrangements and mutations in tumor cells remains an elusive goal in cancer therapy. Here, we used Cas9-based genome editing to introduce the gene encoding the prodrug-converting enzyme herpes simplex virus type 1 thymidine kinase (HSV1-tk) into the genomes of cancer cells carrying unique sequences resulting from genome rearrangements. Specifically, we targeted the breakpoints of TMEM135-CCDC67 and MAN2A1-FER fusions in human prostate cancer or hepatocellular carcinoma cells in vitro and in mouse xenografts...
June 2017: Nature Biotechnology
https://www.readbyqxmd.com/read/28453432/multiregional-radiogenomic-assessment-of-prostate-microenvironments-with-multiparametric-mr-imaging-and-dna-whole-exome-sequencing-of-prostate-glands-with-adenocarcinoma
#14
Neema Jamshidi, Daniel J Margolis, Steven Raman, Jiaoti Huang, Robert E Reiter, Michael D Kuo
Purpose To assess the underlying genomic variation of prostate gland microenvironments of patients with prostate adenocarcinoma in the context of colocalized multiparametric magnetic resonance (MR) imaging and histopathologic assessment of normal and abnormal regions by using whole-exome sequencing. Materials and Methods Six patients with prostate adenocarcinoma who underwent robotic prostatectomy with whole-mount preservation of the prostate were identified, which enabled spatial mapping between preoperative multiparametric MR imaging and the gland...
July 2017: Radiology
https://www.readbyqxmd.com/read/28448495/dysregulation-of-inf2-mediated-mitochondrial-fission-in-spop-mutated-prostate-cancer
#15
Xiaofeng Jin, Jie Wang, Kun Gao, Pingzhao Zhang, Longfang Yao, Yan Tang, Lisha Tang, Jian Ma, Jiantao Xiao, Enceng Zhang, Jie Zhu, Bin Zhang, Shi-Min Zhao, Yao Li, Shancheng Ren, Haojie Huang, Long Yu, Chenji Wang
Next-generation sequencing of the exome and genome of prostate cancers has identified numerous genetic alternations. SPOP (Speckle-type POZ Protein) was one of the most frequently mutated genes in primary prostate cancer, suggesting SPOP is a potential driver of prostate cancer development and progression. However, how SPOP mutations contribute to prostate cancer pathogenesis remains poorly understood. SPOP acts as an adaptor protein of the CUL3-RBX1 E3 ubiquitin ligase complex that generally recruits substrates for ubiquitination and subsequent degradation...
April 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28424341/alterations-in-three-dimensional-organization-of-the-cancer-genome-and-epigenome
#16
Joanna Achinger-Kawecka, Phillippa C Taberlay, Susan J Clark
The structural and functional basis of the genome is provided by the three-dimensional (3D) chromatin state. To enable accurate gene regulation, enhancer elements and promoter regions are brought into close spatial proximity to ensure proper, cell type-specific gene expression. In cancer, genetic and epigenetic processes can deregulate the transcriptional program. To investigate whether the 3D chromatin state is also disrupted in cancer we performed Hi-C chromosome conformation sequencing in normal and prostate cancer cells and compared the chromatin interaction maps with changes to the genome and epigenome...
April 19, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28423598/next-generation-mapping-reveals-novel-large-genomic-rearrangements-in-prostate-cancer
#17
Weerachai Jaratlerdsiri, Eva K F Chan, Desiree C Petersen, Claire Yang, Peter I Croucher, M S Riana Bornman, Palak Sheth, Vanessa M Hayes
Complex genomic rearrangements are common molecular events driving prostate carcinogenesis. Clinical significance, however, has yet to be fully elucidated. Detecting the full range and subtypes of large structural variants (SVs), greater than one kilobase in length, is challenging using clinically feasible next generation sequencing (NGS) technologies. Next generation mapping (NGM) is a new technology that allows for the interrogation of megabase length DNA molecules outside the detection range of single-base resolution NGS...
April 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28415558/family-with-sequence-similarity-13c-fam13c-overexpression-is-an-independent-prognostic-marker-in-prostate-cancer
#18
Christoph Burdelski, Laura Borcherding, Martina Kluth, Claudia Hube-Magg, Nathaniel Melling, Ronald Simon, Christina Möller-Koop, Philipp Weigand, Sarah Minner, Alexander Haese, Hans Uwe Michl, Maria Christina Tsourlakis, Frank Jacobsen, Andrea Hinsch, Corinna Wittmer, Patrick Lebok, Stefan Steurer, Jakob R Izbicki, Guido Sauter, Till Krech, Franziska Büscheck, Till Clauditz, Thorsten Schlomm, Waldemar Wilczak
FAM13C, a gene with unknown function is included in several mRNA signatures for prostate cancer aggressiveness. To understand the impact of FAM13C on prognosis and its relationship to molecularly defined subsets, we analyzed FAM13C expression by immunohistochemistry on a tissue microarray containing 12,400 prostate cancer specimens. Results were compared to phenotype, ERG status, genomic deletions of 3p, 5q, 6q and PTEN, and biochemical recurrence. FAM13C was detectable in cell nuclei of cancerous and non-neoplastic prostate cells...
May 9, 2017: Oncotarget
https://www.readbyqxmd.com/read/28413162/whole-genome-sequence-of-the-metastatic-pc3-and-lncap-human-prostate-cancer-cell-lines
#19
Inge Seim, Penny L Jeffery, Patrick B Thomas, Colleen C Nelson, Lisa K Chopin
The bone metastasis-derived PC3 and the lymph node metastasis-derived LNCaP prostate cancer cell lines are widely studied, having been described in thousands of publications over the last four decades. Here, we report short-read whole-genome sequencing and de novo assembly of PC3 (ATCC CRL-1435) and LNCaP (clone FGC; ATCC CRL-1740) at ~70X coverage. A known homozygous mutation in TP53 and homozygous loss of PTEN were robustly identified in the PC3 cell line, whereas the LNCaP cell line exhibited a larger number of putative inactivating somatic point and indel mutations (and in particular loss of stop codon events)...
April 16, 2017: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/28393575/using-circulating-cell-free-dna-to-monitor-personalized-cancer-therapy
#20
Michael Oellerich, Ekkehard Schütz, Julia Beck, Philipp Kanzow, Piers N Plowman, Glen J Weiss, Philip D Walson
High-quality genomic analysis is critical for personalized pharmacotherapy in patients with cancer. Tumor-specific genomic alterations can be identified in cell-free DNA (cfDNA) from patient blood samples and can complement biopsies for real-time molecular monitoring of treatment, detection of recurrence, and tracking resistance. cfDNA can be especially useful when tumor tissue is unavailable or insufficient for testing. For blood-based genomic profiling, next-generation sequencing (NGS) and droplet digital PCR (ddPCR) have been successfully applied...
May 2017: Critical Reviews in Clinical Laboratory Sciences
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