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N LA, Gathmann I, Capdeville R, Hensley M, Polymeropoulos MH: Correlation of major cytogenetic response with a pharmacogenetic marker in chronic myeloid leukemia patients treated with imatinib (STI571). Clin order Q-VD-OPh Cancer Res 2004, 10:2265-2271. 51. Kim DH, Kong JH, Byeun JY, Jung CW, Xu W, Liu X, Kamel-Reid S, Kim YK, Kim HJ, Lipton JH: The IFNG (IFN-gamma) genotype predicts cytogenetic and molecular response to imatinib therapy in chronic myeloid leukemia. Clin Cancer Res 2010, 16:5339-5350. 52. Zach O, Krieger O, Foedermayr M, Zellhofer B, Lutz D: OCT1 (SLC22A1) R61C polymorphism and response to imatinib treatment in chronic myeloid leukemia patients. Leuk Lymphoma 2008, 49:2222-2223. 53. Entrez SNP [http://www.ncbi.nlm.nih.gov/sites/entrez?db=snp]doi:10.1186/gm206 Cite this article as: Dulucq S, Krajinovic M: The pharmacogenetics of imanitib. Genome Medicine 2010, 2:85.
Kumar et al. Genome Medicine 2011, 3:23 http://genomemedicine.com/content/3/4/RESEARCH HIGHLIGHTGenome interrupted: sequencing of prostate cancer reveals the importance of chromosomal rearrangementsAkash Kumar1, Jay Shendure1 and Peter S Nelson*e genomes of a number of carcinomas, including breast, lung and skin, have been sequenced (Table 1). ese studies have provided fascinating insights into tumor biology, and have identified new leads for diagnosis and therapy [2-4]. A recent Nature article by Berger and colleagues [1] details the first whole genome study of prostate cancer. e work builds on earlier findings concerning the genetic make-up of cancers and highlights aspects that appear to be unique to prostate tumors.Abstract A recent study involving whole genome sequencing of seven prostate cancers has provided the rst comprehensive assessment of genomic changes that underlie this common malignancy. Point mutations were found to be infrequent but changes in chromosome structure were common. Rearrangements were linked to chromatin organization and associated with regions involved in transcription factor binding. Novel candidate prostate cancer genes were also identi ed, highlighting the importance of genome sequencing to identify oncogenic changes that are otherwise invisible to detection. From genetics to genomics in prostate cancer research Prostate cancer is diagnosed in more than 200,000 men and accounts for more than 30,000 fatalities in the USA every year [1]. e course of this disease is remarkably heterogeneous; some cancers remain asymptomatic for decades, while others rapidly metastasize to bone and other tissues, resulting in substantial morbidity and mortality. Although several genetic abnormalities have previously been identified in prostate cancer, including recurrent rearrangements involving the androgenregulated serine protease gene TMPRSS2 and members of the ETS family of oncogenic transcription factors [1], a complete view of the prostate cancer genome has been lacking. Major advances in DNA sequencing technology have recently enabled the exploration of the genetic underpinnings of cancer to an unprecedented level of detail.*Correspondence: [email protected] 2 Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N., Seattle, WA 98109, USA Full list of author information is available at the end of the article?2010 PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28914615 BioMed Central Ltd ?2011 BioMed Central LtdRelatively few point mutations in prostate cancer Berger et al. [1] sequenced the genomes of seven highgrade aggressive primary prostate cancers and corresponding normal tissues by generating ap.