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Characterization of the genomic architecture and mutational spectrum of a small cell prostate carcinoma.
Scott, Alan F; Mohr, David W; Ling, Hua; Scharpf, Robert B; Zhang, Peng; Liptak, Gregory S.
Afiliação
  • Scott AF; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. afscott@jhmi.edu.
  • Mohr DW; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. dwmohr@jhmi.edu.
  • Ling H; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. hling1@jhmi.edu.
  • Scharpf RB; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. rscharpf@jhsph.edu.
  • Zhang P; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. pzhang13@jhmi.edu.
  • Liptak GS; Department of Pediatrics, SUNY Upstate Medical Center, Golisano Children's Hospital, Syracuse, NY 13210, USA. gliptak@rochester.rr.com.
Genes (Basel) ; 5(2): 366-84, 2014 May 12.
Article em En | MEDLINE | ID: mdl-24823478
We present the use of a series of laboratory, analytical and interpretation methods to investigate personalized cancer care for a case of small cell prostate carcinoma (SCPC), a rare and aggressive tumor with poor prognosis, for which the underlying genomic architecture and mutational spectrum has not been well characterized. We performed both SNP genotyping and exome sequencing of a Virchow node metastasis from a patient with SCPC. A variety of methods were used to analyze and interpret the tumor genome for copy number variation, loss of heterozygosity (LOH), somatic mosaicism and mutations in genes from known cancer pathways. The combination of genotyping and exome sequencing approaches provided more information than either technique alone. The results showed widespread evidence of copy number changes involving most chromosomes including the possible loss of both alleles of CDKN1B (p27/Kip1). LOH was observed for the regions encompassing the tumor suppressors TP53, RB1, and CHD1. Predicted damaging somatic mutations were observed in the retained TP53 and RB1 alleles. Mutations in other genes that may be functionally relevant were noted, especially the recently reported high confidence cancer drivers FOXA1 and CCAR1. The disruption of multiple cancer drivers underscores why SCPC may be such a difficult cancer to manage.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2014 Tipo de documento: Article