Recurrent Hemizygous Deletions in Cancers May Optimize Proliferative Potential

Author:

Solimini Nicole L.1,Xu Qikai1,Mermel Craig H.23,Liang Anthony C.1,Schlabach Michael R.1,Luo Ji1,Burrows Anna E.1,Anselmo Anthony N.1,Bredemeyer Andrea L.1,Li Mamie Z.1,Beroukhim Rameen234,Meyerson Matthew23,Elledge Stephen J.1

Affiliation:

1. Department of Genetics, Harvard University Medical School, and Division of Genetics, Howard Hughes Medical Institute, Brigham and Women’s Hospital, Boston, MA 02115, USA.

2. Departments of Medical Oncology and Cancer Biology and Center for Cancer Genome Discovery, Dana-Farber Cancer Institute, Boston, MA 02215, USA.

3. Cancer Program, Broad Institute of MIT and Harvard, Cambridge, MA 02141, USA.

4. Departments of Medicine, Harvard University Medical School and Brigham and Women’s Hospital, Boston, MA 02115, USA.

Abstract

Cancer Gene Islands Human tumors are riddled with genomic alterations that rearrange, remove, amplify, or otherwise disrupt a wide spectrum of genes, and a key challenge is identifying which of these alterations are causally involved in tumorigenesis. The role of recurrent hemizygous focal deletions is especially puzzling because these deletions preferentially affect certain chromosomal regions and result in the loss of one copy of a whole cluster of adjacent genes. Solimini et al. (p. 104 , published online 24 May; see the Perspective by Greenman ) found that these deletions span genomic regions that are enriched in genes that negatively regulate cell proliferation. The cumulative reduction in dosage and tumor suppressive function of the genes within these “cancer gene islands” may represent a critical factor driving tumor growth.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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