New breast cancer susceptibility gene identified

Women with mutations in a gene called BRIP1 have twice the normal risk of breast cancer, according to a study to be published in the November issue of Nature Genetics.

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New breast cancer susceptibility gene identified - Nature Genetics

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[1] New breast cancer susceptibility gene identified

DOI: 10.1038/ng1902

Women with mutations in a gene called BRIP1 have twice the normal risk of breast cancer, according to a study to be published in the November issue of Nature Genetics.

Mutations in three genes - BRCA1, BRCA2, and TP53 - are known to greatly increase the chance of developing breast cancer over a lifetime: for example, women carrying a BRCA mutation have a 50-80% chance of developing the disease. Mutations in two other genes - CHEK2 and ATM - confer a much more modest risk. Nazneen Rahman and colleagues screened 1,212 women with breast cancer, who did not have mutations in BRCA1 and BRCA2, for mutations in BRIP1. They report that nine of these women had mutations in the BRIP1 gene, which most likely inactivates the BRIP1 protein; only two of 2,081 women in a 'control' group without breast cancer demonstrated such mutations.

The authors estimate - by taking into consideration information from the control group and the families of affected individuals - that BRIP1 mutations result in an approximately two-fold increase in the risk of breast cancer, which puts the gene into the same class as CHEK2 and ATM. They believe that mutations in these so-called ‘low-penetrance’ susceptibility genes likely only predispose to cancer in concert with other mutations and/or environmental factors, and account for only a small fraction of the familial risk of breast cancer. Like the other risk genes, BRIP1 is involved in DNA repair, lending support to the idea that unrepaired DNA damage is a key trigger for breast cancer development.

Author contact:
Nazneen Rahman (Institute of Cancer Research, Sutton, UK)
Tel: +44 208 722 4026; E-mail: [email protected]

Other papers from Nature Genetics to be published online at the same time and with the same embargo

[2] DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis

DOI: 10.1038/ng1868

[3] Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism
DOI: 10.1038/ng1905

[4] Nuclear organization of active and inactive chromatin domains uncovered by colocalized chromatin capture and characterization (4C)

DOI: 10.1038/ng1896

[5] Circular chromosome conformation capture (4C) uncovers extensive networks of epigenetically regulated intra- and interchromosomal interactions

DOI: 10.1038/ng1891

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[6] Surface expression of MHC class II in dendritic cells is controlled by regulated ubiquitination

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[8] Probing cell division phenotype space and mitotic spindle assembly mechanisms using small molecule inhibitors
DOI: 10.1038/nchembio826

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[13] Limited transfer of learning between unimanual and bimanual skills within the same limb
DOI: 10.1038/nn1785

[14] Ongoing eye movements constrain visual perception
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[15] Force field effects on cerebellar Purkinje cell discharge with implications for internal models
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[16] An allocentric rather than perceptual deficit in patient D.F.
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[23] RNA polymerase II C-terminal domain mediates regulation of alternative splicing by SRp20
DOI: 10.1038/nsmb1155

[24] Amino acid residues in Rag1 crucial for DNA hairpin formation
DOI: 10.1038/nsmb1154

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Montreal: 2, 3
Ottawa: 3

FRANCE
Grenoble: 9
Paris: 9

GERMANY
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Frankfurt am Main: 2
Freiburg: 18
Hanau: 2
Leipzig: 21
Munich: 2
Munich-Neuherberg: 2

ISRAEL
Rehovot: 10

JAPAN
Fukuoka: 22
Hiroshima: 22
Kumamoto: 22
Kure: 22
Saitama: 13
Sendai: 22
Tokushima: 22
Tokyo: 13

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Rotterdam: 4

SOUTH KOREA
Incheon: 12

SPAIN
Zaragoza: 2

SWEDEN
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UNITED KINGDOM
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Dundee: 7
Durham: 16
Edinburgh: 7
Glasgow: 7
Hinxton: 1
London: 17
Manchester: 1
Nottingham: 7, 17
Southampton: 1
Sutton: 1

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Pasadena: 21
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Kansas
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Massachusetts
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New York
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Ohio
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Texas
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Houston: 24
Utah
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Wisconsin
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Published: 08 Oct 2006

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