(Q54603929)

1 June 2018

title

BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer. (English)

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1 June 2018

author name string

Michelle W Wong

1

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1 June 2018

Cecilia Nordfors

2

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1 June 2018

David Mossman

3

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1 June 2018

Gordana Pecenpetelovska

4

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1 June 2018

Kelly A Avery-Kiejda

5

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1 June 2018

Bente Talseth-Palmer

6

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1 June 2018

Nikola A Bowden

7

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1 June 2018

Rodney J Scott

8

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1 June 2018

language of work or name

English

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publication date

16 March 2011

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1 June 2018

Breast Cancer Research and Treatment

published in

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1 June 2018

volume

127

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1 June 2018

issue

3

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1 June 2018

page(s)

853-859

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1 June 2018

https://scigraph.springernature.com/pub.10.1007/s10549-011-1443-0

exact match

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cites work

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Genome-wide linkage scan reveals three putative breast-cancer-susceptibility loci

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TGFB1 and TGFBR1 polymorphisms and breast cancer risk in the Nurses' Health Study

21 January 2018

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Germline mutations in breast and ovarian cancer pedigrees establish RAD51C as a human cancer susceptibility gene

21 January 2018

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Fanconi anemia and breast cancer susceptibility meet again

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Truncating mutations in the Fanconi anemia J gene BRIP1 are low-penetrance breast cancer susceptibility alleles

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FANCJ/BRIP1 recruitment and regulation of FANCD2 in DNA damage responses.

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Control of BRCA2 cellular and clinical functions by a nuclear partner, PALB2.

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PALB2, which encodes a BRCA2-interacting protein, is a breast cancer susceptibility gene

21 January 2018

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Fanconi anemia is associated with a defect in the BRCA2 partner PALB2.

21 January 2018

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The BRCA1-interacting helicase BRIP1 is deficient in Fanconi anemia

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Mutation of the RAD51C gene in a Fanconi anemia-like disorder

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BACH1, a novel helicase-like protein, interacts directly with BRCA1 and contributes to its DNA repair function

21 January 2018

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The BRCT Domain Is a Phospho-Protein Binding Domain

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The BRCA1-associated protein BACH1 is a DNA helicase targeted by clinically relevant inactivating mutations

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PALB2 is an integral component of the BRCA complex required for homologous recombination repair

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Biallelic mutations in PALB2 cause Fanconi anemia subtype FA-N and predispose to childhood cancer

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Association of BRCA1 with Rad51 in mitotic and meiotic cells

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Linking the cellular functions of BRCA genes to cancer pathogenesis and treatment

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Breast cancer susceptibility: current knowledge and implications for genetic counselling

21 January 2018

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Analysis of PALB2/FANCN-associated breast cancer families

21 January 2018

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Mutational analysis of the BRCA1-interacting genes ZNF350/ZBRK1 and BRIP1/BACH1 among BRCA1 and BRCA2-negative probands from breast-ovarian cancer families and among early-onset breast cancer cases and reference individuals

21 January 2018

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Predicting the effects of coding non-synonymous variants on protein function using the SIFT algorithm

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21 January 2018

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PALB2/FANCN: recombining cancer and Fanconi anemia

21 January 2018

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Identification of a novel truncating PALB2 mutation and analysis of its contribution to early-onset breast cancer in French-Canadian women

21 January 2018

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Structural basis for recruitment of BRCA2 by PALB2

21 January 2018

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https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

PALB2 functionally connects the breast cancer susceptibility proteins BRCA1 and BRCA2.

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

PALB2 links BRCA1 and BRCA2 in the DNA-damage response

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

Cooperation of breast cancer proteins PALB2 and piccolo BRCA2 in stimulating homologous recombination

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

Cancer Incidence in BRCA1 mutation carriers

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

Cancer risks in BRCA2 mutation carriers

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10549-011-1443-0

10.1007/S10549-011-1443-0

21 January 2018

Identifiers

DOI

1 reference

1 June 2018

1 reference

1 June 2018