Somatic recombination redux

Jay A. Tischfield; Changshun Shao

doi:10.1038/ng0103-5

Somatic recombination redux

Jay A. Tischfield
, Changshun Shao

Research output: Contribution to journal › Short survey › peer-review

23 Scopus citations

Abstract

A mouse model for familial adenomatous polyposis has been used to distinguish between possible mechanisms leading to loss of function of the Apc tumor-suppressor gene. Somatic recombination rather than chromosome loss associated with genetic instability is the primary cause of these cancers. Moreover, the data suggest that interphase nuclear architecture is a key factor in facilitating this process.

Original language	English (US)
Pages (from-to)	5-6
Number of pages	2
Journal	Nature genetics
Volume	33
Issue number	1
DOIs	https://doi.org/10.1038/ng0103-5
State	Published - Jan 1 2003

All Science Journal Classification (ASJC) codes

Genetics

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10.1038/ng0103-5

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abstract = "A mouse model for familial adenomatous polyposis has been used to distinguish between possible mechanisms leading to loss of function of the Apc tumor-suppressor gene. Somatic recombination rather than chromosome loss associated with genetic instability is the primary cause of these cancers. Moreover, the data suggest that interphase nuclear architecture is a key factor in facilitating this process.",

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AB - A mouse model for familial adenomatous polyposis has been used to distinguish between possible mechanisms leading to loss of function of the Apc tumor-suppressor gene. Somatic recombination rather than chromosome loss associated with genetic instability is the primary cause of these cancers. Moreover, the data suggest that interphase nuclear architecture is a key factor in facilitating this process.

UR - https://www.scopus.com/pages/publications/0037228054

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JO - Nature genetics

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Somatic recombination redux

Abstract

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