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Germline Mutations in Oncogene-Induced Senescence Pathways Are Associated With Multiple Sessile Serrated Adenomas

Little is known about the genetic factors that contribute to the development of sessile serrated adenomas (SSAs). SSAs contain somatic mutations in AF or KRAS early in development. However, evidence from humans and mouse models indicates that these mutations result in oncogene-induced senescence (OI... Full description

Journal Title: Gastroenterology February 2014, Vol.146(2), pp.520-529.e6
Main Author: Gala, Manish K
Other Authors: Mizukami, Yusuke , Le, Long P , Moriichi, Kentaro , Austin, Thomas , Yamamoto, Masayoshi , Lauwers, Gregory Y , Bardeesy, Nabeel , Chung, Daniel C
Format: Electronic Article Electronic Article
Language: English
Subjects:
Ci
Ddr
Lof
Ois
OR
SSA
ID: ISSN: 0016-5085 ; E-ISSN: 1528-0012 ; DOI: 10.1053/j.gastro.2013.10.045
Link: http://dx.doi.org/10.1053/j.gastro.2013.10.045
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recordid: elsevier_sdoi_10_1053_j_gastro_2013_10_045
title: Germline Mutations in Oncogene-Induced Senescence Pathways Are Associated With Multiple Sessile Serrated Adenomas
format: Article
creator:
  • Gala, Manish K
  • Mizukami, Yusuke
  • Le, Long P
  • Moriichi, Kentaro
  • Austin, Thomas
  • Yamamoto, Masayoshi
  • Lauwers, Gregory Y
  • Bardeesy, Nabeel
  • Chung, Daniel C
subjects:
  • Serrated Polyposis Syndrome
  • Hereditary Colon Cancer
  • Sessile Serrated Polyp
  • Rnf43
  • Serrated Polyposis Syndrome
  • Hereditary Colon Cancer
  • Sessile Serrated Polyp
  • Rnf43
  • Ci
  • Ddr
  • Gwas
  • Lof
  • Ois
  • OR
  • SSA
  • Medicine
ispartof: Gastroenterology, February 2014, Vol.146(2), pp.520-529.e6
description: Little is known about the genetic factors that contribute to the development of sessile serrated adenomas (SSAs). SSAs contain somatic mutations in AF or KRAS early in development. However, evidence from humans and mouse models indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt cells. Progression to serrated neoplasia requires cells to escape OIS via inactivation of tumor suppressor pathways. We investigated whether subjects with multiple SSAs carry germline loss-of-function mutations (nonsense and splice site) in genes that regulate OIS: the p16-Rb and ATM-ATR DNA damage response pathways. Through a bioinformatic analysis of the literature, we identified a set of genes that function at the main nodes of the p16-Rb and ATM-ATR DNA damage response pathways. We performed whole-exome sequencing of 20 unrelated subjects with multiple SSAs; most had features of serrated polyposis. We compared sequences with those from...
language: eng
source:
identifier: ISSN: 0016-5085 ; E-ISSN: 1528-0012 ; DOI: 10.1053/j.gastro.2013.10.045
fulltext: fulltext
issn:
  • 0016-5085
  • 00165085
  • 1528-0012
  • 15280012
url: Link


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titleGermline Mutations in Oncogene-Induced Senescence Pathways Are Associated With Multiple Sessile Serrated Adenomas
creatorGala, Manish K ; Mizukami, Yusuke ; Le, Long P ; Moriichi, Kentaro ; Austin, Thomas ; Yamamoto, Masayoshi ; Lauwers, Gregory Y ; Bardeesy, Nabeel ; Chung, Daniel C
ispartofGastroenterology, February 2014, Vol.146(2), pp.520-529.e6
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subjectSerrated Polyposis Syndrome ; Hereditary Colon Cancer ; Sessile Serrated Polyp ; Rnf43 ; Serrated Polyposis Syndrome ; Hereditary Colon Cancer ; Sessile Serrated Polyp ; Rnf43 ; Ci ; Ddr ; Gwas ; Lof ; Ois ; OR ; SSA ; Medicine
descriptionLittle is known about the genetic factors that contribute to the development of sessile serrated adenomas (SSAs). SSAs contain somatic mutations in AF or KRAS early in development. However, evidence from humans and mouse models indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt cells. Progression to serrated neoplasia requires cells to escape OIS via inactivation of tumor suppressor pathways. We investigated whether subjects with multiple SSAs carry germline loss-of-function mutations (nonsense and splice site) in genes that regulate OIS: the p16-Rb and ATM-ATR DNA damage response pathways. Through a bioinformatic analysis of the literature, we identified a set of genes that function at the main nodes of the p16-Rb and ATM-ATR DNA damage response pathways. We performed whole-exome sequencing of 20 unrelated subjects with multiple SSAs; most had features of serrated polyposis. We compared sequences with those from...
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titleGermline Mutations in Oncogene-Induced Senescence Pathways Are Associated With Multiple Sessile Serrated Adenomas
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Little is known about the genetic factors that contribute to the development of sessile serrated adenomas (SSAs). SSAs contain somatic mutations in BRAF or KRAS early in development. However, evidence from humans and mouse models indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt cells. Progression to serrated neoplasia requires cells to escape OIS via inactivation of tumor suppressor pathways. We investigated whether subjects with multiple SSAs carry germline loss-of-function mutations (nonsense and splice site) in genes that regulate OIS: the p16-Rb and ATM-ATR DNA damage response pathways.

Through a bioinformatic analysis of the literature, we identified a set of genes that function at the main nodes of the p16-Rb and ATM-ATR DNA damage response pathways. We performed whole-exome sequencing of 20 unrelated subjects with multiple SSAs; most had features of serrated polyposis. We compared sequences with those from...

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abstract

Little is known about the genetic factors that contribute to the development of sessile serrated adenomas (SSAs). SSAs contain somatic mutations in BRAF or KRAS early in development. However, evidence from humans and mouse models indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt cells. Progression to serrated neoplasia requires cells to escape OIS via inactivation of tumor suppressor pathways. We investigated whether subjects with multiple SSAs carry germline loss-of-function mutations (nonsense and splice site) in genes that regulate OIS: the p16-Rb and ATM-ATR DNA damage response pathways.

Through a bioinformatic analysis of the literature, we identified a set of genes that function at the main nodes of the p16-Rb and ATM-ATR DNA damage response pathways. We performed whole-exome sequencing of 20 unrelated subjects with multiple SSAs; most had features of serrated polyposis. We compared sequences with those from...

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date2014-02