schliessen

Filtern

 

Bibliotheken

Concomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers

Aberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and breast cancers, were evaluated using primary lung... Full description

Journal Title: Carcinogenesis 2009, 2009, Vol. 30(7), pp.1132-1138
Main Author: Tessema, Mathewos
Other Authors: Yu, Yang Y , Stidley, Christine A , Machida, Emi O , Schuebel, Kornel E , Baylin, Stephen B , Belinsky, Steven A
Format: Electronic Article Electronic Article
Language:
Subjects:
ID: ISSN: 0143-3334 ; E-ISSN: 1460-2180 ; DOI: 10.1093/carcin/bgp114
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: oxford10.1093/carcin/bgp114
title: Concomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
format: Article
creator:
  • Tessema, Mathewos
  • Yu, Yang Y
  • Stidley, Christine A
  • Machida, Emi O
  • Schuebel, Kornel E
  • Baylin, Stephen B
  • Belinsky, Steven A
subjects:
  • Medicine
ispartof: Carcinogenesis, 2009, 2009, Vol. 30(7), pp.1132-1138
description: Aberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and breast cancers, were evaluated using primary lung adenocarcinomas ( n = 175) from current, former and never smokers. Tumor specificity of methylation was validated through comparison of 14 lung cancer cell lines to normal human bronchial epithelial cells derived from bronchoscopy of 20 cancer-free smokers. Twenty-five genes were methylated in 11–81% of primary tumors. Prevalence for methylation of TNFRSF10C , BHLHB5 and BOLL was significantly higher in adenocarcinomas from never smokers than smokers. The relation between methylation of individual genes was examined using pairwise comparisons. A significant association was seen between 138 (42%) of the possible 325 pairwise comparisons. Most notably, methylation of MMP2 , BHLHB4 or p16 was significantly associated with methylation of 16–19 other genes, thus predicting for a widespread methylation phenotype. Kaplan–Meier log-rank test and proportional hazard models identified a significant association between methylation of SULF2 (a pro-growth, -angiogenesis and -migration gene) and better patient survival (hazard ratio = 0.23). These results demonstrate a high degree of commonality for targeted silencing of genes between lung and other solid tumors and suggest that promoter hypermethylation in cancer is a highly co-ordinated event.
language:
source:
identifier: ISSN: 0143-3334 ; E-ISSN: 1460-2180 ; DOI: 10.1093/carcin/bgp114
fulltext: fulltext
issn:
  • 0143-3334
  • 01433334
  • 1460-2180
  • 14602180
url: Link


@attributes
ID986464439
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid10.1093/carcin/bgp114
sourceidoxford
recordidTN_oxford10.1093/carcin/bgp114
sourceformatXML
sourcesystemPC
pqid67445966
display
typearticle
titleConcomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
creatorTessema, Mathewos ; Yu, Yang Y ; Stidley, Christine A ; Machida, Emi O ; Schuebel, Kornel E ; Baylin, Stephen B ; Belinsky, Steven A
ispartofCarcinogenesis, 2009, 2009, Vol. 30(7), pp.1132-1138
identifier
descriptionAberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and breast cancers, were evaluated using primary lung adenocarcinomas ( n = 175) from current, former and never smokers. Tumor specificity of methylation was validated through comparison of 14 lung cancer cell lines to normal human bronchial epithelial cells derived from bronchoscopy of 20 cancer-free smokers. Twenty-five genes were methylated in 11–81% of primary tumors. Prevalence for methylation of TNFRSF10C , BHLHB5 and BOLL was significantly higher in adenocarcinomas from never smokers than smokers. The relation between methylation of individual genes was examined using pairwise comparisons. A significant association was seen between 138 (42%) of the possible 325 pairwise comparisons. Most notably, methylation of MMP2 , BHLHB4 or p16 was significantly associated with methylation of 16–19 other genes, thus predicting for a widespread methylation phenotype. Kaplan–Meier log-rank test and proportional hazard models identified a significant association between methylation of SULF2 (a pro-growth, -angiogenesis and -migration gene) and better patient survival (hazard ratio = 0.23). These results demonstrate a high degree of commonality for targeted silencing of genes between lung and other solid tumors and suggest that promoter hypermethylation in cancer is a highly co-ordinated event.
source
subjectMedicine;
version6
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
search
creatorcontrib
0Tessema, Mathewos
1Yu, Yang Y
2Stidley, Christine A
3Machida, Emi O
4Schuebel, Kornel E
5Baylin, Stephen B
6Belinsky, Steven A
titleConcomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
descriptionAberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and breast cancers, were evaluated using primary lung adenocarcinomas ( n = 175) from current, former and never smokers. Tumor specificity of methylation was validated through comparison of 14 lung cancer cell lines to normal human bronchial epithelial cells derived from bronchoscopy of 20 cancer-free smokers. Twenty-five genes were methylated in 11–81% of primary tumors. Prevalence for methylation of TNFRSF10C , BHLHB5 and BOLL was significantly higher in adenocarcinomas from never smokers than smokers. The relation between methylation of individual genes was examined using pairwise comparisons. A significant association was seen between 138 (42%) of the possible 325 pairwise comparisons. Most notably, methylation of MMP2 , BHLHB4 or p16 was significantly associated with methylation of 16–19 other genes, thus predicting for a widespread methylation phenotype. Kaplan–Meier log-rank test and proportional hazard models identified a significant association between methylation of SULF2 (a pro-growth, -angiogenesis and -migration gene) and better patient survival (hazard ratio = 0.23). These results demonstrate a high degree of commonality for targeted silencing of genes between lung and other solid tumors and suggest that promoter hypermethylation in cancer is a highly co-ordinated event.
general
010.1093/carcin/bgp114
1Oxford Journals
sourceidoxford
recordidoxford10.1093/carcin/bgp114
issn
00143-3334
101433334
21460-2180
314602180
rsrctypearticle
creationdate2009
addtitleCarcinogenesis
searchscopeoxford
scopeoxford
lsr4120090512
lsr30VSR-Enriched:[subject, pqid]
sort
titleConcomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
authorTessema, Mathewos ; Yu, Yang Y ; Stidley, Christine A ; Machida, Emi O ; Schuebel, Kornel E ; Baylin, Stephen B ; Belinsky, Steven A
creationdate200907
facets
frbrgroupid5448549872821863531
frbrtype5
creationdate2009
collectionOxford Journals (Oxford University Press)
prefilterarticles
rsrctypearticles
creatorcontrib
0Tessema, Mathewos
1Yu, Yang Y
2Stidley, Christine A
3Machida, Emi O
4Schuebel, Kornel E
5Baylin, Stephen B
6Belinsky, Steven A
jtitleCarcinogenesis
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Tessema
1Yu
2Stidley
3Machida
4Schuebel
5Baylin
6Belinsky
aufirst
0Mathewos
1Yang Y.
2Christine A.
3Emi O.
4Kornel E.
5Stephen B.
6Steven A.
au
0Tessema, Mathewos
1Yu, Yang Y.
2Stidley, Christine A.
3Machida, Emi O.
4Schuebel, Kornel E.
5Baylin, Stephen B.
6Belinsky, Steven A.
atitleConcomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
jtitleCarcinogenesis
date
0200907
120090512
risdate200907
volume30
issue7
spage1132
epage1138
pages1132-1138
issn0143-3334
eissn1460-2180
formatjournal
genrearticle
ristypeJOUR
abstractAberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and breast cancers, were evaluated using primary lung adenocarcinomas ( n = 175) from current, former and never smokers. Tumor specificity of methylation was validated through comparison of 14 lung cancer cell lines to normal human bronchial epithelial cells derived from bronchoscopy of 20 cancer-free smokers. Twenty-five genes were methylated in 11–81% of primary tumors. Prevalence for methylation of TNFRSF10C , BHLHB5 and BOLL was significantly higher in adenocarcinomas from never smokers than smokers. The relation between methylation of individual genes was examined using pairwise comparisons. A significant association was seen between 138 (42%) of the possible 325 pairwise comparisons. Most notably, methylation of MMP2 , BHLHB4 or p16 was significantly associated with methylation of 16–19 other genes, thus predicting for a widespread methylation phenotype. Kaplan–Meier log-rank test and proportional hazard models identified a significant association between methylation of SULF2 (a pro-growth, -angiogenesis and -migration gene) and better patient survival (hazard ratio = 0.23). These results demonstrate a high degree of commonality for targeted silencing of genes between lung and other solid tumors and suggest that promoter hypermethylation in cancer is a highly co-ordinated event.
pubOxford University Press
doi10.1093/carcin/bgp114