Comprehensive molecular characterization of gastric adenocarcinoma. Nature, 513(7517):202-9, 2014. 1476-4687 Cancer Genome Atlas Research Network P30CA16672/CA/NCI NIH HHS/United States U24 CA143882/CA/NCI NIH HHS/United States 5U24CA143840/CA/NCI NIH HHS/United States R01 HG005690/HG/NHGRI NIH HHS/United States 5U24CA143835/CA/NCI NIH HHS/United States U24 CA143843/CA/NCI NIH HHS/United States U24 CA143883/CA/NCI NIH HHS/United States U24 CA143867/CA/NCI NIH HHS/United States 5U24CA143882/CA/NCI NIH HHS/United States 5U24CA143799/CA/NCI NIH HHS/United States P30 CA016672/CA/NCI NIH HHS/United States K99 CA166729/CA/NCI NIH HHS/United States P01 CA028842/CA/NCI NIH HHS/United States 5U24CA143843/CA/NCI NIH HHS/United States U54 HG003067/HG/NHGRI NIH HHS/United States U54HG003273/HG/NHGRI NIH HHS/United States U24 CA143835/CA/NCI NIH HHS/United States 5U24CA143867/CA/NCI NIH HHS/United States P30 CA006973/CA/NCI NIH HHS/United States 5U24CA143866/CA/NCI NIH HHS/United States U24 CA143866/CA/NCI NIH HHS/United States K08 CA134931/CA/NCI NIH HHS/United States R01 HG007069/HG/NHGRI NIH HHS/United States U54HG003067/HG/NHGRI NIH HHS/United States U24 CA143845/CA/NCI NIH HHS/United States U24 CA143799/CA/NCI NIH HHS/United States P50 CA098258/CA/NCI NIH HHS/United States 5U24CA144025/CA/NCI NIH HHS/United States U54 HG003273/HG/NHGRI NIH HHS/United States P30 CA008748/CA/NCI NIH HHS/United States U24 CA144025/CA/NCI NIH HHS/United States 5U24CA143848/CA/NCI NIH HHS/United States U54HG003079/HG/NHGRI NIH HHS/United States U24 CA180951/CA/NCI NIH HHS/United States U24 CA143840/CA/NCI NIH HHS/United States R01 CA180006/CA/NCI NIH HHS/United States U24 CA143858/CA/NCI NIH HHS/United States 5U24CA143858/CA/NCI NIH HHS/United States U24 CA143848/CA/NCI NIH HHS/United States U24 CA126543/CA/NCI NIH HHS/United States ImNIH/Intramural NIH HHS/United States 5U24CA143845/CA/NCI NIH HHS/United States U54 HG003079/HG/NHGRI NIH HHS/United States 5U24CA143883/CA/NCI NIH HHS/United States Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural England 2014/08/01 Nature. 2014 Sep 11;513(7517):202-9. doi: 10.1038/nature13480. Epub 2014 Jul 23.doi abstract bibtex Gastric cancer is a leading cause of cancer deaths, but analysis of its molecular and clinical characteristics has been complicated by histological and aetiological heterogeneity. Here we describe a comprehensive molecular evaluation of 295 primary gastric adenocarcinomas as part of The Cancer Genome Atlas (TCGA) project. We propose a molecular classification dividing gastric cancer into four subtypes: tumours positive for Epstein-Barr virus, which display recurrent PIK3CA mutations, extreme DNA hypermethylation, and amplification of JAK2, CD274 (also known as PD-L1) and PDCD1LG2 (also known as PD-L2); microsatellite unstable tumours, which show elevated mutation rates, including mutations of genes encoding targetable oncogenic signalling proteins; genomically stable tumours, which are enriched for the diffuse histological variant and mutations of RHOA or fusions involving RHO-family GTPase-activating proteins; and tumours with chromosomal instability, which show marked aneuploidy and focal amplification of receptor tyrosine kinases. Identification of these subtypes provides a roadmap for patient stratification and trials of targeted therapies.
@article{RN6156,
title = {Comprehensive molecular characterization of gastric adenocarcinoma},
journal = {Nature},
volume = {513},
number = {7517},
pages = {202-9},
note = {1476-4687
Cancer Genome Atlas Research Network
P30CA16672/CA/NCI NIH HHS/United States
U24 CA143882/CA/NCI NIH HHS/United States
5U24CA143840/CA/NCI NIH HHS/United States
R01 HG005690/HG/NHGRI NIH HHS/United States
5U24CA143835/CA/NCI NIH HHS/United States
U24 CA143843/CA/NCI NIH HHS/United States
U24 CA143883/CA/NCI NIH HHS/United States
U24 CA143867/CA/NCI NIH HHS/United States
5U24CA143882/CA/NCI NIH HHS/United States
5U24CA143799/CA/NCI NIH HHS/United States
P30 CA016672/CA/NCI NIH HHS/United States
K99 CA166729/CA/NCI NIH HHS/United States
P01 CA028842/CA/NCI NIH HHS/United States
5U24CA143843/CA/NCI NIH HHS/United States
U54 HG003067/HG/NHGRI NIH HHS/United States
U54HG003273/HG/NHGRI NIH HHS/United States
U24 CA143835/CA/NCI NIH HHS/United States
5U24CA143867/CA/NCI NIH HHS/United States
P30 CA006973/CA/NCI NIH HHS/United States
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R01 HG007069/HG/NHGRI NIH HHS/United States
U54HG003067/HG/NHGRI NIH HHS/United States
U24 CA143845/CA/NCI NIH HHS/United States
U24 CA143799/CA/NCI NIH HHS/United States
P50 CA098258/CA/NCI NIH HHS/United States
5U24CA144025/CA/NCI NIH HHS/United States
U54 HG003273/HG/NHGRI NIH HHS/United States
P30 CA008748/CA/NCI NIH HHS/United States
U24 CA144025/CA/NCI NIH HHS/United States
5U24CA143848/CA/NCI NIH HHS/United States
U54HG003079/HG/NHGRI NIH HHS/United States
U24 CA180951/CA/NCI NIH HHS/United States
U24 CA143840/CA/NCI NIH HHS/United States
R01 CA180006/CA/NCI NIH HHS/United States
U24 CA143858/CA/NCI NIH HHS/United States
5U24CA143858/CA/NCI NIH HHS/United States
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U24 CA126543/CA/NCI NIH HHS/United States
ImNIH/Intramural NIH HHS/United States
5U24CA143845/CA/NCI NIH HHS/United States
U54 HG003079/HG/NHGRI NIH HHS/United States
5U24CA143883/CA/NCI NIH HHS/United States
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
England
2014/08/01
Nature. 2014 Sep 11;513(7517):202-9. doi: 10.1038/nature13480. Epub 2014 Jul 23.},
abstract = {Gastric cancer is a leading cause of cancer deaths, but analysis of its molecular and clinical characteristics has been complicated by histological and aetiological heterogeneity. Here we describe a comprehensive molecular evaluation of 295 primary gastric adenocarcinomas as part of The Cancer Genome Atlas (TCGA) project. We propose a molecular classification dividing gastric cancer into four subtypes: tumours positive for Epstein-Barr virus, which display recurrent PIK3CA mutations, extreme DNA hypermethylation, and amplification of JAK2, CD274 (also known as PD-L1) and PDCD1LG2 (also known as PD-L2); microsatellite unstable tumours, which show elevated mutation rates, including mutations of genes encoding targetable oncogenic signalling proteins; genomically stable tumours, which are enriched for the diffuse histological variant and mutations of RHOA or fusions involving RHO-family GTPase-activating proteins; and tumours with chromosomal instability, which show marked aneuploidy and focal amplification of receptor tyrosine kinases. Identification of these subtypes provides a roadmap for patient stratification and trials of targeted therapies.},
keywords = {Adenocarcinoma/*classification/*genetics/virology
Female
Gene Expression Regulation, Neoplastic
Genome, Human/*genetics
Herpesvirus 4, Human/genetics/isolation & purification
Humans
Male
Mutation
Proteome
Stomach Neoplasms/*classification/*genetics/virology},
ISSN = {0028-0836 (Print)
0028-0836},
DOI = {10.1038/nature13480},
year = {2014},
type = {Journal Article}
}
Downloads: 0
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