Comprehensive molecular portraits of human breast tumours.

Détails

ID Serval
serval:BIB_5B5C7C13B539
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Comprehensive molecular portraits of human breast tumours.
Périodique
Nature
Collaborateur(s)
Cancer Genome Atlas Network
Contributeur(s)
Koboldt D.C., Fulton R.S., McLellan M.D., Schmidt H., Kalicki-Veizer J., McMichael J.F., Fulton L.L., Dooling D.J., Ding L., Mardis E.R., Wilson R.K., Ally A., Balasundaram M., Butterfield Y.S., Carlsen R., Carter C., Chu A., Chuah E., Chun H.J., Coope R.J., Dhalla N., Guin R., Hirst C., Hirst M., Holt R.A., Lee D., Li H.I., Mayo M., Moore R.A., Mungall A.J., Pleasance E., Robertson A., Schein J.E., Shafiei A., Sipahimalani P., Slobodan J.R., Stoll D., Tam A., Thiessen N., Varhol R.J., Wye N., Zeng T., Zhao Y., Birol I., Jones S.J., Marra M.A., Cherniack A.D., Saksena G., Onofrio R.C., Pho N.H., Carter S.L., Schumacher S.E., Tabak B., Hernandez B., Gentry J., Nguyen H., Crenshaw A., Ardlie K., Beroukhim R., Winckler W., Getz G., Gabriel S.B., Meyerson M., Chin L., Park P.J., Kucherlapati R., Hoadley K.A., Auman J., Fan C., Turman Y.J., Shi Y., Li L., Topal M.D., He X., Chao H.H., Prat A., Silva G.O., Iglesia M.D., Zhao W., Usary J., Berg J.S., Adams M., Booker J., Wu J., Gulabani A., Bodenheimer T., Hoyle A.P., Simons J.V., Soloway M.G., Mose L.E., Jefferys S.R., Balu S., Parker J.S., Hayes D., Perou C.M., Malik S., Mahurkar S., Shen H., Weisenberger D.J., Triche T., Lai P.H., Bootwalla M.S., Maglinte D.T., Berman B.P., Van Den Berg D.J., Baylin S.B., Laird P.W., Creighton C.J., Donehower L.A., Getz G., Noble M., Voet D., Saksena G., Gehlenborg N., DiCara D., Zhang J., Zhang H., Wu C.J., Liu S.Y., Lawrence M.S., Zou L., Sivachenko A., Lin P., Stojanov P., Jing R., Cho J., Sinha R., Park R.W., Nazaire M.D., Robinson J., Thorvaldsdottir H., Mesirov J., Park P.J., Chin L., Reynolds S., Kreisberg R.B., Bernard B., Bressler R., Erkkila T., Lin J., Thorsson V., Zhang W., Shmulevich I., Ciriello G., Weinhold N., Schultz N., Gao J., Cerami E., Gross B., Jacobsen A., Sinha R., Aksoy B., Antipin Y., Reva B., Shen R., Taylor B.S., Ladanyi M., Sander C., Anur P., Spellman P.T., Lu Y., Liu W., Verhaak R.R., Mills G.B., Akbani R., Zhang N., Broom B.M., Casasent T.D., Wakefield C., Unruh A.K., Baggerly K., Coombes K., Weinstein J.N., Haussler D., Benz C.C., Stuart J.M., Benz S.C., Zhu J., Szeto C.C., Scott G.K., Yau C., Paull E.O., Carlin D., Wong C., Sokolov A., Thusberg J., Mooney S., Ng S., Goldstein T.C., Ellrott K., Grifford M., Wilks C., Ma S., Craft B., Yan C., Hu Y., Meerzaman D., Gastier-Foster J.M., Bowen J., Ramirez N.C., Black A.D., Pyatt R.E., White P., Zmuda E.J., Frick J., Lichtenberg T.M., Brookens R., George M.M., Gerken M.A., Harper H.A., Leraas K.M., Wise L.J., Tabler T.R., McAllister C., Barr T., Hart-Kothari M., Tarvin K., Saller C., Sandusky G., Mitchell C., Iacocca M.V., Brown J., Rabeno B., Czerwinski C., Petrelli N., Dolzhansky O., Abramov M., Voronina O., Potapova O., Marks J.R., Suchorska W.M., Murawa D., Kycler W., Ibbs M., Korski K., Spychała A., Murawa P., Brzeziński J.J., Perz H., Łaźniak R., Teresiak M., Tatka H., Leporowska E., Bogusz-Czerniewicz M., Malicki J., Mackiewicz A., Wiznerowicz M., Le X.V., Kohl B., Nguyen V.T., Thorp R., Nguyen V.B., Sussman H., Bui D.P., Hajek R., Nguyen P.H., Tran V.T., Huynh Q.T., Khan K.Z., Penny R., Mallery D., Curley E., Shelton C., Yena P., Ingle J.N., Couch F.J., Lingle W.L., King T.A., Gonzalez-Angulo A.M., Mills G.B., Dyer M.D., Liu S., Meng X., Patangan M., Waldman F., Stöppler H., Rathmell W., Thorne L., Huang M., Boice L., Hill A., Morrison C., Gaudioso C., Bshara W., Daily K., Egea S.C., Pegram M., Gomez-Fernandez C., Dhir R., Bhargava R., Brufsky A., Shriver C.D., Hooke J.A., Campbell J.L., Mural R.J., Hu H., Somiari S., Larson C., Deyarmin B., Kvecher L., Kovatich A.J., Ellis M.J., King T.A., Hu H., Couch F.J., Mural R.J., Stricker T., White K., Olopade O., Ingle J.N., Luo C., Chen Y., Marks J.R., Waldman F., Wiznerowicz M., Bose R., Chang L.W., Beck A.H., Gonzalez-Angulo A.M., Pihl T., Jensen M., Sfeir R., Kahn A., Chu A., Kothiyal P., Wang Z., Snyder E., Pontius J., Ayala B., Backus M., Walton J., Baboud J., Berton D., Nicholls M., Srinivasan D., Raman R., Girshik S., Kigonya P., Alonso S., Sanbhadti R., Barletta S., Pot D., Sheth M., Demchok J.A., Shaw K.R., Yang L., Eley G., Ferguson M.L., Tarnuzzer R.W., Zhang J., Dillon L.A., Buetow K., Fielding P., Ozenberger B.A., Guyer M.S., Sofia H.J., Palchik J.D.
ISSN
1476-4687 (Electronic)
ISSN-L
0028-0836
Statut éditorial
Publié
Date de publication
04/10/2012
Peer-reviewed
Oui
Volume
490
Numéro
7418
Pages
61-70
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
Publication Status: ppublish
Résumé
We analysed primary breast cancers by genomic DNA copy number arrays, DNA methylation, exome sequencing, messenger RNA arrays, microRNA sequencing and reverse-phase protein arrays. Our ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity. Somatic mutations in only three genes (TP53, PIK3CA and GATA3) occurred at >10% incidence across all breast cancers; however, there were numerous subtype-associated and novel gene mutations including the enrichment of specific mutations in GATA3, PIK3CA and MAP3K1 with the luminal A subtype. We identified two novel protein-expression-defined subgroups, possibly produced by stromal/microenvironmental elements, and integrated analyses identified specific signalling pathways dominant in each molecular subtype including a HER2/phosphorylated HER2/EGFR/phosphorylated EGFR signature within the HER2-enriched expression subtype. Comparison of basal-like breast tumours with high-grade serous ovarian tumours showed many molecular commonalities, indicating a related aetiology and similar therapeutic opportunities. The biological finding of the four main breast cancer subtypes caused by different subsets of genetic and epigenetic abnormalities raises the hypothesis that much of the clinically observable plasticity and heterogeneity occurs within, and not across, these major biological subtypes of breast cancer.
Mots-clé
Breast Neoplasms/classification, Breast Neoplasms/genetics, Breast Neoplasms/metabolism, Breast Neoplasms/pathology, Class I Phosphatidylinositol 3-Kinases, DNA Copy Number Variations/genetics, DNA Methylation, DNA Mutational Analysis, Exome/genetics, Female, GATA3 Transcription Factor/genetics, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genes, BRCA1, Genes, Neoplasm/genetics, Genes, erbB-2/genetics, Genes, p53/genetics, Genetic Heterogeneity, Genome, Human/genetics, Genomics, Humans, MAP Kinase Kinase Kinase 1/genetics, MicroRNAs/genetics, Mutation/genetics, Oligonucleotide Array Sequence Analysis, Ovarian Neoplasms/genetics, Ovarian Neoplasms/pathology, Phosphatidylinositol 3-Kinases/genetics, Protein Array Analysis, Proteomics, RNA, Messenger/genetics, RNA, Neoplasm/genetics, Receptors, Estrogen/metabolism, Retinoblastoma Protein/genetics, Retinoblastoma Protein/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
06/07/2018 11:02
Dernière modification de la notice
21/08/2019 5:34
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