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Your search keyword '"Haffari, Gholamreza"' showing total 14 results
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14 results on '"Haffari, Gholamreza"'

8. The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups

Author

Curtis, Christina, Shah, Sohrab P, Chin, Suet-Feung, Turashvili, Gulisa, Rueda, Oscar M, Dunning, Mark J, Speed, Doug, Lynch, Andy G, Samarajiwa, Shamith, Yuan, Yinyin, Gräf, Stefan, Ha, Gavin, Haffari, Gholamreza, Bashashati, Ali, Russell, Roslin, McKinney, Steven, METABRIC Group, Langerød, Anita, Green, Andrew, Provenzano, Elena, Wishart, Gordon, Pinder, Sarah, Watson, Peter, Markowetz, Florian, Murphy, Leigh, Ellis, Ian, Purushotham, Arnie, Børresen-Dale, Anne-Lise, Brenton, James D, Tavaré, Simon, Caldas, Carlos, Aparicio, Samuel, Chin, Suet-Feung [0000-0001-5697-1082], Rueda Palacio, Oscar [0000-0003-0008-4884], Dunning, Mark [0000-0002-8853-9435], Lynch, Andy [0000-0002-7876-7338], Samarajiwa, Shamith [0000-0003-1046-0601], Graf, Stefan [0000-0002-1315-8873], Markowetz, Florian [0000-0002-2784-5308], Brenton, James [0000-0002-5738-6683], and Apollo - University of Cambridge Repository

Subjects
DNA Copy Number Variations, Genome, Human, MAP Kinase Kinase 4, Gene Expression Profiling, Breast Neoplasms, Genomics, Kaplan-Meier Estimate, Prognosis, Polymorphism, Single Nucleotide, Gene Expression Regulation, Neoplastic, Treatment Outcome, Humans, Female, Gene Regulatory Networks, Protein Phosphatase 2, Genes, Neoplasm
Abstract

The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA–RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the ‘CNA-devoid’ subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.

Published
2012

11. The clonal and mutational evolution spectrum of primary triple-negative breast cancers

Author

Shah, Sohrab P., primary, Roth, Andrew, additional, Goya, Rodrigo, additional, Oloumi, Arusha, additional, Ha, Gavin, additional, Zhao, Yongjun, additional, Turashvili, Gulisa, additional, Ding, Jiarui, additional, Tse, Kane, additional, Haffari, Gholamreza, additional, Bashashati, Ali, additional, Prentice, Leah M., additional, Khattra, Jaswinder, additional, Burleigh, Angela, additional, Yap, Damian, additional, Bernard, Virginie, additional, McPherson, Andrew, additional, Shumansky, Karey, additional, Crisan, Anamaria, additional, Giuliany, Ryan, additional, Heravi-Moussavi, Alireza, additional, Rosner, Jamie, additional, Lai, Daniel, additional, Birol, Inanc, additional, Varhol, Richard, additional, Tam, Angela, additional, Dhalla, Noreen, additional, Zeng, Thomas, additional, Ma, Kevin, additional, Chan, Simon K., additional, Griffith, Malachi, additional, Moradian, Annie, additional, Cheng, S.-W. Grace, additional, Morin, Gregg B., additional, Watson, Peter, additional, Gelmon, Karen, additional, Chia, Stephen, additional, Chin, Suet-Feung, additional, Curtis, Christina, additional, Rueda, Oscar M., additional, Pharoah, Paul D., additional, Damaraju, Sambasivarao, additional, Mackey, John, additional, Hoon, Kelly, additional, Harkins, Timothy, additional, Tadigotla, Vasisht, additional, Sigaroudinia, Mahvash, additional, Gascard, Philippe, additional, Tlsty, Thea, additional, Costello, Joseph F., additional, Meyer, Irmtraud M., additional, Eaves, Connie J., additional, Wasserman, Wyeth W., additional, Jones, Steven, additional, Huntsman, David, additional, Hirst, Martin, additional, Caldas, Carlos, additional, Marra, Marco A., additional, and Aparicio, Samuel, additional

Published
2012
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14. The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups

Author

Curtis, Christina, Shah, Sohrab P, Chin, Suet-Feung, Turashvili, Gulisa, Rueda, Oscar M, Dunning, Mark J, Speed, Doug, Lynch, Andy G, Samarajiwa, Shamith, Yuan, Yinyin, Gräf, Stefan, Ha, Gavin, Haffari, Gholamreza, Bashashati, Ali, Russell, Roslin, McKinney, Steven, METABRIC Group, Langerød, Anita, Green, Andrew, Provenzano, Elena, Wishart, Gordon, Pinder, Sarah, Watson, Peter, Markowetz, Florian, Murphy, Leigh, Ellis, Ian, Purushotham, Arnie, Børresen-Dale, Anne-Lise, Brenton, James D, Tavaré, Simon, Caldas, Carlos, and Aparicio, Samuel

Subjects
DNA Copy Number Variations, Genome, Human, MAP Kinase Kinase 4, Gene Expression Profiling, Breast Neoplasms, Genomics, Kaplan-Meier Estimate, Prognosis, Polymorphism, Single Nucleotide, 3. Good health, Gene Expression Regulation, Neoplastic, Treatment Outcome, Humans, Female, Gene Regulatory Networks, Protein Phosphatase 2, Genes, Neoplasm
Abstract

The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA–RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the ‘CNA-devoid’ subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.

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