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

Author

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

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Women's Health, Cancer, 4.1 Discovery and preclinical testing of markers and technologies, Alleles, Breast Neoplasms, Clone Cells, DNA Copy Number Variations, DNA Mutational Analysis, Disease Progression, Evolution, Molecular, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genotype, High-Throughput Nucleotide Sequencing, Humans, INDEL Mutation, Mutation, Point Mutation, Precision Medicine, Reproducibility of Results, Sequence Analysis, RNA, General Science & Technology
Abstract

Primary triple-negative breast cancers (TNBCs), a tumour type defined by lack of oestrogen receptor, progesterone receptor and ERBB2 gene amplification, represent approximately 16% of all breast cancers. Here we show in 104 TNBC cases that at the time of diagnosis these cancers exhibit a wide and continuous spectrum of genomic evolution, with some having only a handful of coding somatic aberrations in a few pathways, whereas others contain hundreds of coding somatic mutations. High-throughput RNA sequencing (RNA-seq) revealed that only approximately 36% of mutations are expressed. Using deep re-sequencing measurements of allelic abundance for 2,414 somatic mutations, we determine for the first time-to our knowledge-in an epithelial tumour subtype, the relative abundance of clonal frequencies among cases representative of the population. We show that TNBCs vary widely in their clonal frequencies at the time of diagnosis, with the basal subtype of TNBC showing more variation than non-basal TNBC. Although p53 (also known as TP53), PIK3CA and PTEN somatic mutations seem to be clonally dominant compared to other genes, in some tumours their clonal frequencies are incompatible with founder status. Mutations in cytoskeletal, cell shape and motility proteins occurred at lower clonal frequencies, suggesting that they occurred later during tumour progression. Taken together, our results show that understanding the biology and therapeutic responses of patients with TNBC will require the determination of individual tumour clonal genotypes.

Published
2012

2. Supplementary Figure 3 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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3. Supplementary Tables 1-4 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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4. Data from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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5. Supplementary Figure 1 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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7. Supplementary Figure 2 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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8. Supplementary Methods, Legends for Figures 1-5 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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10. Supplementary Figure 5 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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11. Supplementary Figure 4 from Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., primary, Oloumi, Arusha, primary, Chia, Stephen, primary, Ostlund, Christina, primary, Ahmadi, Ardalan, primary, Kyle, Alastair, primary, auf dem Keller, Ulrich, primary, Leung, Samuel, primary, Huntsman, David, primary, Clarke, Blaise, primary, Sutherland, Brent W., primary, Waterhouse, Dawn, primary, Bally, Marcel, primary, Roskelley, Calvin, primary, Overall, Christopher M., primary, Minchinton, Andrew, primary, Pacchiano, Fabio, primary, Carta, Fabrizio, primary, Scozzafava, Andrea, primary, Touisni, Nadia, primary, Winum, Jean-Yves, primary, Supuran, Claudiu T., primary, and Dedhar, Shoukat, primary

Published
2023
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13. Erratum: The somatic mutation profiles of 2,433 breast cancers refine their genomic and transcriptomic landscapes

Author

Pereira, Bernard, Chin, Suet-Feung, Rueda, Oscar M., Vollan, Hans-Kristian Moen, Provenzano, Elena, Bardwell, Helen A., Pugh, Michelle, Jones, Linda, Russell, Roslin, Sammut, Stephen-John, Tsui, Dana W. Y., Liu, Bin, Dawson, Sarah-Jane, Abraham, Jean, Northen, Helen, Peden, John F., Mukherjee, Abhik, Turashvili, Gulisa, Green, Andrew R., McKinney, Steve, Oloumi, Arusha, Shah, Sohrab, Rosenfeld, Nitzan, Murphy, Leigh, Bentley, David R., Ellis, Ian O., Purushotham, Arnie, Pinder, Sarah E., Børresen-Dale, Anne-Lise, Earl, Helena M., Pharoah, Paul D., Ross, Mark T., Aparicio, Samuel, and Caldas, Carlos

Published
2016
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14. Dynamics of genomic clones in breast cancer patient xenografts at single-cell resolution

Author

Eirew, Peter, Steif, Adi, Khattra, Jaswinder, Ha, Gavin, Yap, Damian, Farahani, Hossein, Gelmon, Karen, Chia, Stephen, Mar, Colin, Wan, Adrian, Laks, Emma, Biele, Justina, Shumansky, Karey, Rosner, Jamie, McPherson, Andrew, Nielsen, Cydney, Roth, Andrew J. L., Lefebvre, Calvin, Bashashati, Ali, de Souza, Camila, Siu, Celia, Aniba, Radhouane, Brimhall, Jazmine, Oloumi, Arusha, Osako, Tomo, Bruna, Alejandra, Sandoval, Jose L., Algara, Teresa, Greenwood, Wendy, Leung, Kaston, Cheng, Hongwei, Xue, Hui, Wang, Yuzhuo, Lin, Dong, Mungall, Andrew J., Moore, Richard, Zhao, Yongjun, Lorette, Julie, Nguyen, Long, Huntsman, David, Eaves, Connie J., Hansen, Carl, Marra, Marco A., Caldas, Carlos, Shah, Sohrab P., and Aparicio, Samuel

Published
2015
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15. ARID1A mutations in endometriosis-associated ovarian carcinomas

Author

Wiegand, Kimberly C., Shah, Sohrab P., Al-Agha, Osama M., Yongjun Zhao, Tse, Kane, Zeng, Thomas, Senz, Janine, McConechy, Melissa K., Anglesio, Michael S., Kalloger, Steve E., Yang, Winnie, Heravi-Moussavi, Alireza, Guiliany, Ryan, Chow, Christine, Fee, John, Zayed, Abdalnasser, Prentice, Leah, Melnyk, Nataliya, Turashvili, Gulisa, Delaney, Allan D., Madore, Jason, Yip, Stephen, McPherson, Andrew W., Ha, Gavin, Bell, Lynda, Fereday, Sian, Tam, Angela, Galletta, Laura, Tonin, Patricia N., Provencher, Diane, Miller, Dianne, Jones, Steven J.M., Moore, Richard A., Morin, Gregg B., Oloumi, Arusha, Boyd, Niki, Aparicio, Samuel A., le_Ming Shih, Mes_Masson, Anne-Marie, Bowtell, David B., Hirst, Martin, Gilks, Blake, Marra, Marco A., and Huntsman, David

Subjects
Ovarian cancer -- Genetic aspects, Ovarian cancer -- Care and treatment, Gene mutations -- Research, Endometriosis -- Genetic aspects, Endometriosis -- Causes of, Tumor suppressor genes -- Research
Abstract

The study attempts to evaluate the data derived from the RNA sequencing of 18 ovarian carcinomas to identify variants in ARID1A mutations. The results indicate that ARIDIA mutations are present in ovarian carcinomas and that it is indicative of an early event in the transformation of endometriosis into cancer.

Published
2010

16. Using next-generation sequencing for the diagnosis of rare disorders : a family with retinitis pigmentosa and skeletal abnormalities

Author

Schrader, Kasmintan, Heravi-Moussavi, Alireza, Waters, Paula J., Senz, Janine, Whelan, James, Eydoux, Patrice, Nielsen, Torsten, Gallagher, Barry, Oloumi, Arusha, Boyd, Niki, Fernandez, Bridget A., Young, Terry-Lynn, Jones, Steve J. M., Hirst, Martin, Shah, Sohrab P., Marra, Marco, and Green, Jane

Abstract

Linkage analysis with subsequent candidate gene sequencing is typically used to diagnose novel inherited syndromes. It is now possible to expedite diagnosis through the sequencing of all coding regions of the genome (the exome) or full genomes. We sequenced the exomes of four members of a family presenting with spondylo-epiphyseal dysplasia and retinitis pigmentosa and identified a six-base-pair (6-bp) deletion in GNPTG, the gene implicated in mucolipidosis type IIIγ. The diagnosis was confirmed by biochemical studies and both broadens the mucolipidosis type III phenotype and demonstrates the clinical utility of nextgeneration sequencing to diagnose rare genetic diseases.

Published
2021
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20. Using next-generation sequencing for the diagnosis of rare disorders: a family with retinitis pigmentosa and skeletal abnormalities

Author

Schrader, Kasmintan A, Heravi-Moussavi, Alireza, Waters, Paula J, Senz, Janine, Whelan, James, Ha, Gavin, Eydoux, Patrice, Nielsen, Torsten, Gallagher, Barry, Oloumi, Arusha, Boyd, Niki, Fernandez, Bridget A, Young, Terry-Lynn, Jones, Steven JM, Hirst, Martin, Shah, Sohrab P, Marra, Marco A, Green, Jane, and Huntsman, David G

Published
2011
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21. Ordering of mutations in preinvasive disease stages of esophageal carcinogenesis

Author

Weaver, Jamie MJ, Ross-Innes, Caryn S, Shannon, Nicholas, Lynch, Andy G, Forshew, Tim, Barbera, Mariagnese, Murtaza, Muhammed, Ong, Chin-Ann J, Lao-Sirieix, Pierre, Dunning, Mark J, Smith, Laura, Smith, Mike L, Anderson, Charlotte L, Carvalho, Benilton, O'Donovan, Maria, Underwood, Timothy J, May, Andrew P, Grehan, Nicola, Hardwick, Richard, Davies, Jim, Oloumi, Arusha, Aparicio, Sam, Caldas, Carlos, Eldridge, Matthew D, Edwards, Paul AW, Rosenfeld, Nitzan, Tavaré, Simon, Fitzgerald, Rebecca C, OCCAMS Consortium, Lynch, Andy [0000-0002-7876-7338], Dunning, Mark [0000-0002-8853-9435], Caldas, Carlos [0000-0003-3547-1489], Eldridge, Matthew [0000-0002-5799-8911], Edwards, Paul [0000-0002-4789-3374], Rosenfeld, Nitzan [0000-0002-2825-4788], Fitzgerald, Rebecca [0000-0002-3434-3568], and Apollo - University of Cambridge Repository

Subjects
Cancer genome sequencing, Adult, Male, Esophageal Neoplasms, Carcinogenesis, ICGC, Biology, Adenocarcinoma, medicine.disease_cause, Malignancy, Somatic evolution in cancer, Article, Barrett Esophagus, Genetics, medicine, Barrett’s esophagus, Humans, esophageal cancer, Barretts esophagus, Aged, Aged, 80 and over, whole genome sequencing, Mutation, Sequence Analysis, DNA, Middle Aged, medicine.disease, digestive system diseases, 3. Good health, Dysplasia, Cancer research, Female, Precancerous Conditions, Genome-Wide Association Study
Abstract

Cancer genome sequencing studies have identified numerous driver genes, but the relative timing of mutations in carcinogenesis remains unclear. The gradual progression from premalignant Barrett's esophagus to esophageal adenocarcinoma (EAC) provides an ideal model to study the ordering of somatic mutations. We identified recurrently mutated genes and assessed clonal structure using whole-genome sequencing and amplicon resequencing of 112 EACs. We next screened a cohort of 109 biopsies from 2 key transition points in the development of malignancy: benign metaplastic never-dysplastic Barrett's esophagus (NDBE; n=66) and high-grade dysplasia (HGD; n=43). Unexpectedly, the majority of recurrently mutated genes in EAC were also mutated in NDBE. Only TP53 and SMAD4 mutations occurred in a stage-specific manner, confined to HGD and EAC, respectively. Finally, we applied this knowledge to identify high-risk Barrett's esophagus in a new non-endoscopic test. In conclusion, mutations in EAC driver genes generally occur exceptionally early in disease development with profound implications for diagnostic and therapeutic strategies.

Published
2020
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23. CDK12 regulates alternative last exon mRNA splicing and promotes breast cancer cell invasion

Author

Tien, Jerry F., primary, Mazloomian, Alborz, additional, Cheng, S.-W. Grace, additional, Hughes, Christopher S., additional, Chow, Christalle C.T., additional, Canapi, Leanna T., additional, Oloumi, Arusha, additional, Trigo-Gonzalez, Genny, additional, Bashashati, Ali, additional, Xu, James, additional, Chang, Vicky C.-D., additional, Shah, Sohrab P., additional, Aparicio, Samuel, additional, and Morin, Gregg B., additional

Published
2017
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24. CLK-dependent exon recognition and conjoined gene formation revealed with a novel small molecule inhibitor

Author

Funnell, Tyler, primary, Tasaki, Shinya, additional, Oloumi, Arusha, additional, Araki, Shinsuke, additional, Kong, Esther, additional, Yap, Damian, additional, Nakayama, Yusuke, additional, Hughes, Christopher S., additional, Cheng, S.-W. Grace, additional, Tozaki, Hirokazu, additional, Iwatani, Misa, additional, Sasaki, Satoshi, additional, Ohashi, Tomohiro, additional, Miyazaki, Tohru, additional, Morishita, Nao, additional, Morishita, Daisuke, additional, Ogasawara-Shimizu, Mari, additional, Ohori, Momoko, additional, Nakao, Shoichi, additional, Karashima, Masatoshi, additional, Sano, Masaya, additional, Murai, Aiko, additional, Nomura, Toshiyuki, additional, Uchiyama, Noriko, additional, Kawamoto, Tomohiro, additional, Hara, Ryujiro, additional, Nakanishi, Osamu, additional, Shumansky, Karey, additional, Rosner, Jamie, additional, Wan, Adrian, additional, McKinney, Steven, additional, Morin, Gregg B., additional, Nakanishi, Atsushi, additional, Shah, Sohrab, additional, Toyoshiba, Hiroyoshi, additional, and Aparicio, Samuel, additional

Published
2017
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25. The somatic mutation profiles of 2,433 breast cancers refine their genomic and transcriptomic landscapes

Author

Pereira, Bernard, primary, Chin, Suet-Feung, additional, Rueda, Oscar M., additional, Vollan, Hans-Kristian Moen, additional, Provenzano, Elena, additional, Bardwell, Helen A., additional, Pugh, Michelle, additional, Jones, Linda, additional, Russell, Roslin, additional, Sammut, Stephen-John, additional, Tsui, Dana W. Y., additional, Liu, Bin, additional, Dawson, Sarah-Jane, additional, Abraham, Jean, additional, Northen, Helen, additional, Peden, John F., additional, Mukherjee, Abhik, additional, Turashvili, Gulisa, additional, Green, Andrew R., additional, McKinney, Steve, additional, Oloumi, Arusha, additional, Shah, Sohrab, additional, Rosenfeld, Nitzan, additional, Murphy, Leigh, additional, Bentley, David R., additional, Ellis, Ian O., additional, Purushotham, Arnie, additional, Pinder, Sarah E., additional, Børresen-Dale, Anne-Lise, additional, Earl, Helena M., additional, Pharoah, Paul D., additional, Ross, Mark T., additional, Aparicio, Samuel, additional, and Caldas, Carlos, additional

Published
2016
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26. Dynamics of genomic clones in breast cancer patient xenografts at single-cell resolution

Author

Eirew, Peter, primary, Steif, Adi, additional, Khattra, Jaswinder, additional, Ha, Gavin, additional, Yap, Damian, additional, Farahani, Hossein, additional, Gelmon, Karen, additional, Chia, Stephen, additional, Mar, Colin, additional, Wan, Adrian, additional, Laks, Emma, additional, Biele, Justina, additional, Shumansky, Karey, additional, Rosner, Jamie, additional, McPherson, Andrew, additional, Nielsen, Cydney, additional, Roth, Andrew J. L., additional, Lefebvre, Calvin, additional, Bashashati, Ali, additional, de Souza, Camila, additional, Siu, Celia, additional, Aniba, Radhouane, additional, Brimhall, Jazmine, additional, Oloumi, Arusha, additional, Osako, Tomo, additional, Bruna, Alejandra, additional, Sandoval, Jose L., additional, Algara, Teresa, additional, Greenwood, Wendy, additional, Leung, Kaston, additional, Cheng, Hongwei, additional, Xue, Hui, additional, Wang, Yuzhuo, additional, Lin, Dong, additional, Mungall, Andrew J., additional, Moore, Richard, additional, Zhao, Yongjun, additional, Lorette, Julie, additional, Nguyen, Long, additional, Huntsman, David, additional, Eaves, Connie J., additional, Hansen, Carl, additional, Marra, Marco A., additional, Caldas, Carlos, additional, Shah, Sohrab P., additional, and Aparicio, Samuel, additional

Published
2014
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27. 935 The Timing of Oncogenic Events in the Evolution of the Oesophageal Adenocarcinoma Genome and Implications for Clinical Diagnostics

Author

Weaver, Jamie M., primary, Ross-Innes, Caryn, additional, Shannon, Nicholas B., additional, Lynch, Andy, additional, Forshew, Tim, additional, Barbera, Mariagnese, additional, Ong, Chin-Ann J., additional, Murtaza, Muhammed, additional, Lao-Sirieix, Pierre, additional, Dunning, Mark J., additional, Smith, Laura, additional, Smith, Mike, additional, Carvalho, Benilton, additional, Underwood, Timothy, additional, May, Andrew, additional, Grehan, Nicola, additional, Anderson, Charlotte, additional, Davies, Jim, additional, Hardwick, Richard H., additional, ODonovan, Maria, additional, Oloumi, Arusha, additional, Aparicio, Sam, additional, Caldas, Carlos, additional, Eldridge, Matthew D., additional, Edwards, Paul A., additional, Rosenfeld, Nitzan, additional, Tavaré, Simon, additional, and Fitzgerald, Rebecca, additional

Published
2014
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28. Integrin-linked kinase as a target for ERG-mediated invasive properties in prostate cancer models

Author

Becker-Santos, Daiana, Guo, Yubin, Ghaffari, Mazyar, Vickers, Elaine, Lehman, Melanie, Altamirano-Dimas, Manuel, Oloumi, Arusha, Furukawa, Junya, Sharma, Manju, Wang, Yuzhuo, Dedhar, Shoukat, Cox, Michael, Becker-Santos, Daiana, Guo, Yubin, Ghaffari, Mazyar, Vickers, Elaine, Lehman, Melanie, Altamirano-Dimas, Manuel, Oloumi, Arusha, Furukawa, Junya, Sharma, Manju, Wang, Yuzhuo, Dedhar, Shoukat, and Cox, Michael

Abstract

Approximately half of prostate cancers (PCa) carry TMPRSS2-ERG translocations; however, the clinical impact of this genomic alteration remains enigmatic. Expression of v-ets erythroblastosis virus E26 oncogene like (avian) gene (ERG) promotes prostatic epithelial dysplasia in transgenic mice and acquisition of epithelial-to-mesenchymal transition (EMT) characteristics in human prostatic epithelial cells (PrECs). To explore whether ERG-induced EMT in PrECs was associated with therapeutically targetable transformation characteristics, we established stable populations of BPH-1, PNT1B and RWPE-1 immortalized human PrEC lines that constitutively express flag-tagged ERG3 (fERG). All fERG-expressing populations exhibited characteristics of in vitro and in vivo transformation. Microarray analysis revealed >2000 commonly dysregulated genes in the fERG-PrEC lines. Functional analysis revealed evidence that fERG cells underwent EMT and acquired invasive characteristics. The fERG-induced EMT transcript signature was exemplified by suppressed expression of E-cadherin and keratins 5, 8, 14 and 18; elevated expression of N-cadherin, N-cadherin 2 and vimentin, and of the EMT transcriptional regulators Snail, Zeb1 and Zeb2, and lymphoid enhancer-binding factor-1 (LEF-1). In BPH-1 and RWPE-1-fERG cells, fERG expression is correlated with increased expression of integrin-linked kinase (ILK) and its downstream effectors Snail and LEF-1. Interfering RNA suppression of ERG decreased expression of ILK, Snail and LEF-1, whereas small interfering RNA suppression of ILK did not alter fERG expression. Interfering RNA suppression of ERG or ILK impaired fERG-PrEC Matrigel invasion. Treating fERG-BPH-1 cells with the small molecule ILK inhibitor, QLT-0267, resulted in dose-dependent suppression of Snail and LEF-1 expression, Matrigel invasion and reversion of anchorage-independent growth. These results suggest that ILK is a therapeutically targetable mediator of ERG-induced EMT and transformati

Published
2012

29. Mutation Discovery in Regions of Segmental Cancer Genome Amplifications with CoNAn-SNV: A Mixture Model for Next Generation Sequencing of Tumors

Author

Crisan, Anamaria, primary, Goya, Rodrigo, additional, Ha, Gavin, additional, Ding, Jiarui, additional, Prentice, Leah M., additional, Oloumi, Arusha, additional, Senz, Janine, additional, Zeng, Thomas, additional, Tse, Kane, additional, Delaney, Allen, additional, Marra, Marco A., additional, Huntsman, David G., additional, Hirst, Martin, additional, Aparicio, Sam, additional, and Shah, Sohrab, additional

Published
2012
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30. Integrative analysis of genome-wide loss of heterozygosity and monoallelic expression at nucleotide resolution reveals disrupted pathways in triple-negative breast cancer

Author

Ha, Gavin, primary, Roth, Andrew, additional, Lai, Daniel, additional, Bashashati, Ali, additional, Ding, Jiarui, additional, Goya, Rodrigo, additional, Giuliany, Ryan, additional, Rosner, Jamie, additional, Oloumi, Arusha, additional, Shumansky, Karey, additional, Chin, Suet-Feung, additional, Turashvili, Gulisa, additional, Hirst, Martin, additional, Caldas, Carlos, additional, Marra, Marco A., additional, Aparicio, Samuel, additional, and Shah, Sohrab P., additional

Published
2012
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32. Targeting Tumor Hypoxia: Suppression of Breast Tumor Growth and Metastasis by Novel Carbonic Anhydrase IX Inhibitors

Author

Lou, Yuanmei, primary, McDonald, Paul C., additional, Oloumi, Arusha, additional, Chia, Stephen, additional, Ostlund, Christina, additional, Ahmadi, Ardalan, additional, Kyle, Alastair, additional, auf dem Keller, Ulrich, additional, Leung, Samuel, additional, Huntsman, David, additional, Clarke, Blaise, additional, Sutherland, Brent W., additional, Waterhouse, Dawn, additional, Bally, Marcel, additional, Roskelley, Calvin, additional, Overall, Christopher M., additional, Minchinton, Andrew, additional, Pacchiano, Fabio, additional, Carta, Fabrizio, additional, Scozzafava, Andrea, additional, Touisni, Nadia, additional, Winum, Jean-Yves, additional, Supuran, Claudiu T., additional, and Dedhar, Shoukat, additional

Published
2011
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33. ARID1AMutations in Endometriosis-Associated Ovarian Carcinomas

Author

Wiegand, Kimberly C., primary, Shah, Sohrab P., additional, Al-Agha, Osama M., additional, Zhao, Yongjun, additional, Tse, Kane, additional, Zeng, Thomas, additional, Senz, Janine, additional, McConechy, Melissa K., additional, Anglesio, Michael S., additional, Kalloger, Steve E., additional, Yang, Winnie, additional, Heravi-Moussavi, Alireza, additional, Giuliany, Ryan, additional, Chow, Christine, additional, Fee, John, additional, Zayed, Abdalnasser, additional, Prentice, Leah, additional, Melnyk, Nataliya, additional, Turashvili, Gulisa, additional, Delaney, Allen D., additional, Madore, Jason, additional, Yip, Stephen, additional, McPherson, Andrew W., additional, Ha, Gavin, additional, Bell, Lynda, additional, Fereday, Sian, additional, Tam, Angela, additional, Galletta, Laura, additional, Tonin, Patricia N., additional, Provencher, Diane, additional, Miller, Dianne, additional, Jones, Steven J.M., additional, Moore, Richard A., additional, Morin, Gregg B., additional, Oloumi, Arusha, additional, Boyd, Niki, additional, Aparicio, Samuel A., additional, Shih, Ie-Ming, additional, Mes-Masson, Anne-Marie, additional, Bowtell, David D., additional, Hirst, Martin, additional, Gilks, Blake, additional, Marra, Marco A., additional, and Huntsman, David G., additional

Published
2010
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35. Abstract 455: Hypoxia induced carbonic anhydrase IX is essential for the growth and metastasis of breast tumors

Author

Lou, Yuanmei, primary, McDonald, Paul C., additional, Oloumi, Arusha, additional, Chia, Stephen, additional, Kyle, Alastair, additional, dem Keller, Ulrich auf, additional, Fotovati, Abbas, additional, Gray, Virginia, additional, Leung, Samuel, additional, Huntsman, David, additional, Clarke, Blaise, additional, Waterhouse, Dawn, additional, Bally, Marcel, additional, Roskelley, Calvin, additional, Overall, Christopher, additional, Minchinton, Andrew, additional, Supuran, Claudiu T., additional, and Dedhar, Shoukat, additional

Published
2010
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38. Critical Role of Integrin-Linked Kinase in Granule Cell Precursor Proliferation and Cerebellar Development.

Author

Mills, Julia, Niewmierzycka, Agnieszka, Oloumi, Arusha, Rico, Beatriz, St-Arnaud, Rene, Mackenzie, Ian R., Mawji, Nasrin M., Wilson, Jason, Reichardt, Louis F., and Dedhar, Shoukat

Subjects
INTEGRINS, CELL proliferation, PROTEIN kinases, CENTRAL nervous system, CELLULAR signal transduction, CEREBELLUM, HEDGEHOG signaling proteins
Abstract

Integrin-linked kinase (ILK) is a serine/threonine protein kinase that plays an important role in integrin signaling and cell proliferation. We used Cre recombinase (Cre)-loxP technology to study CNS restricted knock-out of the ilk gene by either Nestin-driven or gfap-driven Cre-mediated recombination. Developmental changes in ilk-excised brain regions are similar to those observed in mice lacking the integrin β1 subunit in the CNS, including defective laminin deposition, abnormal glial morphology, and alterations in granule cell migration. Decreases in 6-bromodeoxyuridine (BrdU) pulse labeling and proliferating cell nuclear antigen expression in the external granule cell layer of the cerebellum demonstrated that proliferation is disrupted in granule cells lacking ILK. Previous studies have shown that laminin-sonic hedgehog (Shh)-induced granule cell precursor (GCP) proliferation is dependent on β1 integrins, several of which bind laminin and interact with ILK through the β1 cytoplasmic domain. Both ex vivo deletion of ilk and a small molecule inhibitor of ILK kinase activity decreased laminin-Shh-induced BrdU labeling in cultured GCPs. Together, these results implicate ILK as a critical effector in a signaling pathway necessary for granule cell proliferation and cerebellar development. [ABSTRACT FROM AUTHOR]

Published
2006
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39. The somatic mutation profiles of 2,433 breast cancers refines their genomic and transcriptomic landscapes

Author

Pereira, Bernard, Chin, Suet-Feung, Rueda, Oscar M., Vollan, Hans-Kristian Moen, Provenzano, Elena, Bardwell, Helen A., Pugh, Michelle, Jones, Linda, Russell, Roslin, Sammut, Stephen-John, Tsui, Dana W.Y., Liu, Bin, Dawson, Sarah-Jane, Abraham, Jean, Northen, Helen, Peden, John F., Mukherjee, Abhik, Turashvili, Gulisa, Green, Andrew R., McKinney, Steve, Oloumi, Arusha, Shah, Sohrab, Rosenfeld, Nitzan, Murphy, Leigh, Bentley, David R., Ellis, Ian O., Purushotham, Arnie, Pinder, Sarah E., Earl, Helena M., Pharoah, Paul D., Ross, Mark T., Aparicio, Samuel, and Caldas, Carlos

Subjects
Nottingham Breast Cancer Research Centre
Abstract

The genomic landscape of breast cancer is complex, and inter- and intra-tumour heterogeneity are important challenges in treating the disease. In this study, we sequence 173 genes in 2,433 primary breast tumours that have copy number aberration (CNA), gene expression and long-term clinical follow-up data. We identify 40 mutation-driver (Mut-driver) genes, and determine associations between mutations, driver CNA profiles, clinical-pathological parameters and survival. We assess the clonal states of Mut-driver mutations, and estimate levels of intra-tumour heterogeneity using mutant-allele fractions. Associations between PIK3CA mutations and reduced survival are identified in three subgroups of ER-positive cancer (defined by amplification of 17q23, 11q13–14 or 8q24). High levels of intra-tumour heterogeneity are in general associated with a worse outcome, but highly aggressive tumours with 11q13–14 amplification have low levels of intra-tumour heterogeneity. These results emphasize the importance of genome-based stratification of breast cancer, and have important implications for designing therapeutic strategies.

40. The somatic mutation profiles of 2,433 breast cancers refines their genomic and transcriptomic landscapes

Author

Pereira, Bernard, Chin, Suet-Feung, Rueda, Oscar M., Vollan, Hans-Kristian Moen, Provenzano, Elena, Bardwell, Helen A., Pugh, Michelle, Jones, Linda, Russell, Roslin, Sammut, Stephen-John, Tsui, Dana W.Y., Liu, Bin, Dawson, Sarah-Jane, Abraham, Jean, Northen, Helen, Peden, John F., Mukherjee, Abhik, Turashvili, Gulisa, Green, Andrew R., McKinney, Steve, Oloumi, Arusha, Shah, Sohrab, Rosenfeld, Nitzan, Murphy, Leigh, Bentley, David R., Ellis, Ian O., Purushotham, Arnie, Pinder, Sarah E., Børresen-Dale, Anne-Lise, Earl, Helena M., Pharoah, Paul D., Ross, Mark T., Aparicio, Samuel, Caldas, Carlos, Pereira, Bernard, Chin, Suet-Feung, Rueda, Oscar M., Vollan, Hans-Kristian Moen, Provenzano, Elena, Bardwell, Helen A., Pugh, Michelle, Jones, Linda, Russell, Roslin, Sammut, Stephen-John, Tsui, Dana W.Y., Liu, Bin, Dawson, Sarah-Jane, Abraham, Jean, Northen, Helen, Peden, John F., Mukherjee, Abhik, Turashvili, Gulisa, Green, Andrew R., McKinney, Steve, Oloumi, Arusha, Shah, Sohrab, Rosenfeld, Nitzan, Murphy, Leigh, Bentley, David R., Ellis, Ian O., Purushotham, Arnie, Pinder, Sarah E., Børresen-Dale, Anne-Lise, Earl, Helena M., Pharoah, Paul D., Ross, Mark T., Aparicio, Samuel, and Caldas, Carlos

Abstract

The genomic landscape of breast cancer is complex, and inter- and intra-tumour heterogeneity are important challenges in treating the disease. In this study, we sequence 173 genes in 2,433 primary breast tumours that have copy number aberration (CNA), gene expression and long-term clinical follow-up data. We identify 40 mutation-driver (Mut-driver) genes, and determine associations between mutations, driver CNA profiles, clinical-pathological parameters and survival. We assess the clonal states of Mut-driver mutations, and estimate levels of intra-tumour heterogeneity using mutant-allele fractions. Associations between PIK3CA mutations and reduced survival are identified in three subgroups of ER-positive cancer (defined by amplification of 17q23, 11q13–14 or 8q24). High levels of intra-tumour heterogeneity are in general associated with a worse outcome, but highly aggressive tumours with 11q13–14 amplification have low levels of intra-tumour heterogeneity. These results emphasize the importance of genome-based stratification of breast cancer, and have important implications for designing therapeutic strategies.

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41. Ordering of mutations in preinvasive disease stages of esophageal carcinogenesis.

Author

Weaver JMJ, Ross-Innes CS, Shannon N, Lynch AG, Forshew T, Barbera M, Murtaza M, Ong CJ, Lao-Sirieix P, Dunning MJ, Smith L, Smith ML, Anderson CL, Carvalho B, O'Donovan M, Underwood TJ, May AP, Grehan N, Hardwick R, Davies J, Oloumi A, Aparicio S, Caldas C, Eldridge MD, Edwards PAW, Rosenfeld N, Tavaré S, and Fitzgerald RC

Subjects
Adenocarcinoma genetics, Adenocarcinoma pathology, Adult, Aged, Aged, 80 and over, Barrett Esophagus genetics, Barrett Esophagus pathology, Esophageal Neoplasms pathology, Female, Genome-Wide Association Study methods, Humans, Male, Middle Aged, Precancerous Conditions pathology, Sequence Analysis, DNA methods, Carcinogenesis genetics, Esophageal Neoplasms genetics, Mutation, Precancerous Conditions genetics
Abstract

Cancer genome sequencing studies have identified numerous driver genes, but the relative timing of mutations in carcinogenesis remains unclear. The gradual progression from premalignant Barrett's esophagus to esophageal adenocarcinoma (EAC) provides an ideal model to study the ordering of somatic mutations. We identified recurrently mutated genes and assessed clonal structure using whole-genome sequencing and amplicon resequencing of 112 EACs. We next screened a cohort of 109 biopsies from 2 key transition points in the development of malignancy: benign metaplastic never-dysplastic Barrett's esophagus (NDBE; n=66) and high-grade dysplasia (HGD; n=43). Unexpectedly, the majority of recurrently mutated genes in EAC were also mutated in NDBE. Only TP53 and SMAD4 mutations occurred in a stage-specific manner, confined to HGD and EAC, respectively. Finally, we applied this knowledge to identify high-risk Barrett's esophagus in a new non-endoscopic test. In conclusion, mutations in EAC driver genes generally occur exceptionally early in disease development with profound implications for diagnostic and therapeutic strategies.

Published
2014
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