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Article ; Online: An open access pilot freely sharing cancer genomic data from participants in Texas.

Becnel, Lauren B / Pereira, Stacey / Drummond, Jennifer A / Gingras, Marie-Claude / Covington, Kyle R / Kovar, Christie L / Doddapaneni, Harsha Vardhan / Hu, Jianhong / Muzny, Donna / McGuire, Amy L / Wheeler, David A / Gibbs, Richard A

Scientific data

2016 Volume 3, Page(s) 160010

Abstract: Genomic data sharing in cancer has been restricted to aggregate or controlled-access initiatives to protect the privacy of research participants. By limiting access to these data, it has been argued that the autonomy of individuals who decide to ... ...

Abstract	Genomic data sharing in cancer has been restricted to aggregate or controlled-access initiatives to protect the privacy of research participants. By limiting access to these data, it has been argued that the autonomy of individuals who decide to participate in data sharing efforts has been superseded and the utility of the data as research and educational tools reduced. In a pilot Open Access (OA) project from the CPRIT-funded Texas Cancer Research Biobank, many Texas cancer patients were willing to openly share genomic data from tumor and normal matched pair specimens. For the first time, genetic data from 7 human cancer cases with matched normal are freely available without requirement for data use agreements nor any major restriction except that end users cannot attempt to re-identify the participants (http://txcrb.org/open.html).
MeSH term(s)	Access to Information ; Biological Specimen Banks ; DNA, Neoplasm ; Databases, Genetic ; Genome, Human ; Humans ; Information Dissemination ; Pancreatic Neoplasms/genetics ; Texas
Chemical Substances	DNA, Neoplasm
Language	English
Publishing date	2016-02-16
Publishing country	England
Document type	Dataset ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2775191-0
ISSN	2052-4463 ; 2052-4463
ISSN (online)	2052-4463
ISSN	2052-4463
DOI	10.1038/sdata.2016.10
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mutational landscape of aggressive cutaneous squamous cell carcinoma.

Pickering, Curtis R / Zhou, Jane H / Lee, J Jack / Drummond, Jennifer A / Peng, S Andrew / Saade, Rami E / Tsai, Kenneth Y / Curry, Jonathan L / Tetzlaff, Michael T / Lai, Stephen Y / Yu, Jun / Muzny, Donna M / Doddapaneni, Harshavardhan / Shinbrot, Eve / Covington, Kyle R / Zhang, Jianhua / Seth, Sahil / Caulin, Carlos / Clayman, Gary L /

El-Naggar, Adel K / Gibbs, Richard A / Weber, Randal S / Myers, Jeffrey N / Wheeler, David A / Frederick, Mitchell J

Clinical cancer research : an official journal of the American Association for Cancer Research

2014 Volume 20, Issue 24, Page(s) 6582–6592

Abstract: Purpose: Aggressive cutaneous squamous cell carcinoma (cSCC) is often a disfiguring and lethal disease. Very little is currently known about the mutations that drive aggressive cSCC.: Experimental design: Whole-exome sequencing was performed on 39 ... ...

Abstract	Purpose: Aggressive cutaneous squamous cell carcinoma (cSCC) is often a disfiguring and lethal disease. Very little is currently known about the mutations that drive aggressive cSCC. Experimental design: Whole-exome sequencing was performed on 39 cases of aggressive cSCC to identify driver genes and novel therapeutic targets. Significantly, mutated genes were identified with MutSig or complementary methods developed to specifically identify candidate tumor suppressors based upon their inactivating mutation bias. Results: Despite the very high-mutational background caused by UV exposure, 23 candidate drivers were identified, including the well-known cancer-associated genes TP53, CDKN2A, NOTCH1, AJUBA, HRAS, CASP8, FAT1, and KMT2C (MLL3). Three novel candidate tumor suppressors with putative links to cancer or differentiation, NOTCH2, PARD3, and RASA1, were also identified as possible drivers in cSCC. KMT2C mutations were associated with poor outcome and increased bone invasion. Conclusions: The mutational spectrum of cSCC is similar to that of head and neck squamous cell carcinoma and dominated by tumor-suppressor genes. These results improve the foundation for understanding this disease and should aid in identifying and treating aggressive cSCC.
MeSH term(s)	Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/mortality ; Carcinoma, Squamous Cell/pathology ; Cluster Analysis ; Computational Biology ; DNA Copy Number Variations ; Disease Progression ; Exome ; Genomics ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation ; Prognosis ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology
Language	English
Publishing date	2014-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-14-1768
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Article ; Online: Cross-species identification of genomic drivers of squamous cell carcinoma development across preneoplastic intermediates.

Chitsazzadeh, Vida / Coarfa, Cristian / Drummond, Jennifer A / Nguyen, Tri / Joseph, Aaron / Chilukuri, Suneel / Charpiot, Elizabeth / Adelmann, Charles H / Ching, Grace / Nguyen, Tran N / Nicholas, Courtney / Thomas, Valencia D / Migden, Michael / MacFarlane, Deborah / Thompson, Erika / Shen, Jianjun / Takata, Yoko / McNiece, Kayla / Polansky, Maxim A /

Abbas, Hussein A / Rajapakshe, Kimal / Gower, Adam / Spira, Avrum / Covington, Kyle R / Xiao, Weimin / Gunaratne, Preethi / Pickering, Curtis / Frederick, Mitchell / Myers, Jeffrey N / Shen, Li / Yao, Hui / Su, Xiaoping / Rapini, Ronald P / Wheeler, David A / Hawk, Ernest T / Flores, Elsa R / Tsai, Kenneth Y

Nature communications

2016 Volume 7, Page(s) 12601

Abstract: Cutaneous squamous cell carcinoma (cuSCC) comprises 15-20% of all skin cancers, accounting for over 700,000 cases in USA annually. Most cuSCC arise in association with a distinct precancerous lesion, the actinic keratosis (AK). To identify potential ... ...

Abstract	Cutaneous squamous cell carcinoma (cuSCC) comprises 15-20% of all skin cancers, accounting for over 700,000 cases in USA annually. Most cuSCC arise in association with a distinct precancerous lesion, the actinic keratosis (AK). To identify potential targets for molecularly targeted chemoprevention, here we perform integrated cross-species genomic analysis of cuSCC development through the preneoplastic AK stage using matched human samples and a solar ultraviolet radiation-driven Hairless mouse model. We identify the major transcriptional drivers of this progression sequence, showing that the key genomic changes in cuSCC development occur in the normal skin to AK transition. Our data validate the use of this ultraviolet radiation-driven mouse cuSCC model for cross-species analysis and demonstrate that cuSCC bears deep molecular similarities to multiple carcinogen-driven SCCs from diverse sites, suggesting that cuSCC may serve as an effective, accessible model for multiple SCC types and that common treatment and prevention strategies may be feasible.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Carcinogenesis/genetics ; Carcinoma, Squamous Cell/etiology ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/prevention & control ; DNA Mutational Analysis ; Disease Progression ; Female ; Gene Expression Profiling ; Genomics ; High-Throughput Nucleotide Sequencing ; Humans ; Keratosis, Actinic/pathology ; Mice ; Mice, Hairless ; Molecular Targeted Therapy/methods ; Precancerous Conditions/genetics ; Precancerous Conditions/pathology ; Sequence Analysis, RNA ; Skin/pathology ; Skin Neoplasms/etiology ; Skin Neoplasms/genetics ; Skin Neoplasms/prevention & control ; Ultraviolet Rays/adverse effects ; Whole Exome Sequencing
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2016-08-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms12601
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Article ; Online: Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1.

Agrawal, Nishant / Frederick, Mitchell J / Pickering, Curtis R / Bettegowda, Chetan / Chang, Kyle / Li, Ryan J / Fakhry, Carole / Xie, Tong-Xin / Zhang, Jiexin / Wang, Jing / Zhang, Nianxiang / El-Naggar, Adel K / Jasser, Samar A / Weinstein, John N / Treviño, Lisa / Drummond, Jennifer A / Muzny, Donna M / Wu, Yuanqing / Wood, Laura D /

Hruban, Ralph H / Westra, William H / Koch, Wayne M / Califano, Joseph A / Gibbs, Richard A / Sidransky, David / Vogelstein, Bert / Velculescu, Victor E / Papadopoulos, Nickolas / Wheeler, David A / Kinzler, Kenneth W / Myers, Jeffrey N

Science (New York, N.Y.)

2011 Volume 333, Issue 6046, Page(s) 1154–1157

Abstract: Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. To explore the genetic origins of this cancer, we used whole-exome sequencing and gene copy number analyses to study 32 primary tumors. Tumors from patients with a ... ...

Abstract	Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. To explore the genetic origins of this cancer, we used whole-exome sequencing and gene copy number analyses to study 32 primary tumors. Tumors from patients with a history of tobacco use had more mutations than did tumors from patients who did not use tobacco, and tumors that were negative for human papillomavirus (HPV) had more mutations than did HPV-positive tumors. Six of the genes that were mutated in multiple tumors were assessed in up to 88 additional HNSCCs. In addition to previously described mutations in TP53, CDKN2A, PIK3CA, and HRAS, we identified mutations in FBXW7 and NOTCH1. Nearly 40% of the 28 mutations identified in NOTCH1 were predicted to truncate the gene product, suggesting that NOTCH1 may function as a tumor suppressor gene rather than an oncogene in this tumor type.
MeSH term(s)	Carcinoma/drug therapy ; Carcinoma/genetics ; Carcinoma/virology ; Carcinoma, Squamous Cell ; Cell Cycle Proteins/genetics ; Codon, Nonsense ; Exons ; F-Box Proteins/genetics ; F-Box-WD Repeat-Containing Protein 7 ; Gene Dosage ; Genes, Tumor Suppressor ; Genes, p53 ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/virology ; Humans ; INDEL Mutation ; Mutation ; Mutation, Missense ; Neoplasms, Squamous Cell/drug therapy ; Neoplasms, Squamous Cell/genetics ; Neoplasms, Squamous Cell/virology ; Oligonucleotide Array Sequence Analysis ; Oncogenes ; Papillomaviridae/isolation & purification ; Papillomavirus Infections/virology ; Receptor, Notch1/chemistry ; Receptor, Notch1/genetics ; Sequence Analysis, DNA ; Smoking ; Squamous Cell Carcinoma of Head and Neck ; Nicotiana ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Cell Cycle Proteins ; Codon, Nonsense ; F-Box Proteins ; F-Box-WD Repeat-Containing Protein 7 ; FBXW7 protein, human ; NOTCH1 protein, human ; Receptor, Notch1 ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2011-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.1206923
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Article ; Online: Comprehensive Molecular Characterization of Papillary Renal-Cell Carcinoma.

Linehan, W Marston / Spellman, Paul T / Ricketts, Christopher J / Creighton, Chad J / Fei, Suzanne S / Davis, Caleb / Wheeler, David A / Murray, Bradley A / Schmidt, Laura / Vocke, Cathy D / Peto, Myron / Al Mamun, Abu Amar M / Shinbrot, Eve / Sethi, Anurag / Brooks, Samira / Rathmell, W Kimryn / Brooks, Angela N / Hoadley, Katherine A / Robertson, A Gordon /

Brooks, Denise / Bowlby, Reanne / Sadeghi, Sara / Shen, Hui / Weisenberger, Daniel J / Bootwalla, Moiz / Baylin, Stephen B / Laird, Peter W / Cherniack, Andrew D / Saksena, Gordon / Haake, Scott / Li, Jun / Liang, Han / Lu, Yiling / Mills, Gordon B / Akbani, Rehan / Leiserson, Mark D M / Raphael, Benjamin J / Anur, Pavana / Bottaro, Donald / Albiges, Laurence / Barnabas, Nandita / Choueiri, Toni K / Czerniak, Bogdan / Godwin, Andrew K / Hakimi, A Ari / Ho, Thai H / Hsieh, James / Ittmann, Michael / Kim, William Y / Krishnan, Bhavani / Merino, Maria J / Mills Shaw, Kenna R / Reuter, Victor E / Reznik, Ed / Shelley, Carl S / Shuch, Brian / Signoretti, Sabina / Srinivasan, Ramaprasad / Tamboli, Pheroze / Thomas, George / Tickoo, Satish / Burnett, Kenneth / Crain, Daniel / Gardner, Johanna / Lau, Kevin / Mallery, David / Morris, Scott / Paulauskis, Joseph D / Penny, Robert J / Shelton, Candace / Shelton, W Troy / Sherman, Mark / Thompson, Eric / Yena, Peggy / Avedon, Melissa T / Bowen, Jay / Gastier-Foster, Julie M / Gerken, Mark / Leraas, Kristen M / Lichtenberg, Tara M / Ramirez, Nilsa C / Santos, Tracie / Wise, Lisa / Zmuda, Erik / Demchok, John A / Felau, Ina / Hutter, Carolyn M / Sheth, Margi / Sofia, Heidi J / Tarnuzzer, Roy / Wang, Zhining / Yang, Liming / Zenklusen, Jean C / Zhang, Jiashan / Ayala, Brenda / Baboud, Julien / Chudamani, Sudha / Liu, Jia / Lolla, Laxmi / Naresh, Rashi / Pihl, Todd / Sun, Qiang / Wan, Yunhu / Wu, Ye / Ally, Adrian / Balasundaram, Miruna / Balu, Saianand / Beroukhim, Rameen / Bodenheimer, Tom / Buhay, Christian / Butterfield, Yaron S N / Carlsen, Rebecca / Carter, Scott L / Chao, Hsu / Chuah, Eric / Clarke, Amanda / Covington, Kyle R / Dahdouli, Mahmoud / Dewal, Ninad / Dhalla, Noreen / Doddapaneni, Harsha V / Drummond, Jennifer A / Gabriel, Stacey B / Gibbs, Richard A / Guin, Ranabir / Hale, Walker / Hawes, Alicia / Hayes, D Neil / Holt, Robert A / Hoyle, Alan P / Jefferys, Stuart R / Jones, Steven J M / Jones, Corbin D / Kalra, Divya / Kovar, Christie / Lewis, Lora / Li, Jie / Ma, Yussanne / Marra, Marco A / Mayo, Michael / Meng, Shaowu / Meyerson, Matthew / Mieczkowski, Piotr A / Moore, Richard A / Morton, Donna / Mose, Lisle E / Mungall, Andrew J / Muzny, Donna / Parker, Joel S / Perou, Charles M / Roach, Jeffrey / Schein, Jacqueline E / Schumacher, Steven E / Shi, Yan / Simons, Janae V / Sipahimalani, Payal / Skelly, Tara / Soloway, Matthew G / Sougnez, Carrie / Tam, Angela / Tan, Donghui / Thiessen, Nina / Veluvolu, Umadevi / Wang, Min / Wilkerson, Matthew D / Wong, Tina / Wu, Junyuan / Xi, Liu / Zhou, Jane / Bedford, Jason / Chen, Fengju / Fu, Yao / Gerstein, Mark / Haussler, David / Kasaian, Katayoon / Lai, Phillip / Ling, Shiyun / Radenbaugh, Amie / Van Den Berg, David / Weinstein, John N / Zhu, Jingchun / Albert, Monique / Alexopoulou, Iakovina / Andersen, Jeremiah J / Auman, J Todd / Bartlett, John / Bastacky, Sheldon / Bergsten, Julie / Blute, Michael L / Boice, Lori / Bollag, Roni J / Boyd, Jeff / Castle, Erik / Chen, Ying-Bei / Cheville, John C / Curley, Erin / Davies, Benjamin / DeVolk, April / Dhir, Rajiv / Dike, Laura / Eckman, John / Engel, Jay / Harr, Jodi / Hrebinko, Ronald / Huang, Mei / Huelsenbeck-Dill, Lori / Iacocca, Mary / Jacobs, Bruce / Lobis, Michael / Maranchie, Jodi K / McMeekin, Scott / Myers, Jerome / Nelson, Joel / Parfitt, Jeremy / Parwani, Anil / Petrelli, Nicholas / Rabeno, Brenda / Roy, Somak / Salner, Andrew L / Slaton, Joel / Stanton, Melissa / Thompson, R Houston / Thorne, Leigh / Tucker, Kelinda / Weinberger, Paul M / Winemiller, Cynthia / Zach, Leigh Anne / Zuna, Rosemary

The New England journal of medicine

2016 Volume 374, Issue 2, Page(s) 135–145

Abstract: Background: Papillary renal-cell carcinoma, which accounts for 15 to 20% of renal-cell carcinomas, is a heterogeneous disease that consists of various types of renal cancer, including tumors with indolent, multifocal presentation and solitary tumors ... ...

Abstract	Background: Papillary renal-cell carcinoma, which accounts for 15 to 20% of renal-cell carcinomas, is a heterogeneous disease that consists of various types of renal cancer, including tumors with indolent, multifocal presentation and solitary tumors with an aggressive, highly lethal phenotype. Little is known about the genetic basis of sporadic papillary renal-cell carcinoma, and no effective forms of therapy for advanced disease exist. Methods: We performed comprehensive molecular characterization of 161 primary papillary renal-cell carcinomas, using whole-exome sequencing, copy-number analysis, messenger RNA and microRNA sequencing, DNA-methylation analysis, and proteomic analysis. Results: Type 1 and type 2 papillary renal-cell carcinomas were shown to be different types of renal cancer characterized by specific genetic alterations, with type 2 further classified into three individual subgroups on the basis of molecular differences associated with patient survival. Type 1 tumors were associated with MET alterations, whereas type 2 tumors were characterized by CDKN2A silencing, SETD2 mutations, TFE3 fusions, and increased expression of the NRF2-antioxidant response element (ARE) pathway. A CpG island methylator phenotype (CIMP) was observed in a distinct subgroup of type 2 papillary renal-cell carcinomas that was characterized by poor survival and mutation of the gene encoding fumarate hydratase (FH). Conclusions: Type 1 and type 2 papillary renal-cell carcinomas were shown to be clinically and biologically distinct. Alterations in the MET pathway were associated with type 1, and activation of the NRF2-ARE pathway was associated with type 2; CDKN2A loss and CIMP in type 2 conveyed a poor prognosis. Furthermore, type 2 papillary renal-cell carcinoma consisted of at least three subtypes based on molecular and phenotypic features. (Funded by the National Institutes of Health.).
MeSH term(s)	Carcinoma, Papillary/genetics ; Carcinoma, Papillary/metabolism ; CpG Islands/physiology ; DNA Methylation ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; MicroRNAs/chemistry ; Mutation ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Phenotype ; Proto-Oncogene Proteins c-met/chemistry ; Proto-Oncogene Proteins c-met/genetics ; Proto-Oncogene Proteins c-met/metabolism ; RNA, Messenger/chemistry ; RNA, Neoplasm/chemistry ; Sequence Analysis, RNA ; Signal Transduction/physiology
Chemical Substances	MicroRNAs ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; RNA, Messenger ; RNA, Neoplasm ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2016-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMoa1505917
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Characterization of HPV and host genome interactions in primary head and neck cancers

Parfenov, Michael / Pedamallu, Chandra Sekhar / Gehlenborg, Nils / Freeman, Samuel S. / Danilova, Ludmila / Bristow, Christopher A. / Lee, Semin / Hadjipanayis, Angela G. / Ivanova, Elena V. / Wilkerson, Matthew D. / Protopopov, Alexei / Yang, Lixing / Seth, Sahil / Song, Xingzhi / Tang, Jiabin / Ren, Xiaojia / Zhang, Jianhua / Pantazi, Angeliki / Santoso, Netty /

Xu, Andrew W. / Mahadeshwar, Harshad / Wheeler, David A. / Haddad, Robert I. / Jung, Joonil / Ojesina, Akinyemi I. / Issaeva, Natalia / Yarbrough, Wendell G. / Hayes, D. Neil / Grandis, Jennifer R. / El-Naggar, Adel K. / Meyerson, Matthew / Park, Peter J. / Chin, Lynda / Seidman, J. G. / Hammerman, Peter S. / Kucherlapati, Raju / Ally, Adrian / Balasundaram, Miruna / Birol, Inanc / Bowlby, Reanne / Butterfield, Yaron S.N. / Carlsen, Rebecca / Cheng, Dean / Chu, Andy / Dhalla, Noreen / Guin, Ranabir / Holt, Robert A. / Jones, Steven J.M. / Lee, Darlene / Li, Haiyan I. / Marra, Marco A. / Mayo, Michael / Moore, Richard A. / Mungall, Andrew J. / Robertson, A. Gordon / Schein, Jacqueline E. / Sipahimalani, Payal / Tam, Angela / Thiessen, Nina / Wong, Tina / Mahadeshwar, Harshad S. / Haseley, Psalm / Zeng, Dong / Bristow, Christopher / Hadjipanayis, Angela / Seidman, Jonathan / Akbani, Rehan / Casasent, Tod / Liu, Wenbin / Lu, Yiling / Mills, Gordon / Motter, Thomas / Weinstein, John / Diao, Lixia / Wang, Jing / Fan, You Hong / Liu, Jinze / Wang, Kai / Auman, J. Todd / Balu, Saianand / Bodenheimer, Thomas / Buda, Elizabeth / Hoadley, Katherine A. / Hoyle, Alan P. / Jefferys, Stuart R. / Jones, Corbin D. / Kimes, Patrick K. / Marron, J.S. / Meng, Shaowu / Mieczkowski, Piotr A. / Mose, Lisle E. / Parker, Joel S. / Perou, Charles M. / Prins, Jan F. / Roach, Jeffrey / Shi, Yan / Simons, Janae V. / Darashana Siṅgha / Soloway, Mathew G. / Tan, Donghui / Veluvolu, Umadevi / Walter, Vonn / Waring, Scot / Wu, Junyuan / Zhao, Ni / Cherniack, Andrew D. / Tward, Aaron D. / Saksena, Gordon / Carter, Scott L. / Zack, Travis I. / Schumacher, Steven E. / Beroukhim, Rameen / Cho, Juok / Getz, Gad / Noble, Michael S. / DiCara, Daniel / Zhang, Hailei / Heiman, David I. / Voet, Doug / Lin, Pei / Frazer, Scott / Stojanov, Petar / Liu, Yingchun / Zou, Lihua / Kim, Jaegil / Lawrence, Michael S. / Sougnez, Carrie / Lichtenstein, Lee / Cibulskis, Kristian / Lander, Eric / Gabriel, Stacey B. / Muzny, Donna / Doddapaneni, HarshaVardhan / Kovar, Christie / Reid, Jeff / Morton, Donna / Han, Yi / Hale, Walker / Chao, Hsu / Chang, Kyle / Drummond, Jennifer A. / Gibbs, Richard / Kakkar, Nipun / Wheeler, David / Xi, Liu / Ciriello, Giovanni / Ladanyi, Marc / Lee, William / Ramirez, Ricardo / Sander, Chris / Shen, Ronglai / Sinha, Rileen / Weinhold, Nils / Taylor, Barry S. / Aksoy, B. Arman / Dresdner, Gideon / Gao, Jianjiong / Gross, Benjamin / Jacobsen, Anders / Reva, Boris / Schultz, Nikolaus / Sumer, S. Onur / Sun, Yichao / Chan, Timothy / Morris, Luc / Stuart, Joshua / Benz, Stephen / Ng, Sam / Benz, Christopher / Yau, Christina / Baylin, Stephen B. / Cope, Leslie / Herman, James G. / Bootwalla, Moiz / Maglinte, Dennis T. / Laird, Peter W. / Triche, Timothy / Weisenberger, Daniel J. / Van Den Berg, David J. / Agrawal, Nishant / Bishop, Justin / Boutros, Paul C. / Bruce, Jeff P / Byers, Lauren Averett / Califano, Joseph / Carey, Thomas E. / Chen, Zhong / Cheng, Hui / Chiosea, Simion I. / Cohen, Ezra / Diergaarde, Brenda / Egloff, Ann Marie / Ferris, Robert L. / Frederick, Mitchell J. / Guo, Yan / Harris, Thomas / Hui, Angela BY / Lee, J. Jack / Lippman, Scott M. / Liu, Feifei / McHugh, Jonathan B. / Myers, Jeff / Ng, Patrick Kwok Shing / Perez-Ordonez, Bayardo / Pickering, Curtis R. / Prystowsky, Michael / Romkes, Marjorie / Saleh, Anthony D. / Sartor, Maureen A. / Seethala, Raja / Seiwert, Tanguy Y. / Si, Han / Van Waes, Carter / Waggott, Daryl M. / Wiznerowicz, Maciej / Yarbrough, Wendell / Zhang, Jiexin / Zuo, Zhixiang / Burnett, Ken / Crain, Daniel / Gardner, Johanna / Lau, Kevin / Mallery, David / Morris, Scott / Paulauskis, Joseph / Penny, Robert / Shelton, Candance / Shelton, Troy / Sherman, Mark / Yena, Peggy / Black, Aaron D. / Bowen, Jay / Frick, Jessica / Gastier-Foster, Julie M. / Harper, Hollie A. / Lichtenberg, Tara M. / Ramirez, Nilsa C. / Wise, Lisa / Zmuda, Erik / Baboud, Julien / Jensen, Mark A. / Kahn, Ari B. / Pihl, Todd D. / Pot, David A. / Srinivasan, Deepak / Walton, Jessica S. / Wan, Yunhu / Burton, Robert / Davidsen, Tanja / Demchok, John A. / Eley, Greg / Ferguson, Martin L. / Shaw, Kenna R. Mills / Ozenberger, Bradley A. / Sheth, Margi / Sofia, Heidi J. / Tarnuzzer, Roy / Wang, Zhining / Yang, Liming / Zenklusen, Jean Claude / Saller, Charles / Tarvin, Katherine / Chen, Chu / Bollag, Roni / Weinberger, Paul / Golusiński, Wojciech / Golusińński, Paweł / Ibbs, Matthiew / Korski, Konstanty / Mackiewicz, Andrzej / Suchorska, Wiktoria / Szybiak, Bartosz / Curley, Erin / Beard, Christina / Mitchell, Colleen / Sandusky, George / Ahn, Julie / Khan, Zubair / Irish, Jonathan / Waldron, John / Egea, Sophie / Gomez-Fernandez, Carmen / Herbert, Lynn / Bradford, Carol R. / Chepeha, Douglas B. / Haddad, Andrea S. / Jones, Tamara R. / Komarck, Christine M. / Malakh, Mayya / Moyer, Jeffrey S. / Nguyen, Ariane / Peterson, Lisa A. / Prince, Mark E. / Rozek, Laura S. / Taylor, Evan G. / Walline, Heather M. / Wolf, Gregory T. / Boice, Lori / Chera, Bhishamjit S. / Funkhouser, William K. / Gulley, Margaret L. / Hackman, Trevor G. / Hayward, Michele C. / Huang, Mei / Rathmell, W. Kimryn / Salazar, Ashley H. / Shockley, William W. / Shores, Carol G. / Thorne, Leigh / Weissler, Mark C. / Wrenn, Sylvia / Zanation, Adam M. / Brown, Brandee T. / Pham, Michelle

Proceedings of the National Academy of Sciences of the United States of America. 2014 Oct. 28, v. 111, no. 43 p.15544-15549

2014

Abstract: Significance A significant proportion of head and neck cancer is driven by human papillomavirus (HPV) infection, and the expression of viral oncogenes is involved in the development of these tumors. However, the role of HPV integration in primary tumors ... ...

Abstract	Significance A significant proportion of head and neck cancer is driven by human papillomavirus (HPV) infection, and the expression of viral oncogenes is involved in the development of these tumors. However, the role of HPV integration in primary tumors beyond increasing the expression of viral oncoproteins is not understood. Here, we describe how HPV integration impacts the host genome by amplification of oncogenes and disruption of tumor suppressors as well as driving inter- and intrachromosomal rearrangements. Tumors that do and do not have HPV integrants display distinct gene expression profiles and DNA methylation patterns, which further support the view that the mechanisms by which tumors with integrated and nonintegrated HPV arise are distinct. Previous studies have established that a subset of head and neck tumors contains human papillomavirus (HPV) sequences and that HPV-driven head and neck cancers display distinct biological and clinical features. HPV is known to drive cancer by the actions of the E6 and E7 oncoproteins, but the molecular architecture of HPV infection and its interaction with the host genome in head and neck cancers have not been comprehensively described. We profiled a cohort of 279 head and neck cancers with next generation RNA and DNA sequencing and show that 35 (12.5%) tumors displayed evidence of high-risk HPV types 16, 33, or 35. Twenty-five cases had integration of the viral genome into one or more locations in the human genome with statistical enrichment for genic regions. Integrations had a marked impact on the human genome and were associated with alterations in DNA copy number, mRNA transcript abundance and splicing, and both inter- and intrachromosomal rearrangements. Many of these events involved genes with documented roles in cancer. Cancers with integrated vs. nonintegrated HPV displayed different patterns of DNA methylation and both human and viral gene expressions. Together, these data provide insight into the mechanisms by which HPV interacts with the human genome beyond expression of viral oncoproteins and suggest that specific integration events are an integral component of viral oncogenesis.
Keywords	DNA fingerprinting ; DNA methylation ; Papillomaviridae ; gene expression ; head ; head and neck neoplasms ; humans ; oncogene proteins ; oncogenes ; cancer ; head and neck ; papilloma virus ; genome rearrangement ; integration sites
Language	English
Dates of publication	2014-1028
Size	p. 15544-15549.
Publishing place	National Academy of Sciences
Document type	Article ; Online
Note	Resource is Open Access
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1416074111
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Multilevel Genomics-Based Taxonomy of Renal Cell Carcinoma.

Chen, Fengju / Zhang, Yiqun / Şenbabaoğlu, Yasin / Ciriello, Giovanni / Yang, Lixing / Reznik, Ed / Shuch, Brian / Micevic, Goran / De Velasco, Guillermo / Shinbrot, Eve / Noble, Michael S / Lu, Yiling / Covington, Kyle R / Xi, Liu / Drummond, Jennifer A / Muzny, Donna / Kang, Hyojin / Lee, Junehawk / Tamboli, Pheroze /

Cell reports

2016 Volume 14, Issue 10, Page(s) 2476–2489

Abstract: On the basis of multidimensional and comprehensive molecular characterization (including DNA methalylation and copy number, RNA, and protein expression), we classified 894 renal cell carcinomas (RCCs) of various histologic types into nine major genomic ... ...

Abstract	On the basis of multidimensional and comprehensive molecular characterization (including DNA methalylation and copy number, RNA, and protein expression), we classified 894 renal cell carcinomas (RCCs) of various histologic types into nine major genomic subtypes. Site of origin within the nephron was one major determinant in the classification, reflecting differences among clear cell, chromophobe, and papillary RCC. Widespread molecular changes associated with TFE3 gene fusion or chromatin modifier genes were present within a specific subtype and spanned multiple subtypes. Differences in patient survival and in alteration of specific pathways (including hypoxia, metabolism, MAP kinase, NRF2-ARE, Hippo, immune checkpoint, and PI3K/AKT/mTOR) could further distinguish the subtypes. Immune checkpoint markers and molecular signatures of T cell infiltrates were both highest in the subtype associated with aggressive clear cell RCC. Differences between the genomic subtypes suggest that therapeutic strategies could be tailored to each RCC disease subset.
MeSH term(s)	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/mortality ; Carcinoma, Renal Cell/pathology ; Chromatin/metabolism ; Gene Expression Profiling ; Genomics ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/mortality ; Kidney Neoplasms/pathology ; MicroRNAs/metabolism ; Mutation ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/metabolism ; Signal Transduction/genetics ; Survival Rate ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Chromatin ; MicroRNAs ; RNA, Messenger ; TFE3 protein, human ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2016-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2211-1247
ISSN (online)	2211-1247
DOI	10.1016/j.celrep.2016.02.024
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Multilevel Genomics-Based Taxonomy of Renal Cell Carcinoma.

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