@article{RN6115,
   author = {Barthel, F. P. and Wei, W. and Tang, M. and Martinez-Ledesma, E. and Hu, X. and Amin, S. B. and Akdemir, K. C. and Seth, S. and Song, X. and Wang, Q. and Lichtenberg, T. and Hu, J. and Zhang, J. and Zheng, S. and Verhaak, R. G.},
   title = {Systematic analysis of telomere length and somatic alterations in 31 cancer types},
   journal = {Nat Genet},
   volume = {49},
   number = {3},
   pages = {349-357},
   note = {1546-1718
Barthel, Floris P
Wei, Wei
Tang, Ming
Orcid: 0000-0002-7739-8913
Martinez-Ledesma, Emmanuel
Hu, Xin
Amin, Samirkumar B
Akdemir, Kadir C
Seth, Sahil
Orcid: 0000-0003-4579-3959
Song, Xingzhi
Wang, Qianghu
Lichtenberg, Tara
Hu, Jian
Zhang, Jianhua
Zheng, Siyuan
Orcid: 0000-0002-7176-5348
Verhaak, Roel G W
P01 CA085878/CA/NCI NIH HHS/United States
P30 CA016672/CA/NCI NIH HHS/United States
P30 CA034196/CA/NCI NIH HHS/United States
R01 CA190121/CA/NCI NIH HHS/United States
Journal Article
United States
2017/01/31
Nat Genet. 2017 Mar;49(3):349-357. doi: 10.1038/ng.3781. Epub 2017 Jan 30.},
   abstract = {Cancer cells survive cellular crisis through telomere maintenance mechanisms. We report telomere lengths in 18,430 samples, including tumors and non-neoplastic samples, across 31 cancer types. Telomeres were shorter in tumors than in normal tissues and longer in sarcomas and gliomas than in other cancers. Among 6,835 cancers, 73% expressed telomerase reverse transcriptase (TERT), which was associated with TERT point mutations, rearrangements, DNA amplifications and transcript fusions and predictive of telomerase activity. TERT promoter methylation provided an additional deregulatory TERT expression mechanism. Five percent of cases, characterized by undetectable TERT expression and alterations in ATRX or DAXX, demonstrated elongated telomeres and increased telomeric repeat-containing RNA (TERRA). The remaining 22% of tumors neither expressed TERT nor harbored alterations in ATRX or DAXX. In this group, telomere length positively correlated with TP53 and RB1 mutations. Our analysis integrates TERT abnormalities, telomerase activity and genomic alterations with telomere length in cancer.},
   keywords = {DNA Methylation/genetics
Glioma/genetics
Humans
Neoplasms/*genetics
Point Mutation/*genetics
Promoter Regions, Genetic/genetics
Retinoblastoma Binding Proteins/genetics
Sarcoma/genetics
Telomerase/genetics
Telomere/*genetics
Tumor Suppressor Protein p53/genetics
Ubiquitin-Protein Ligases/genetics},
   ISSN = {1061-4036 (Print)
1061-4036},
   DOI = {10.1038/ng.3781},
   year = {2017},
   type = {Journal Article}
}

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G."],"year":2017,"bibtype":"article","biburl":"https://verhaaklab.com/files/verhaak.bib","bibdata":{"bibtype":"article","type":"Journal Article","author":[{"propositions":[],"lastnames":["Barthel"],"firstnames":["F.","P."],"suffixes":[]},{"propositions":[],"lastnames":["Wei"],"firstnames":["W."],"suffixes":[]},{"propositions":[],"lastnames":["Tang"],"firstnames":["M."],"suffixes":[]},{"propositions":[],"lastnames":["Martinez-Ledesma"],"firstnames":["E."],"suffixes":[]},{"propositions":[],"lastnames":["Hu"],"firstnames":["X."],"suffixes":[]},{"propositions":[],"lastnames":["Amin"],"firstnames":["S.","B."],"suffixes":[]},{"propositions":[],"lastnames":["Akdemir"],"firstnames":["K.","C."],"suffixes":[]},{"propositions":[],"lastnames":["Seth"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Song"],"firstnames":["X."],"suffixes":[]},{"propositions":[],"lastnames":["Wang"],"firstnames":["Q."],"suffixes":[]},{"propositions":[],"lastnames":["Lichtenberg"],"firstnames":["T."],"suffixes":[]},{"propositions":[],"lastnames":["Hu"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Zhang"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Zheng"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Verhaak"],"firstnames":["R.","G."],"suffixes":[]}],"title":"Systematic analysis of telomere length and somatic alterations in 31 cancer types","journal":"Nat Genet","volume":"49","number":"3","pages":"349-357","note":"1546-1718 Barthel, Floris P Wei, Wei Tang, Ming Orcid: 0000-0002-7739-8913 Martinez-Ledesma, Emmanuel Hu, Xin Amin, Samirkumar B Akdemir, Kadir C Seth, Sahil Orcid: 0000-0003-4579-3959 Song, Xingzhi Wang, Qianghu Lichtenberg, Tara Hu, Jian Zhang, Jianhua Zheng, Siyuan Orcid: 0000-0002-7176-5348 Verhaak, Roel G W P01 CA085878/CA/NCI NIH HHS/United States P30 CA016672/CA/NCI NIH HHS/United States P30 CA034196/CA/NCI NIH HHS/United States R01 CA190121/CA/NCI NIH HHS/United States Journal Article United States 2017/01/31 Nat Genet. 2017 Mar;49(3):349-357. doi: 10.1038/ng.3781. Epub 2017 Jan 30.","abstract":"Cancer cells survive cellular crisis through telomere maintenance mechanisms. We report telomere lengths in 18,430 samples, including tumors and non-neoplastic samples, across 31 cancer types. Telomeres were shorter in tumors than in normal tissues and longer in sarcomas and gliomas than in other cancers. Among 6,835 cancers, 73% expressed telomerase reverse transcriptase (TERT), which was associated with TERT point mutations, rearrangements, DNA amplifications and transcript fusions and predictive of telomerase activity. TERT promoter methylation provided an additional deregulatory TERT expression mechanism. Five percent of cases, characterized by undetectable TERT expression and alterations in ATRX or DAXX, demonstrated elongated telomeres and increased telomeric repeat-containing RNA (TERRA). The remaining 22% of tumors neither expressed TERT nor harbored alterations in ATRX or DAXX. In this group, telomere length positively correlated with TP53 and RB1 mutations. Our analysis integrates TERT abnormalities, telomerase activity and genomic alterations with telomere length in cancer.","keywords":"DNA Methylation/genetics Glioma/genetics Humans Neoplasms/*genetics Point Mutation/*genetics Promoter Regions, Genetic/genetics Retinoblastoma Binding Proteins/genetics Sarcoma/genetics Telomerase/genetics Telomere/*genetics Tumor Suppressor Protein p53/genetics Ubiquitin-Protein Ligases/genetics","issn":"1061-4036 (Print) 1061-4036","doi":"10.1038/ng.3781","year":"2017","bibtex":"@article{RN6115,\n author = {Barthel, F. P. and Wei, W. and Tang, M. and Martinez-Ledesma, E. and Hu, X. and Amin, S. B. and Akdemir, K. C. and Seth, S. and Song, X. and Wang, Q. and Lichtenberg, T. and Hu, J. and Zhang, J. and Zheng, S. and Verhaak, R. G.},\n title = {Systematic analysis of telomere length and somatic alterations in 31 cancer types},\n journal = {Nat Genet},\n volume = {49},\n number = {3},\n pages = {349-357},\n note = {1546-1718\nBarthel, Floris P\nWei, Wei\nTang, Ming\nOrcid: 0000-0002-7739-8913\nMartinez-Ledesma, Emmanuel\nHu, Xin\nAmin, Samirkumar B\nAkdemir, Kadir C\nSeth, Sahil\nOrcid: 0000-0003-4579-3959\nSong, Xingzhi\nWang, Qianghu\nLichtenberg, Tara\nHu, Jian\nZhang, Jianhua\nZheng, Siyuan\nOrcid: 0000-0002-7176-5348\nVerhaak, Roel G W\nP01 CA085878/CA/NCI NIH HHS/United States\nP30 CA016672/CA/NCI NIH HHS/United States\nP30 CA034196/CA/NCI NIH HHS/United States\nR01 CA190121/CA/NCI NIH HHS/United States\nJournal Article\nUnited States\n2017/01/31\nNat Genet. 2017 Mar;49(3):349-357. doi: 10.1038/ng.3781. Epub 2017 Jan 30.},\n abstract = {Cancer cells survive cellular crisis through telomere maintenance mechanisms. We report telomere lengths in 18,430 samples, including tumors and non-neoplastic samples, across 31 cancer types. Telomeres were shorter in tumors than in normal tissues and longer in sarcomas and gliomas than in other cancers. Among 6,835 cancers, 73% expressed telomerase reverse transcriptase (TERT), which was associated with TERT point mutations, rearrangements, DNA amplifications and transcript fusions and predictive of telomerase activity. TERT promoter methylation provided an additional deregulatory TERT expression mechanism. Five percent of cases, characterized by undetectable TERT expression and alterations in ATRX or DAXX, demonstrated elongated telomeres and increased telomeric repeat-containing RNA (TERRA). The remaining 22% of tumors neither expressed TERT nor harbored alterations in ATRX or DAXX. In this group, telomere length positively correlated with TP53 and RB1 mutations. 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