Journal
CANCER CELL
Volume 26, Issue 3, Pages 319-330Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.07.014
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Funding
- NIH [5U24CA143843, U54HG003273, 5U24CA143866, KL2TR001109, UL1TR001111, 5P50CA101942, U54 HG003067, K24CA172355]
- NIH, National Cancer Institute, Center for Cancer Research
- Frederick National Lab, NIH [HHSN261200800001E]
- NIH, National Institute of Environmental Health Sciences
- Keck Center for Interdisciplinary Bioscience Training of the Gulf Coast Consortia [T15 LM007093]
- J. Randall AMP
- Kathleen L. MacDonald Kidney Cancer Research Fund
- Tuttle Family Kidney Cancer Research Fund
- Ministry of Health AMP
- Welfare, Republic of Korea [HI13C2096]
- Korea Institute of Science and Technology Information [K-14-L01-C02-S04, KSC-2013-C3-037]
- Direct For Biological Sciences [0845783] Funding Source: National Science Foundation
- Div Of Biological Infrastructure [0845783] Funding Source: National Science Foundation
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We describe the landscape of somatic genomic alterations of 66 chromophobe renal cell carcinomas (ChRCCs) on the basis of multidimensional and comprehensive characterization, including mtDNA and whole-genome sequencing. The result is consistent that ChRCC originates from the distal nephron compared with other kidney cancers with more proximal origins. Combined mtDNA and gene expression analysis implicates changes in mitochondrial function as a component of the disease biology, while suggesting alternative roles for mtDNA mutations in cancers relying on oxidative phosphorylation. Genomic rearrangements lead to recurrent structural breakpoints within TERT promoter region, which correlates with highly elevated TERT expression and manifestation of kataegis, representing a mechanism of TERT upregulation in cancer distinct from previously observed amplifications and point mutations.
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