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Understanding the biological processes of kidney carcinogenesis: an integrative multi-omics approach
R. Cortez Cardoso Penha, A. Sexton Oates, S. Senkin, HA. Park, J. Atkins, I. Holcatova, A. Hornakova, S. Savic, S. Ognjanovic, B. Świątkowska, J. Lissowska, D. Zaridze, A. Mukeria, V. Janout, A. Chabrier, V. Cahais, C. Cuenin, G. Scelo, M. Foll,...
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články
Grantová podpora
GeniLuc2017-1-TABAC-03-CIRC-1-[TABAC17-022]
Institut National Du Cancer (INCa)
U01CA155309
HHS | National Institutes of Health (NIH)
U01 CA155309
NCI NIH HHS - United States
C98/A24032
Cancer Research UK (CRUK)
001
World Health Organization - International
- MeSH
- DNA vazebné proteiny genetika metabolismus MeSH
- epigeneze genetická MeSH
- epitelo-mezenchymální tranzice * genetika MeSH
- glutathion-S-transferasa fí genetika metabolismus MeSH
- histonlysin-N-methyltransferasa genetika metabolismus MeSH
- karcinogeneze * genetika MeSH
- lidé MeSH
- metylace DNA * MeSH
- multiomika MeSH
- mutace * MeSH
- nádorové supresorové proteiny genetika metabolismus MeSH
- nádory ledvin * genetika patologie MeSH
- regulace genové exprese u nádorů MeSH
- stárnutí genetika MeSH
- thiolesterasa ubikvitinu MeSH
- transkripční faktory genetika metabolismus MeSH
- transkriptom MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Biological mechanisms related to cancer development can leave distinct molecular fingerprints in tumours. By leveraging multi-omics and epidemiological information, we can unveil relationships between carcinogenesis processes that would otherwise remain hidden. Our integrative analysis of DNA methylome, transcriptome, and somatic mutation profiles of kidney tumours linked ageing, epithelial-mesenchymal transition (EMT), and xenobiotic metabolism to kidney carcinogenesis. Ageing process was represented by associations with cellular mitotic clocks such as epiTOC2, SBS1, telomere length, and PBRM1 and SETD2 mutations, which ticked faster as tumours progressed. We identified a relationship between BAP1 driver mutations and the epigenetic upregulation of EMT genes (IL20RB and WT1), correlating with increased tumour immune infiltration, advanced stage, and poorer patient survival. We also observed an interaction between epigenetic silencing of the xenobiotic metabolism gene GSTP1 and tobacco use, suggesting a link to genotoxic effects and impaired xenobiotic metabolism. Our pan-cancer analysis showed these relationships in other tumour types. Our study enhances the understanding of kidney carcinogenesis and its relation to risk factors and progression, with implications for other tumour types.
Cancer Epidemiology Unit University of Oxford Oxford Oxford OX3 7LF UK
Department of Environmental Epidemiology Nofer Institute of Occupational Medicine Łódź 90 950 Poland
Department of Urology Kliničko Bolnički Centar Dr Dragiša Mišović Belgrade Serbia
Faculty of Health Sciences Palacký University Olomouc 77900 Olomouc Czechia
Institute of Hygiene and Epidemiology Charles University Prague 12800 Czechia
Institute of Public Health and Preventive Medicine Charles University Prague 15000 Czechia
International Organization for Cancer Prevention and Research Belgrade 11070 Serbia
Maria Sklodowska Curie National Research Institute of Oncology Warszawa 00 001 Poland
N N Blokhin Cancer Research Center Moscow 115478 Russia
The Observational and Pragmatic Research Institute Midview City 573969 Singapore
Citace poskytuje Crossref.org
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