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000177482 037__ $$aDKFZ-2021-02569
000177482 041__ $$aEnglish
000177482 082__ $$a500
000177482 1001_ $$00000-0003-0265-0835$$aBhandari, Vinayak$$b0
000177482 245__ $$aDivergent mutational processes distinguish hypoxic and normoxic tumours.
000177482 260__ $$a[London]$$bNature Publishing Group UK$$c2020
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000177482 500__ $$asiehe Correction: DKFZ Autoren affiliiert im PCAWG Consortium:https://inrepo02.dkfz.de/record/212440 /https://doi.org/10.1038/s41467-022-32339-4
000177482 520__ $$aMany primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
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000177482 650_7 $$2NLM Chemicals$$aTP53 protein, human
000177482 650_7 $$2NLM Chemicals$$aTumor Suppressor Protein p53
000177482 650_7 $$0EC 3.1.3.67$$2NLM Chemicals$$aPTEN Phosphohydrolase
000177482 650_7 $$0EC 3.1.3.67$$2NLM Chemicals$$aPTEN protein, human
000177482 650_2 $$2MeSH$$aCell Hypoxia: genetics
000177482 650_2 $$2MeSH$$aGenes, myc
000177482 650_2 $$2MeSH$$aGenome, Human
000177482 650_2 $$2MeSH$$aGenomic Structural Variation
000177482 650_2 $$2MeSH$$aHumans
000177482 650_2 $$2MeSH$$aMutation
000177482 650_2 $$2MeSH$$aNeoplasms: genetics
000177482 650_2 $$2MeSH$$aNeoplasms: pathology
000177482 650_2 $$2MeSH$$aPTEN Phosphohydrolase: genetics
000177482 650_2 $$2MeSH$$aPolymorphism, Single Nucleotide
000177482 650_2 $$2MeSH$$aTumor Hypoxia: genetics
000177482 650_2 $$2MeSH$$aTumor Microenvironment: genetics
000177482 650_2 $$2MeSH$$aTumor Suppressor Protein p53: genetics
000177482 650_2 $$2MeSH$$aWhole Genome Sequencing
000177482 7001_ $$00000-0002-5487-7225$$aLi, Constance H$$b1
000177482 7001_ $$00000-0002-8553-9544$$aBristow, Robert G$$b2
000177482 7001_ $$00000-0003-0553-7520$$aBoutros, Paul C$$b3
000177482 7001_ $$0P:(DE-HGF)0$$aPCAWGConsortium$$b4
000177482 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-019-14052-x$$gVol. 11, no. 1, p. 737$$n1$$p737$$tNature Communications$$v11$$x2041-1723$$y2020
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