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Jonathan Hinton

Researcher at Wellcome Trust Sanger Institute

Publications -  26
Citations -  10332

Jonathan Hinton is an academic researcher from Wellcome Trust Sanger Institute. The author has contributed to research in topics: Biology & Cancer. The author has an hindex of 15, co-authored 19 publications receiving 8545 citations. Previous affiliations of Jonathan Hinton include Wellcome Trust & European Bioinformatics Institute.

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Mutational Processes Molding the Genomes of 21 Breast Cancers

TL;DR: This work generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes, finding a remarkable phenomenon of localized hypermutation, termed “kataegis,” was observed.
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The landscape of cancer genes and mutational processes in breast cancer

Philip J. Stephens, +69 more
- 21 Jun 2012 - 
TL;DR: Strong correlations between mutation number, age at which cancer was diagnosed and cancer histological grade are found, and multiple mutational signatures are observed, including one present in about ten per cent of tumours characterized by numerous mutations of cytosine at TpC dinucleotides.
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Pan-cancer analysis of whole genomes

Peter J. Campbell, +1332 more
- 06 Feb 2020 - 
TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
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The Life History of 21 Breast Cancers

TL;DR: Algorithms were developed to decipher this narrative and applied them to 21 breast cancers, finding that expansion of the dominant subclone to an appreciable mass may represent the final rate-limiting step in a breast cancer's development, triggering diagnosis.
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Somatic mutations of the histone H3K27 demethylase gene UTX in human cancer

TL;DR: UTX reintroduction into cancer cells with inactivating UTX mutations resulted in slowing of proliferation and marked transcriptional changes, identifying UTX as a new human cancer gene.