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Sean M. Grimmond

Researcher at University of Melbourne

Publications -  302
Citations -  51131

Sean M. Grimmond is an academic researcher from University of Melbourne. The author has contributed to research in topics: Gene & Cancer. The author has an hindex of 88, co-authored 278 publications receiving 43895 citations. Previous affiliations of Sean M. Grimmond include Medical Research Council & Ludwig Institute for Cancer Research.

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Signatures of mutational processes in human cancer

Ludmil B. Alexandrov, +84 more
- 22 Aug 2013 - 
TL;DR: It is shown that hypermutation localized to small genomic regions, ‘kataegis’, is found in many cancer types, and this results reveal the diversity of mutational processes underlying the development of cancer.
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The Transcriptional Landscape of the Mammalian Genome

Piero Carninci, +197 more
- 02 Sep 2005 - 
TL;DR: Detailed polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.
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Genomic analyses identify molecular subtypes of pancreatic cancer

Peter Bailey, +128 more
- 03 Mar 2016 - 
TL;DR: Detailed genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing.
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International network of cancer genome projects

Thomas J. Hudson, +273 more
TL;DR: Systematic studies of more than 25,000 cancer genomes will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
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Whole genomes redefine the mutational landscape of pancreatic cancer.

Nicola Waddell, +88 more
- 26 Feb 2015 - 
TL;DR: Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency, and 4 of 5 individuals with these measures of defective DNA maintenance responded to platinum therapy.