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Emily K. Colvin

Researcher at University of Sydney

Publications -  50
Citations -  8967

Emily K. Colvin is an academic researcher from University of Sydney. The author has contributed to research in topics: Pancreatic cancer & Cancer. The author has an hindex of 22, co-authored 46 publications receiving 7244 citations. Previous affiliations of Emily K. Colvin include Kolling Institute of Medical Research & Garvan Institute of Medical Research.

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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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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.
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Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes

Andrew V. Biankin, +140 more
- 15 Nov 2012 - 
TL;DR: It is found that frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, are also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement ofAxon guidance genes in pancreatic carcinogenesis.
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Whole-genome landscape of pancreatic neuroendocrine tumours

Aldo Scarpa, +129 more
- 02 Mar 2017 - 
TL;DR: In this paper, the authors performed whole-genome sequencing of 102 primary pancreatic neuroendocrine tumours and defined the genomic events that characterize their pathogenesis, including a deficiency in G:C,>T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase.