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Alan Ashworth
Researcher at University of California, San Francisco
Publications - 589
Citations - 82138
Alan Ashworth is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 134, co-authored 578 publications receiving 72089 citations. Previous affiliations of Alan Ashworth include Imperial College London & Papworth Hospital.
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DNA amplifications in breast cancer: genotypic-phenotypic correlations.
TL;DR: DNA copy number changes in cancer cells, in particular, amplifications, occur frequently, have prognostic impact and are associated with subtypes of breast cancer, including luminal (ER+)/HER2(-)), HER2+ and basal-like (ER(-)/HER1(-) and discusses their known or potential roles in cancer biology and their clinical implications.
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A Modified Method for Whole Exome Resequencing from Minimal Amounts of Starting DNA
Iwanka Kozarewa,Juan Manuel Rosa-Rosa,Christopher P. Wardell,Brian A Walker,Kerry Fenwick,Ioannis Assiotis,Costas Mitsopoulos,Marketa Zvelebil,Gareth J. Morgan,Alan Ashworth,J Christopher +10 more
TL;DR: This work presents a method for exome capture and resequencing using as little as 50 ng of starting DNA, which can be performed in most laboratories using commonly available reagents and has the potential to enhance large scale profiling efforts such as the resequenced of tumour exomes.
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An in vivo model of intratumoural aromatase using aromatase‐transfected MCF7 human breast cancer cells
Kathryn Lee,Valentine M. Macaulay,Joanne E. Nicholls,Simone Detre,Alan Ashworth,Mitchell Dowsett +5 more
TL;DR: The results indicate that Δ4A‐dependent growth of Arom 1 tumours in vivo is mediated through the action of intratumoural aromatase, which should allow an assessment of the critical levels of aromat enzyme required for tumour growth support.
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An RNA interference screen for identifying downstream effectors of the p53 and pRB tumour suppressor pathways involved in senescence
TL;DR: The senescence bypass screen identified TMEM9B, ATXN10, LAYN and LTBP2/3 as novel downstream effectors of the p53-p21 and p16-pRB tumour suppressor pathways.
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NLK Is a Novel Therapeutic Target for PTEN Deficient Tumour Cells
TL;DR: Evidence that PTEN defective cells targeted by NLK gene depletion undergo senescence, suggesting that NLK function is critical for the continued proliferation of PTEN deficient cells, provides new insight into the potential of targeting of NLK to treat a range of tumourigenic conditions characterised by PTEN deficiency.