Alan Ashworth
| Alan Ashworth | |
|---|---|
| Born | 1960 (age 57–58) Bolton, Lancashire |
| Nationality | British |
| Alma mater |
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| Scientific career | |
| Institutions | |
| Thesis | Cloning and characterisation of cDNAs derived from cytochrome P-450 mRNAs (1984) |
| Doctoral students | Elizabeth Iorns |
| Website | cancer |
Alan Ashworth, FRS (born 1960 in Bolton, Lancashire) is a British molecular biologist, noted for his work on genes involved in cancer susceptibility. He is currently the President of the UCSF Helen Diller Family Comprehensive Cancer Center at the University of California, San Francisco, a multidisciplinary research and clinical care organisation that is one of the largest cancer centres in the Western United States. He was previously CEO of the Institute of Cancer Research (ICR) in London.
Ashworth was educated at St Mary's Primary School and Thornleigh Salesian College, Bolton. He completed his Bachelor of Science in Chemistry and Biochemistry at Imperial College, London, and was awarded a PhD in Biochemistry at University College, London.
Ashworth joined the Institute for Cancer Research (ICR) in London in 1986 as a Postdoctoral research Scientist in the Section of Cell and Molecular Biology and in 1999 he was appointed the first Director of the Breakthrough Breast Cancer Research Centre (BBCRC). The Centre is now recognised internationally and has more than 120 scientists and researchers working on aspects of the disease ranging from basic molecular and cellular biology through to translational research and clinical trials. Ashworth's Directorship ended in January 2011 when he took up the position of Chief Executive of the ICR which he held until December 2014.
One of Ashworth's major contributions to cancer research has been his work on genes involved in cancer risk. He was a key part of the team that in 1995 discovered the BRCA2 gene, which is linked to an increased risk of some types of cancers/ which is now used to identify women at high risk of the disease. Ten years later, Ashworth identified a way to exploit genetic weaknesses in cancer cells including mutated BRCA 1 or BRCA2, leading to a new approach to work on Poly ADP ribose polymerase (PARP as a drug target for cancer.
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