Patel is of Gujarati Indian origin and was born in Nairobi, Kenya. His early education took place in his home country at Hospital Hill Primary School and Banda Preparatory School. In 1976, Patel left Kenya to continue his secondary education at Marlborough College in Wiltshire. He subsequently went to medical school at the Royal Free Hospital and the University of London where he qualified as a doctor with distinctions in Medicine and Surgery. Patel originally trained as a gastroenterologist but also was awarded an MRC training fellowship to work with Michael Neuberger FRS at the MRC Laboratory of Molecular Biology. He completed a PhD in which he conducted research to understand the role the membrane bound form of the antibody molecule.
Career and Research
After his PhD, Patel was awarded an MRC Clinician Scientist Fellowship and started working with A. Venkitaraman where he contributed to the discovery that the BRCA2 protein functions in repairing damaged DNA. Patel eventually joined the LMB as a tenure track group leader and was later on promoted to tenured principal investigator at the LMB. Patel's research is mainly concerned with how living cells repair DNA crosslinks. These lesions cause the two opposing strands of DNA to be covalently bound together. Such crosslinks are lethal to cells since they would prevent DNA from being copied or for the genes it carries to be read. DNA crosslinks are caused by numerous anti-cancer drugs, but they also must arise naturally since individuals carrying a genetic defect in crosslink repair suffer from the illness Fanconi anaemia. This devastating inherited illness leads to congenital defects, progressive loss of blood production and an enormous lifetime risk of certain cancers. Patel's research on the Fanconi pathway has provided key molecular insights into how cells remove DNA crosslinks and, most recently, his lab discovered that reactive aldehydes are the likely natural agents that produce them. Aldehydes are ubiquitous metabolites, arising not only from many metabolic pathways but also when cells process alcohol. His lab showed that mammals use a two-tier protection mechanism to counteract aldehydes, consisting of enzymatic clearance of aldehydes by aldehyde dehydrogenases and the Fanconi DNA repair pathway. Although Fanconi anaemia is a very rare condition, genetic deficiency of this two-tier protection mechanism is actually very common in man: up to 500 million Asians are deficient in first tier protection due to mutations in the gene ALDH2.
