Contact info

Dr Pavel Hamet
CRCHUM � Pavillon R
900, Saint-Denis � Room R08.464
Montreal, QC H2X 0A9

Tel: 1-514-890-8246
Fax: 1-514-412-7682
E-mail: [email protected]

Research keywords

Dr Hamet holds a Canada Research Chair in Predictive Genomics of hypertension and cardiovascular diseases. He is Professor of Medicine at Universit� de Montr�al, Adjunct Professor of Experimental Medicine at McGill University, and Visiting Professor at the First Faculty of Medicine at Charles University, Prague, Czech Republic. He founded and directed the Centre Hospitalier de l'Universit� de Montr�al's Research Centre (CRCHUM) from 1996 to 2006. He is currently Chief of Gene Medicine and member of the Endocrinology Services, and Director of the Laboratory of Molecular Medicine at the CHUM.

Dr Hamet received his Doctorate in Medicine in 1967 from Charles University in Prague, Czech Republic, a PhD in Experimental Medicine from McGill University in 1972, and a CSPQ in Endocrinology from Universit� de Montr�al in 1974. He then completed two years of postdoctoral training at Vanderbilt University in the USA. He is a Fellow of the Royal College of Physicians and Surgeons of Canada since 1984, Fellow of the American Heart Association since 1985, Fellow of the Royal Society of Medicine since 1986 and Fellow of the Canadian Academy of Health Science since 2005.

Dr Hamet is the author or co-author of over 535 scientific publications and holds several international patents. He serves on many national and international boards, including the Institute of Circulatory and Respiratory Health of the Canadian Institutes of Health Research (CIHR). His major scientific contributions are in the areas of hypertension, diabetes and cardiovascular diseases, using approaches that range from bench to bedside to population health. He is also President of Prognomix and Medpharmgene, two academic biotechnology societies devoted to the conduct of high-level science and results-oriented clinical research programs, and to the development of diagnostic and predictive technology aimed at delivering the promises of personalized medicine.

Dr Hamet receives financial support from major funding agencies, including the CIHR, the Canada Foundation for Innovation, Genome Quebec, and from the pharmaceutical industry. Active in many societies, he is President of the International Society of Pathophysiology. He was President of the Canadian and Quebec Hypertension Societies and General-Secretary of the International Society of Hypertension. He has received many honours, including the Harry Goldblatt Award from the American Heart Association, the J.E. Purkyne Golden Medal by the Czech Academy of Sciences, the Distinguished Scientist Award from the Canadian Society for Clinical Investigation and the Achievement Award from the Canadian Cardiovascular Society. In 2001, he was honoured with the prestigious Wilder Penfield Award by the Government of Qu�bec. In 2008, Dr Hamet was named as an Officer of the Ordre national du Qu�bec and he received the prestigious Okamoto Award by the Japan Vascular Disease Research Foundation. L'Association des M�decins de Langue Fran�aise du Canada awarded him the Prize of the scientific work for 2010. In 2011, Dr Hamet was appointed Honorary Member of the Canadian Medical Association and named by the Council of Ministers of Quebec, member of the Committee of Ethics in Science and in Technology. In 2012, The Soci�t� Francophone du Diab�te, in France, honoured him with the Roger Assan Award.

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Contribution to the establishment of the role of the second messenger cGMP in signal transduction of hormones. Discovery of cGMP-binding phosphodiesterase, its purification and characterisation. This enzyme became later the target of Viagra. Publication of a novel method for generation of anti-cGMP antibody for its detection in human and animal fluids and in cell culture. The antibody is still largely used in many laboratories (Richman et al., J Cycl Nucleotide Res 6:461-8, 1980). Discovery that cGMP is the second messenger of the atrial natriuretic peptide, ANP. Use of radiolabelled ANP to visualise the kidney mass.

Contribution to improved treatment of hypertension. STONE (Shanghai trial of Nifedipine in the Elderly) study was the first demonstration that a new type of antihypertensive agent can decrease cardiovascular outcomes. This study was a significant argument used in the calcium channel blocker (CCB) controversy of that time, to prove the absence of detrimental effect of CCB in cardiovascular area and cancer. Demonstration that intensive blood pressure and glycemic control improve mortality in diabetes in 12,000 subjects of ADVANCE study.

Demonstration of elevated proliferation and apoptosis in target organs of hypertension. We have been first to demonstrate an increased proliferation of vascular smooth muscle cells from genetic rodent models of hypertension in response to growth factors, through shortening of the G₁-S transition phase of the cell cycle. We also introduced the notion that apoptosis is increased not only in response to acute blood pressure overload but also chronically in spontaneous hypertension or during the vascular regression induced by antihypertensive. This led us to propose the hypothesis that hypertension exhibits a state of increased cellular turnover which leads to an accelerated ageing.

Contribution to the genetics of hypertension.
Experimental genetics. We have identified the genetic basis of increased sensitivity to environmental stress in hypertensive rats and reported that hsp70 polymorphism is associated with hypertension in the recombinant inbred strains of the genetically hypertensive rat and by whole genome scan, identified the quantitative trait loci (QTL) of stress response in the rat. We also discovered a pleiotropic effect of response to stress by a first linkage analysis of mRNA accumulation of stress genes as a phenotype, leading to identification of a SNP in the heat shock transcription factor, hstf. We have established a novel model of familial combined hyperlipidemia in the rat by comparative genomics and established the genetic architecture of the metabolic syndrome. Using recombinant congenic strains of mice and in silico analysis we have identified several genes involved in stress response.
Human genetics. I have established a French-Canadian family cohort affected with hypertension and dyslipidemia and compared it with Afro-Americans. We established a quantitative founder effect in complex diseases which led to the identification of the most comprehensive QTL map of hypertension and metabolic traits. We have then proceeded to the first partitioning of hypertension subtypes with and without obesity and determined their clearly distinct genetic determinants.

Discovery of a new etiology of Cushing Syndrome by ectopic expression of adrenal receptors. I have identified a new cause and with my collaborators, we have established its mechanisms as adrenal ectopic expression of several hormone receptors including GIP, vasopressin, beta-adrenergic receptor and luteinizing hormone.

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