Associate professor, Department of Medicine, McGill University
Lady Davis Institute for Medical Research
Sir Mortimer B. Davis-Jewish General Hospital
3755 Cote-Ste-Catherine Road
Montreal, Quebec H3T 1E2
Tel.: 514-340-8222 ext. 5269
mark [dot] trifiro [at] mcgill [dot] ca (Email)
Dr. Trifiro's Web Page
Expertise: Androgen Receptor – Mechanism of Action, genetic instability of androgen independent prostate carcinoma
Summary of Research Activities
Dr. Trifiro’s laboratory studies Androgen Receptor (AR) mutations and their associated diseases. One facet of his studies focuses on trinucleotide repeat polymorphism in the AR. An expansion in the CAG repeats leads to spinobulbar muscular atrophy, an adult onset neurodegenerative disorder. A shortening in the trinucloetide repeats has been linked to an increased risk of prostate cancer and has been found in individuals with prostate cancer. They are developing transgenic mice with varying repeat lengths of the polyglutamine tract in order to study the effects of polyCAG tract length, somatic polyCAG instability and AR missense mutations on the pathogenesis of AR related disease.
A second facet of his studies involves the human Androgen Insensitivity Syndrome. They functionally characterize AR mutants responsible for this disease and curate a world wide database of AR mutants. Methods for the characterization of these mutants include receptor binding studies, genomic and expression studies, and computer modeling.
Di Fabio F, Alvarado C, Majdan A, Gologan A, Voda L, Mitmaker E, Beitel LK, Gordon PH, Trifiro M. Underexpression of Mineralocorticoid Receptor in Colorectal Carcinomas and Association with VEGFR-2 Overexpression. J Gastrointest Surg. 2007 Nov;11(11):1521-8. Epub 2007 Aug 17.
Gottlieb B, Beitel LK, Trifiro M. Will knowledge of human genome variation result in changing cancer paradigms? Bioessays. 2007 Jul;29(7):678-85. Review.
Elhaji YA, Stoica I, Dennis S, Purisima EO, Trifiro MA. Impaired helix 12 dynamics due to proline 892 substitutions in the androgen receptor are associated with complete androgen insensitivity. Hum Mol Genet. 2006 Mar 15;15(6):921-31. Epub 2006 Jan 31.