McGill Alert / Alerte de McGill

Updated: Mon, 07/15/2024 - 16:07

Gradual reopening continues on downtown campus. See Campus Public Safety website for details.

La réouverture graduelle du campus du centre-ville se poursuit. Complément d'information : Direction de la protection et de la prévention.

Nicole Beauchemin

Academic title(s): 

Emeritus Professor

Nicole Beauchemin
Area(s): 
Basic and Translational Cancer Research
Biography: 

Dr. Nicole Beauchemin was a McGill University Professor in the Gerald Bronfman Department of Oncology as well as in the Departments of Biochemistry and Medicine, and a member of the Goodman Cancer Research Institute. She completed her Ph.D. in Biochemistry at the University of Montreal in 1985 and trained as a post-doctoral fellow from 1985-1988 with Dr. Clifford P. Stanners at McGill University. These were the most exciting times in the study of carcinoembryonic antigen (CEA) and its functions and her expertise was key in identifying the gene and the initial functions of CEA. The Faculty of Medicine through the Department of Biochemistry and the McGill Cancer Centre recognized the importance of this work and offered her a position to work on the role of CEACAM1 (CarcinoEmbryonic Antigen Cell Adhesion Molecule 1) in colorectal cancer and metastasis. 

Her work rapidly gained international recognition in the field of CEACAM1, a close relative to CEA. With continuous funding from CIHR and the Cancer Research Society, among many other discoveries, her research team developed the first mouse models of CEACAM1, allowing in vivo studies on its function; these mouse models have now been distributed in over 35 different laboratories worldwide. The major focus of her group's work was the identification of CEACAM1 as a co-receptor for the insulin, the VEGFR2 and now the EphA2 tyrosine kinase receptors. These functional associations with the receptors defined a role for CEACAM1 in liver lipid metabolism, basal and tumour angiogenesis as well as migration and liver metastasis of colorectal cancer (CRC) cells. These phenotypes occur though a common mechanism that was first delineated in 1997 in her laboratory. Remarkably for the time, they showed that various tyrosine kinases (receptors and Src-like) were phosphorylating CEACAM1 creating docking sites for the recruitment of Tyr phosphatases, which in turn served to turn off many different signaling pathways downstream of the kinases. They also focused on clinically exploiting the biology of CEACAM1 itself as either a checkpoint inhibitor regulating TIM-3-mediated immune tolerance or targeting CEACAM1 partners in CRC liver metastasis. 

In addition to her work on CEACAM1, she collaborated with Dr. Philippe Gros on the identification and targeting of CRC and CA-CRC susceptibility gene loci and several gene candidates from carcinogen-induced mouse models.

Group: 
Emeritus Professors
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