Nicole Beauchemin, Ph.D.

Academic title(s): 

 

 

 

 

 

 

 

 

 

 

 

Rosalind and Morris Goodman Cancer Institute
Departments of Biochemistry, Medicine and Oncology
McGill University

* Please note: Dr. Beauchemin is no longer accepting graduate students or Postdoctoral Fellows*

Contact Information
Address: 

McIntyre Medical Sciences Building
Montreal, Quebec H3G 1Y6
Office: GCRC Room 613
Lab: Room 708
 

Phone: 
514-398-3541 (Office)
514-398-3542 (Lab)
Fax number: 
514-398-6769
Email address: 
nicole.beauchemin [at] mcgill.ca
Awards, honours, and fellowships: 

1. Salary Award from Fonds de la recherche en santé du Québec, 1988-2005
2. Recipient of the Abbott Award for Research, International Society for Oncodevelopmental Biology and Medicine, 1999


 

Selected publications: 
Current research: 

Investigations on the role of inflammatory gene drivers in the development and progression of colitis-associated colorectal cancer (CA-CRC), particularly prevalent in IBD patients.

* Please note: Dr. Beauchemin is no longer accepting graduate students or Postdoctoral Fellows*

Dr. Beauchemin’s research deals with colon cancer and focuses on the molecular mechanisms of pathways involving CEACAM1 in cancer progression and metastasis. Colon cancer remains a leading cause of death in Canada. It is estimated that 10,000 Canadians succombed of this disease in 2018.

Dr. Beauchemin’s team analyzes:

1. Whether the CEACAM1 gene, an Ig and carcinoembryonic antigen (CEA) family member, represents a good target for colorectal cancer treatment options.

CEACAM1 (CC1) is dysregulated in many human tumors, including colon tumors. Its expression pattern is paradoxical: it is absent in the very early stages of tumor development, but strongly overexpressed later in stages 3 and 4 human colon cancer. Dr. Beauchemin’s team has shown that Ceacam1-/- normal colonocytes exhibit increased proliferation and decreased apoptosis. This leads to increased colon tumor multiplicity in azoxymethane (AOM)-induced carcinogenesis compared to wild-type littermate controls. Deletion of CC1 also contributes to development of Adenomatous polyposis coli (Apc)-driven intestinal cancer with Ceacam1-/- intestine having decreased intestinal apoptosis. Importantly, CEACAM1 deletion has more impact on tumor progression leading to increased tumor size and more advanced staging. Dr. Beauchemin’s research team has now mapped a whole signalling network involving CEACAM1-L with Receptor Tyrosine Kinases, the STAT3 transcription factor, several chemokines and cytokines. CEACAM1 influences metastasis progression in vivo through this signalling pathway. We are also investigating how the tumor stroma responds to CEACAM1-positive tumors via endothelial cells and myeloid-derived suppressor cells. Furthermore, members of this laboratory are developing new CEACAM1-based inhibitory compounds that would prevent such dramatic cancer progression.

2. Dr. Beauchemin has also developed a long-standing collaboration with Dr. Philippe Gros to identify and characterize colon cancer susceptibility genes using the power of reverse genetics.

A novel gene locus has been identified for azoxymethane-induced colorectal cancer development using A/J-B6 congenic mice and another locus has also been found with a gene(s) responding to azoxymethane and sodium dextran sulfate-induced treatment for inflammation-CRC. These genes have now been mapped and are being functionally analyzed. In addition, this team has identified that the IRF1 gene, known as a susceptibility factor in IBD, causes the development of CA-CRC in Irf1-/- mice upon treatment with AOM-DSS. Differential susceptibility to CA-CRC of Irf1-/-vs. C57B6 controls is fully transferable through hematopoietic cells as observed in bone marrow chimera studies. IRF1 expression in the human colon is significantly decreased in late stage colorectal cancer (stages 3, 4) and is associated with poorer prognosis. This indicates that partial or complete loss of IRF1 expression alters the type, number, and function of immune cells in situ during chronic inflammation, possibly via the creation of a tumor-promoting environment (Jeyakumar et al. Scientific Reports, in press 2020).

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