Ï㽶ÊÓƵ

Beauchemin, Nicole, Professor (Please note: No longer accepting graduate students or post-doctoral fellows)
nicole.beauchemin [at] mcgill.ca
Studies on the functions of the mouse CEACAM1 proteins in various tissues, their association with intracytoplasmic proteins and their connection with signaling cascades using transgenic and knockout mouse models. Role of the CEACAM1 proteins in colon tumor development, progression, and metastasis in genetic models. Role of the CEACAM1 proteins in angiogenesis in transgenic mice.

Bouchard, Maxime, Professor
maxime.bouchard [at] mcgill.ca
Molecular mechanisms of urogenital system development and tumor formation. Role of transcription factors and cell signaling in tissue morphogenesis, tubulogenesis and cell survival. Mouse models of renal and prostate cancer.

Natasha Chang, Assistant Professor
natasha.chang [at] mcgill.ca
The focus of the Chang lab is to elucidate the molecular pathways that regulate stem cell function. We employ muscle stem cells as a model to study stem cell biology and tissue regeneration. Dysregulation of the pathways that control muscle stem cell function contribute to muscle degeneration and disease. We investigate how stem cell function is impaired in muscle degenerative disease and cancer in order to gain insight into mechanisms of disease and develop novel regenerative medicine strategies.

Dostie, Josee, Professor
josee.dostie [at] mcgill.ca
The Dostie lab is working towards defining how the human genome is organized in three-dimensions, and identifying mechanisms that regulate spatial chromatin organization. We are applying genomics and molecular biology approaches to understand how genome folding impinges on gene expression in normal and diseased tissues such as in cancers.

Duchaine, Thomas, Professor
thomas.duchaine [at] mcgill.ca
Ï㽶ÊÓƵi is the process through which small non-coding Ï㽶ÊÓƵs direct a diverse set of gene-silencing processes. My group is interested in the underlying mechanisms, and their implications in development and cancer. Through a combination of genetics, cell biology, biochemistry and proteomics and using the nematode C. elegans, we examine the molecular machines involved in Ï㽶ÊÓƵi, and decipher how they orchestrate gene silencing. Currently, my group focuses on two distinct ‘branches’ of the Ï㽶ÊÓƵi processes: endoÏ㽶ÊÓƵi and microÏ㽶ÊÓƵ-mediated silencing. First, we examine a phenomenon termed endogenous Ï㽶ÊÓƵi (endoÏ㽶ÊÓƵ) which is naturally initiated on certain messenger Ï㽶ÊÓƵs, and results in the shutdown of the gene's expression. We are particularly interested in the functional interactions between endoÏ㽶ÊÓƵi and chromatin, the physiological scaffold of the genome. Second, we are interested in how microÏ㽶ÊÓƵ-mediated gene silencing touches upon genetic programs in the developing embryo, and in cancer cells. Our findings have implications for the understanding of gene networks in all animals, including humans.

Gallouzi, Imed, Professor
imed.gallouzi [at] mcgill.ca
Our general research area is mÏ㽶ÊÓƵ metabolism during the cell cycle and cell differentiation. We use the tools of molecular and cell biology to study problems in this field. The long-term research goals focus on understanding the cellular mechanisms involved in the regulation of mÏ㽶ÊÓƵ half-lives and how they affect cell growth and differentiation.

Gros, Philippe, Professor
philippe.gros [at] mcgill.ca
Our laboratory uses a genetic approach in mouse to discover genes, proteins and pathways that play an important role in complex human diseases. Our long-term objectives are to translate knowledge obtained in laboratory mouse models, into clinical outcomes through the creation of novel diagnostic tools or new small molecules modulators with therapeutic value in the corresponding human disease. We are currently focusing on three major human diseases known to have clear genetic component: infectious diseases, cancer, and the birth defect spina bifida. Our genetic platform is based on the use of genetically diverse mouse inbred strains, recombinant congenic strains, and experimentally induced mutagenized mouse stocks (ENU mutants).

Huang, Sidong, Associate Professor
sidong.huang [at] mcgill.ca
Our laboratory uses functional genomic tools to study cancer-relevant pathways and to guide targeted cancer therapy. We aim to identify novel genes and networks that modulate response to cancer drugs, and to uncover genetic dependencies between the major signaling pathways in cancer that can be exploited therapeutically.

Kazak, Lawrence, Assistant Professor
lawrence.kazak [at] mcgill.ca
The Kazak lab combines mouse genetics, mass spectrometry, molecular and cell biology, biochemistry and bioenergetics to study the molecular control of mammalian energy metabolism. Our efforts are concentrated on the molecules and metabolic pathways that control mitochondrial energetics in adipocytes and cancer cells. We have generated novel genetically-engineered mouse models to accurately study cellular metabolism, in vivo. In the case of adipose tissue, we systematically examine mechanisms supporting adipocyte energy expenditure, which has tremendous promise for combating obesity. In the case of cancer, we are leveraging our expertise of mitochondrial biology and cellular energetics to explore novel metabolic pathways that are critical for tumorigenesis.

Muller, William, Professor
william.muller [at] mcgill.ca
The progression of the primary mammary epithelial cell to malignant phenotype involves multiple genetic events including the activation of dominant activating oncogenes and inactivation of specific tumor suppressor genes. Our laboratory has focused on the role of a class of receptor tyrosine kinases known as the epidermal growth factor receptor (EGFR) family in the induction of breast cancer .Elevated expression of the various EGFR family members has been observed in a large proportion of sporadic breast cancers and their derived cell lines. For example, amplification and overexpression of erbB-2/neu proto-oncogene is observed in 20-30% human breast cancer and is inversely correlated with the survival of the patient. The major focus of our laboratory is to determine the relative contribution of the various EGFR family members and their coupled signaling pathways in ErbB-2 induced mammary tumor progression. Given the fact that germline inactivation of these signaling pathways results in either embryonic or perinatal lethality, we have used use Cre/Lox recombination system to specifically inactivate each of these signaling molecules members in the mammary epithelium of mice expressing activated erbB-2. The results of these biochemical and genetic analyses will provide important insight in molecular basis for erbB-2 induced tumorigenesis and metastasis.

Nepveu, Alain, Professor
alain.nepveu [at] mcgill.ca
Transcriptional regulation in normal and cancer cells (expression profiling, genome-wide location arrays (ChIP-chip)). Post-translational regulation by cyclin-dependent kinases during cell cycle progression, and by checkpoint kinases following DNA damage. The spindle assembly checkpoint and the control of genomic instability. Spontaneous and induced point mutations. Transgenic mouse models of breast cancer: a model for the basal-like group of breast cancers and transcriptional regulation of the Wnt/beta-catenin pathway.

Park, Morag, Professor
morag.park [at] mcgill.ca
Deregulation of receptor tyrosine kinases is a common event in the development and progression of human cancers. We propose to examine the signals regulated by receptor tyrosine kinases that promote cell transformation, tumor formation and metastatic spread of tumors with a focus on breast cancer.

Pause, Arnim, Professor
arnim.pause [at] mcgill.ca
(1) Molecular characterization of the von Hippel-Lindau (VHL) tumor suppressor gene pathway, identification of new targets of the VHL ubiquitin ligase, mechanism of tumorigenesis in VHL tumors (renal cell carcinoma) and C.elegans, development of animal models of kidney cancer (mice and C.elegans). (2) Functional characterization of the Birt-Hogge-Dube (BHD) tumor suppressor protein in kidney cancer and in cellular and whole animal metabolism (mice and C.elegans). (3) Functional characterization of a tyrosine phosphatase involved in tumor suppression, studies in cellular and animal models.

Pelletier, Jerry M., Professor
jjerry.pelletier [at] mcgill.ca
Chemical Biology Approach to Study Regulation of Eukaryotic Translation — Chemical Biology Approach to Interdict miÏ㽶ÊÓƵ—mediated Repression — Targeting Translation Initiation in Cancer as a Therapeutic Avenue — Use of Mechanism Based Mouse Models to Study Response to Chemotherapy — Biology of Ï㽶ÊÓƵ Helicases.

Sonenberg, Nahum, Professor
nahum.sonenberg [at] mcgill.ca
Control of translation in eukaryotes; translational control cancer, obesity and neurodegenerative diseases; translational control of learning and memory; ‘knock-out’ mice in translation initiation factors.

Teodoro, Jose, Professor
jose.teodoro [at] mcgill.ca
Projects in the lab identify and characterize pathways that target tumour growth. The first project studies how the p53 tumour suppressor pathway is able to inhibit angiogenesis. Angiogenesis is the process of blood vessel formation that is required for tumour formation. Molecular and proteomic approaches are used to identify p53-induced angiogenesis inhibitors and define how such factors work. The second project in the lab studies cytotoxic viral proteins and how such factors destroy cancer cells. A number of such viral proteins interact with and inhibit a protein complex called the Anaphase Promoting Complex/Cyclosome (APC/C). Work in the lab seeks to determine why the APC/C is a general target of many viruses and how inhibition of this complex can lead to specific destruction of cancer cells.

Tremblay, Michel L., Professor
michel.tremblay [at] mcgill.ca
In vitroÌý²¹²Ô»åÌýin vivo characterization of protein tyrosine phosphatases in the mouse. Generation of PTPase mouse models using homologous recombination in embryonic stem cells and transgenic technology.

Watson, Ian, Associate Professor
ian.watson2 [at] mcgill.ca
My lab is interested in understanding the biological function and therapeutic relevance of novel significantly mutated genes discovered in our melanoma genome- and exome-sequencing studies by employing computational approaches, in vivo models and biochemical techniques studying patient samples, cell lines and genetically engineered mice.