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.
Dostie, Josee, Professor
josee.dostie [at] mcgill.ca
Our goal is to understand the role of spatial chromatin organization in the regulation of gene expression in mammalian cells. We are particularly interested in defining how epigenetic modifications affect chromatin structure and genome function in “normal” and cancer cells. We are characterizing the molecular mechanisms involved in regulating the three-dimensional chromatin architecture and expression of Hox genes in leukemia cell models.
Duchaine, Thomas, Associate Professor
thomas.duchaine [at] mcgill.ca
RNAi is the process through which small non-coding RNAs 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 RNAi, and decipher how they orchestrate gene silencing. Currently, my group focuses on two distinct ‘branches’ of the RNAi processes: endoRNAi and microRNA-mediated silencing. First, we examine a phenomenon termed endogenous RNAi (endoRNA) which is naturally initiated on certain messenger RNAs, and results in the shutdown of the gene's expression. We are particularly interested in the functional interactions between endoRNAi and chromatin, the physiological scaffold of the genome. Second, we are interested in how microRNA-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 mRNA 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 mRNA 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, Assistant 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.
McInnes, Roderick, Professor
roderick.mcinnes [at] mcgill.ca
Our lab is interested in two major questions in biology and medicine. First, in inherited neurodegenerations, we wish to understand what is happening in the mutant neurons, in the years to decades between their birth and their death years to decades later. After decades of normal function, why do the neurons suddenly die? To address this question, we are identifying molecular mechanisms that contribute to, or protect against the death of mutant photoreceptors (PRs) in inherited photoreceptor degenerations (IPDs) using mouse models of these diseases. Understanding of these mechanisms is likely to suggest therapeutic opportunities that will slow or arrest PR death. Second, we wish to understand the roles of “accessory” proteins in the regulation of ion channels in neurons, particularly at synapses. Our focus is on two such proteins that we discovered, Neto1 and Neto2. The Neto proteins are multifunctional, as indicated by their loss-of-function phenotypes, which include defects in axon guidance, seizures in some genetic backgrounds, defects in memory and learning, and abnormal regulation of neuronal excitability. To date, we have identified at least 5 ion channels or other neuronal proteins whose activity is or appears to be regulated by a Neto. Elucidation of the role of the Netos in the brain is increasing our understanding of a surprisingly broad range of fundamental neuronal processes.
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.
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
Pelletier, Jerry M., Professor
jerry.pelletier [at] mcgill.ca
Chemical Biology Approach to Study Regulation of Eukaryotic Translation — Chemical Biology Approach to Interdict miRNA—mediated Repression — Targeting Translation Initiation in Cancer as a Therapeutic Avenue — Use of Mechanism Based Mouse Models to Study Response to Chemotherapy — Biology of RNA 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, Associate 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.
Thomas, David Y
Thomas, David Y., Professor
david.thomas [at] mcgill.ca
There are two major projects in this group. Cell signaling pathways and molecular chaperone systems in the endoplasmic reticulum and their role in diseases. We use a variety of genetic, biochemical informatics and structural approaches to these problems.
Watson, Ian, Assistant 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.