Recruitment at the
Rosalind & Morris
Goodman Cancer Institute
The Rosalind and Morris Goodman Cancer Instittue (GCI) is dedicated to shaping the future of cancer research by recruiting exceptional graduate students from across Canada and beyond. Our Annual Recruitment Event is a key part of this mission, connecting aspiring researchers with the institute's vibrant academic community.
Through the Annual Graduate Recruitment Event, we offer top applicants a unique chance to visit the institute, meet current graduate students and faculty, and learn about cutting-edge research opporunities.
Applications for 2026
are now open
Are you interested in pursuing graduate studies in cancer research with us?
Apply to attend our annual Graduate Student Recruitment Event for a unique opportunity to explore the GCI and learn about our cutting-edge research and scientific platforms.
Top applicants will be invited to attend the event that aims to be both informative and convivial. We will introduce the GCI’s extensive training program and provide an opportunity to meet with existing graduate students and cancer scientists.
Selected invitees will then be offered a scholarship for Fall 2026 or Winter 2027 admission. Please note that all travel expenses will be covered for invited students unless specified otherwise.
The deadline to apply is December 1st, 2025.
Join us for a live information session to ask questions and learn more about the program. More details regarding day and time of the information session will be added soon. Check back to sign up!
Interested candidates must complete an online registration form HERE.
Within the online registration form, applicants will be asked to upload the following information in 1 single pdf:
- An up-to-date CV with valid contact information
- A letter of intent (maximum 2 pages) and
- A copy of your most recent transcripts (these do not need to be official for the purpose of this event)
Registration is open
Deadline to submit an application
December 1st, 2024
In-person Events
January 23rd - 24th 2025
- Demonstrated interest in biomedical research
- Enrolled in a B.Sc. or M.Sc. program
- GPA of 3.6 out of 4.3 for M.Sc. & Ph.D. candidates; international students will be evaluated on individual basis.
The GCI is committed to equity and diversity in the recruitment of its trainees. We welcome and encourage applications from racialized persons/visible minorities, women, Indigenous persons, persons with disabilities, ethnic minorities, and persons of minority sexual orientations and gender identities as well as others who may contribute to diversification.
The following investigators are recruiting new students:
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).
What we are
currently
working on
Our laboratory uses genetic analysis in experimental mouse models to identify genes and pathways that are required for the function of lymphoid and myeloid immune cells and for protection against infections such as malaria and tuberculosis. Using phenotype-driven genetic screen in mutagenized mice, we identify genes which inactivation protects mice against acute neuroinflammation, a pathological feature of cerebral malaria caused by Plasmodium berghei. The discovered genes include Ccdc88b, a protein essential for the migratory function of myeloid cells, Themis and Zbtb7b, two proteins that are required for development and pro-inflammatory function of T cells, and Usp15, a de-ubiquitinase that activates type I interferon response in the brain and in immune cells via RIG-I signaling, and IRF1 and IRF8, 2 transcription factors that are necessary for the development and pro-inflammatory function of dendritic cells, and NK cells. Using a similar approach, we have shown that deficiency in the erythrocyte enzyme Bpgm, protects mice against both blood stage (P. chabaudi) and cerebral (P. berghei) malaria through modification of the intracellular milieu of the erythrocyte, the replicative niche of Plasmodium parasites in the blood. Finally, we have used genomic and epigenetic approaches to identify the pathways regulated by IRF1 and IRF8 (IRF1/IRF8 regulome) in myeloid cells. In collaboration with other laboratories (JL Casanova), we have determined that several of the genes in the IRF1/IRF8 regulome are mutated in patients suffering from primary immunodeficiencies. In addition, several of these genes are associated with susceptibility to chronic inflammatory conditions in humans, such as Inflammatory Bowel Disease, Multiple Sclerosis, Rheumatoid Arthritis and Lupus. Several of these genes are now being investigated in the lab as potential targets for drug development and therapeutic intervention in these common human diseases.
- Cancer Notre laboratoire a travaillé depuis de nombreuses années sur le phénomène de la résistance aux médicaments chez les cellules tumorales, causée par les membres de la famille des P-glycoprotéines (MDR) et des protéines associées à la résistance aux médicaments (MRP). Plus récemment, nous avons étudié la résistance à deux groupes de médicaments utilisés dans le traitement du myélome multiple, à savoir l'analogie nucléosidique arabinocytosine (cytarabine) et l'inhibiteur de protéasome Bortezomib (Valcade). Nous étudions actuellement le mécanisme par lequel le Bortezomib induit la mort cellulaire via la formation de granules de stress et l'activation de la mort cellulaire programmée, ainsi que la façon dont les lignées cellulaires résistantes au Bortezomib développées dans notre laboratoire peuvent survivre à ces effets du médicament. Plus récemment, nous avons porté notre attention sur les déterminants génétiques impliqués dans la prédisposition au cancer.
Dans ce nouveau projet, nous avons utilisé la carcinogenèse chimique avec l'azoxyméthane (AOM) pour induire des tumeurs colorectales chez les souris. Nous avons criblé plusieurs souches consanguines de souris pour les différences de susceptibilité au cancer colorectal induit par l'AOM, mesurées par le type, le nombre et la taille des lésions détectées dans le côlon. Dans ce test, les souris A/J sont susceptibles tandis que les souris C57BL/6J sont très résistantes. En utilisant un ensemble unique de lignées de souris recombinantes congéniques AcB/BcA, nous avons déterminé que la base génétique de cette différence de susceptibilité est causée par un seul locus majeur, que nous avons nommé Ccs3. Le locus se trouve sur le chromosome 3, et l'intervalle génétique et physique minimal pour cette région contient environ ~50 gènes. Ces gènes font actuellement l'objet d'investigations pour leur motif d'expression spécifique aux tissus et aux cellules, ainsi que pour la présence de mutations dans les tissus normaux ou dans l'ADN des tumeurs émergentes chez les animaux susceptibles. Nous interrogeons également des échantillons de tumeurs primaires humaines pour détecter des altérations dans les homologues humains des gènes de souris présents dans l'intervalle Ccs3. Enfin, nous avons développé un modèle de cancer colorectal induit par l'inflammation, induit par le sulfate de dextran et l'AOM. Nous étudions la base génétique de la susceptibilité différentielle des souches consanguines de souris aux tumeurs colorectales induites par ce traitement. Cancer Our laboratory has worked for many years on the phenomenon of multidrug resistance in tumor cells, as caused by members of the P-glcoprotein (MDR) and multidrug resistance associated protein (MRP) family. More recently, we have studied resistance to two groups of drugs that are used in the treatment of multiple myeloma, namely the nuceloside analog arabinocytosine (cytarabine), and the proteasome inhibitor Bortezomib (Valcade). We are currently studying the mechanism by which Bortezomib induces cell death via formation of stress granules, and activation of programmed cell death, and how Bortezomib resistant cell lines developed in our laboratory can survive these effects of the drug.
More recently, we have turned our attention to genetic determinants involved in pre-disposition to cancer. In this new project, we have used chemical carcinogenesis with azoxymethane (AOM) to induce colorectal tumors in mice. We have screened several inbred strains of mice for differences in susceptibility to colorectal cancer induced by AOM, measured by the type, number and size of lesions detected in the colon. In this assay, A/J mice are susceptible while C57BL/6J mice are highly resistant. Using a unique set of AcB/BcA recombinant congenic mouse lines, we have determined that the genetic basis for this difference in susceptibility is caused by a single major locus, that we have named Ccs3. The locus maps on chromosome 3, and the minimal genetic and physical interval for this region contains an estimated ~50 genes. These genes are currently being investigated for their pattern of tissue and cell-specific expression, and for the presence of mutations in either normal tissues or in DNA from tumors emerging in susceptible animals. We are also interrogating human primary tumor samples for alterations in human homologs of the mouse genes present in the Ccs3 interval. Finally, we have developed a model of inflammation-induced colorectal cancer, induced by dextran sulfate and AOM. We are investigating the genetic basis of differential susceptibility of inbred mouse strains to colorectal tumors induced by this treatment.
- Maladies Infectieuses Notre recherche sur les maladies infectieuses se concentre sur les agents pathogènes qui envahissent et se reproduisent à l'intérieur des cellules hôtes, et qui utilisent cette stratégie pour échapper au système immunitaire et aux autres défenses normales de l'hôte. Nous nous concentrons particulièrement sur Mycobacterium tuberculosis, Legionella pneumophila, Candida albicans et les espèces de Plasmodium responsables du paludisme. Notre travail consiste à identifier les gènes qui régulent les réponses aux infections. Par exemple, nous avons étudié Nramp1, qui limite la réplication des microbes intracellulaires tels que les mycobactéries chez les souris. Les mutations de Nramp1 affectent non seulement la susceptibilité aux mycobactéries, mais aussi à d'autres agents pathogènes tels que Salmonella et Leishmania chez les souris, et elles sont liées à la susceptibilité chez l'homme à des maladies telles que la tuberculose et la lèpre.
En ce qui concerne Legionella, nous avons découvert que des mutations dans une protéine appelée Naip5/Birc1e affectent la façon dont les macrophages détectent ce pathogène. De plus, nous avons identifié d'autres acteurs clés comme IRF1 et IRF8 qui protègent contre l'infection à Legionella. Notre recherche utilise des méthodes à l'échelle du génome pour comprendre comment ces protéines influencent les réponses à Legionella.
Dans notre exploration de la tuberculose, nous avons identifié des facteurs génétiques influençant la susceptibilité entre différentes souches de souris. Les mutations dans un gène appelé Icsbp/IRF8 compromettent gravement l'immunité non seulement contre la tuberculose, mais aussi contre d'autres infections comme la fièvre typhoïde et le paludisme chez les souris.
Dans nos études sur le paludisme, nous avons cartographié les gènes affectant la réplication du Plasmodium dans les globules rouges. Nous avons également identifié certaines mutations géniques qui affectent la susceptibilité au paludisme, comme celles du gène de la pyruvate kinase ou de Vnn3. De plus, nous avons découvert des pistes prometteuses concernant l'utilisation de la cystéamine comme traitement potentiel.
Notre recherche sur Candida albicans a révélé le rôle de C5a dans la susceptibilité à l'infection et sa fonction dans la mobilisation des cellules immunitaires pour combattre l'infection. Nous étudions actuellement les déterminants génétiques responsables de la susceptibilité à l'infection à Candida dans diverses souches de souris. Infectious Diseases Our research on infectious diseases focuses on pathogens that invade an replicate inside host cells, and that use this strategy to evade the immune system and other normal host defenses. We're particularly focused on Mycobacterium tuberculosis, Legionella pneumophila, Candida albicans, and the malaria-causing Plasmodium species.
Our work involves pinpointing genes that regulate responses to infections. For instance, we've looked at Nramp1, which curtails the replication of intracellular microbes like Mycobacteria in mice. Mutations in Nramp1 not only affect susceptibility to Mycobacteria but also to other pathogens like Salmonella and Leishmania in mice, and they're linked to susceptibility in humans for diseases like tuberculosis and leprosy.
When it comes to Legionella, we've discovered that mutations in a protein called Naip5/Birc1e impact how macrophages sense this pathogen. Plus, we've found other key players like IRF1 and IRF8 that defend against Legionella infection. Our research employs genome-wide methods to understand how these proteins influence responses to Legionella.
In our exploration of tuberculosis, we've identified genetic factors influencing susceptibility between different mouse strains. Mutations in a gene called Icsbp/IRF8 severely compromise immunity not just against TB but also against other infections like typhoid and malaria in mice.
In our malaria studies, we've mapped genes affecting the replication of Plasmodium in red blood cells. We've also identified certain gene mutations that affect susceptibility to malaria, like those in the pyruvate kinase or Vnn3 gene. Additionally, we've found promising leads regarding the use of cysteamine as a potential treatment.
Our research into Candida albicans has revealed the role of C5a in infection susceptibility and its function in rallying immune cells to combat the infection. We're currently investigating the genetic determinants responsible for susceptibility to Candida infection across various mouse strains.
- Malformations du tube neural Les malformations du tube neural (NTD), telles que la spina bifida, sont très courantes chez les humains et ne sont dépassées que par les défauts cardiaques en termes d'erreurs innées. Notre laboratoire étudie deux modèles de NTD chez la souris, à savoir la souris splotch et, plus récemment, la souris looptail (Lp). Les souris homozygotes pour la mutation Lp souffrent d'une forme très sévère de malformation du tube neural appelée craniorachischisis. Cette condition est mortelle in utero. En utilisant une approche de clonage positionnel, nous avons découvert que le défaut Lp est causé par des mutations dans la protéine membranaire Vangl2. Cette protéine est un homologue mammifère du gène mouche Van Ghog/strabisme, un gène connu pour réguler le développement de certaines structures chez la mouche, faisant partie d'une voie appelée voie PCP, pour polarité cellulaire planaire. Les mouches avec des mutations dans cette voie présentent des défauts dans l'organisation de plusieurs appendices et structures (ailes, yeux), causés par une incapacité des cellules épithéliales à s'organiser correctement dans le champ de polarité planaire. Cette voie est hautement conservée des mouches aux humains, et chez les mammifères, cette voie est également impliquée dans certains types de mouvements morphogénétiques pendant l'embryogenèse connus sous le nom d'extension convergente; encore une fois, cette voie implique le réarrangement dynamique et la migration des cellules épithéliales pour former des structures primordiales, y compris le tube neural, le cœur, le rein et d'autres.
Chez les mammifères, il existe deux gènes Vangl, Vangl1 et Vangl2, qui codent pour des protéines membranaires hautement similaires. Nous avons récemment détecté des mutations dans le gène humain VANGL1 dans des cas familiaux et sporadiques de spina bifida. Nous avons également récemment déterminé que VANGL1 et VANGL2 interagissent génétiquement dans la régulation de la neurogenèse et dans l'apparition de malformations du tube neural chez les souris. Ces découvertes passionnantes suggèrent que la famille VANGL peut jouer un rôle critique dans l'étiologie de cette malformation. Nous enquêtons actuellement sur un grand nombre de cas cliniques pour déterminer la fréquence de telles mutations et explorons les bases moléculaires de la perte de fonction chez ces patients. Cela est étudié chez des modèles murins, mais également chez des poissons-zèbres, où le gène humain peut corriger la malformation du tube neural détectée chez les embryons de poisson présentant un défaut dans l'homologue correspondant du poisson. Sur le plan biochimique, nous étudions le complexe multiprotéique formé par les protéines Vangl à la membrane et qui est responsable de fournir des informations de polarité aux cellules, ainsi que la façon dont les altérations de ce complexe peuvent causer la spina bifida chez les humains. Neural tube defects Neural tube defects (NTD) such as spina bifida are very common in humans, and rank second only to cardiac defects in inborn errors. Our laboratory has been studying two mouse models of NTD, namely the splotch mouse, and more recently the looptail (Lp) mouse. Mice homozygote for the Lp mutation suffer from a very severe form of neural tube defect called craniorachischisis. This condition is lethal in utero. Using a positional cloning approach, we found that the Lp defect is caused by mutations in the membrane protein Vangl2. This protein is a mammalian homolog of the fly Van Ghog/strabismus, a gene known to be involved in regulating the development of certain structures in the fly, being part of a pathway known as the PCP pathway, standing for planar cell polarity. Flies with mutations in this pathway have defect in the organization of several appendages and structures (wings, eyes), which is caused by an inability of epithelial cells to properly organize in the planar polarity field. This pathway is highly conserved from flies to humans, and in mammals this pathway is also involved in certain types of morphogenic movements during embryogenesis known as convergent extension; Again, this pathway involves the dynamic rearrangement and migration of epithelial cells to form primordial structures, including the neural tube, the heart, the kidney and others.
In mammals, there are two Vangl genes, Vangl1 and Vangl2 that encode for highly similar membrane proteins. We recently detected mutations in the human VANGL1 gene in familial and sporadic cases of spina bifida. We have also recently determined that VANGL1 and VANGL2 genetically interact in the regulation of neurogenesis and in the appearance of neural tube defects in mice. These exciting findings suggest that the VANGL family may play a critical role in the etiology of this malformation. We are currently investigating large number of clinical cases to determine the frequency of such mutations, and are exploring the molecular basis for the loss of function in these patients. This is being investigated in mouse models, but also in zebra fish, where the human gene can correct the neural tube defect detected in fish embryos showing a defect in the corresponding fish homolog. Biochemically, we are investigating the multiprotein complex formed by Vangl proteins at the membrane and that is responsible for providing polarity information to the cells, and how alterations in this complex may cause spina bifida in humans.
- Professor
Rosalind and Morris Goodman Cancer InstituteDepartment of Biochemistry
Faculty of Medicine and Health Sciences
McGill University - Vice-Dean Life Sciences,
Faculty of Medicine
McGill University
2015- present
- Co-Director, McGill Center for Complex Traits
McGill University
2018-Present
- Deputy Vice-Principal, Research and Innovation
McGill University
2022-Present
- Co-Founder and Executive Director, McGill Institute of Genomic Medicine
- Distinguished James McGill Professor
Royal Society of Canada Fellow
- McLaughlin Medal for Scientific Excellence, Royal Society of Canada, 2014
- Queen Elizabeth II Diamond Jubilee Medal, Association of Universities and Colleges of Canada, 2013
- Killam Prize in Health Sciences, Canada Council for the Arts, 2009
- Prix Wilder-Penfield, Government of Quebec, 2008
Our team
Major discoveries
- 2023 Inherited IRF1 Deficiency Underlies Mycobacterial Disease by Impairing the Production of and Response to Interferon Gamma.
- 2021 Inherited human PD-1 deficiency underlies tuberculosis and autoimmunity in a child
- 2020 Ccdc88b is required for mobility and inflammatory function of dendritic cells.
- 2020 Bisphosphoglycerate Mutase Deficiency Protects Against Malaria.
- 2020 Zbtb7b (ThPOK) is required for pathogenesis of cerebral malaria, and protection against pulmonary tuberculosis.
- 2020 Human T-bet governs both innate and adaptive anti-mycobacterial IFN-γ immunity
- 2019 Inactivation of interferon regulatory factor 1 (IRF1) causes increased susceptibility to colitis associated colorectal cancer.
- 2018 Impaired development of IL-12/IL-23-producing mDC1 and mycobacteria-specific IFN-γ-producing Th cells in patients with inherited SPPL2a deficiency.
- 2018 Rocaglates as novel dual targeting agents for severe malaria.
- 2017 New Insights into Genetics of Infectious and Inflammatory Disease: Overlap Between Discoveries from GWAS and Exome Sequencing.
- 2017 CCDC88B is required for pathogenesis of inflammatory bowel disease.
- 2017 USP15 regulates type I interferon response in vivo and is required for pathogenesis of microbial and autoimmune neuroinflammation.
- 2016 The macrophage IRF1/IRF8 regulome is required for protection against infections and is associated with chronic inflammation.
- 2015 Human intracellular ISG15 prevents IFN-a/b over-amplification and auto-inflammation.
- 2015 Themis is required for pathogenesis of cerebral malaria and for protection against pulmonary tuberculosis.
- 2014 Human Dendritic Cell Immunodeficiency Mutation IRF8K108E Leads To Loss Of Protein Function And Depletion Of Target Gene Expression.
- 2014 Ccdc88b Is A Novel Regulator Of Development And Effector Functions Of T Cells And Is Required For Pathological Inflammation.
- 2013 Irf8-regulated genomic responses drive pathological inflammation during cerebral malaria.
- 2013 Inherited human OX40 deficiency underlying classic Kaposi sarcoma of childhood.
- 2012 Mycobacterial disease and impaired IFN-γ immunity in humans with inherited ISG15 deficiency.
- 2012 An N-Ethyl-N-Nitrosourea (ENU)-Induced Dominant Negative Mutation in the Jak3 Kinase Protects Against Cerebral Malaria.
- 2011 IRF8 mutations and human dendritic cell immunodeficiency.
- 2011 Interferon Regulatory Factor 8 regulates pathways for antigen processing and antigen presentation in myeloid cells.
- 2007 Icsbp1/Irf-8 Is Required For Innate And Adaptive Immune Responses Against Intracellular Pathogens.
- 2005 A mutation in the Icsbp/IRF-8 gene causes susceptibility to infections and a CML-like syndrome in BXH-2 mice.
- 1997 Genetic control of blood parasitemia in murine malaria maps to chromosome 8.
- 1995 The Ity/Lsh/Bcg locus: Natural resistance to infection with intracellular parasites is abrogated by disruption of the Nramp 1 gene.
- 1993 Natural resistance to infection with intracellular parasites:Isolation of a candidate for Bcg.
Research Partners
Get in touch
3655 Promenade Sir William Osler
Montreal, Quebec H3G 1Y6
Office: 366
Lab: 370
T. 514-398-7291
T. 514-398-2542
F. 514-398-2603
philippe.gros@mcgill.ca
Contact us for any questions about
our recruitment process
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