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.

We are accepting applications for our Fall 2026 Recruitment Event.

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 2027 or Winter 2028 admission. Please note that all travel expenses will be covered for invited students unless specified otherwise.

To find out more or ask any questions you might have, join us for a live information session on Thursday, October 1st at 5pm EST.

Click her to register for the Information Session

The deadline to apply is October 15th, 2026.

The Event will take place November 19th and 20th, 2026, on location at the GCI.

Apply

Applications for 2023
are now completed

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 2024 or Winter 2025 admission. Please note that all travel expenses will be covered for invited students unless specified otherwise.

Stay tuned for more information about our upcoming Graduate Recruitment Event

Application process

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)

Summary of the Recruitment process & event

Registration is open

Deadline to submit an application
October 15, 2026

In-person Events
November 19-20, 2026

Eligibility Requirements

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. Potential applicants should not contact these investigators directly. Instead, applicants should indicate the names of the investigators they are interested in on their application.

Our laboratory uses functional genomic tools to study cancer-relevant pathways and to guide cancer therapy. We aim to identify novel genes and networks that modulate response to cancer drugs and to uncover genetic dependencies in cancer that can be exploited therapeutically.

I) Hard-to-Treat Cancer Driver Mutations
Precision oncology has transformed cancer care by targeting oncogenic mutations. However, many common cancer driver mutations, particularly loss-of-function alterations in tumor suppressor genes, remain difficult to drug directly. We aim to identify disease mechanisms and vulnerabilities of these hard-to-treat alterations to develop effective therapeutic strategies.

II) mRNA Translation and Therapeutics
Translational control is a fundamental cellular process often dysregulated in cancer. Since this process integrates multiple upstream oncogenic pathways, targeting translation can overcome tumor heterogeneity for cancer treatment. We aim to uncover the mechanisms governing translation initiation, develop translation-targeted therapies, and advance RNA therapeutics.

What we are
currently
working on

Our laboratory uses functional genomic tools to study cancer-relevant pathways and to guide cancer therapy. We aim to identify novel genes and networks that modulate response to cancer drugs and to uncover genetic dependencies in cancer that can be exploited therapeutically.

Cibler les dépendances génétiques des mutations conductrices du cancer Les médicaments anticancéreux dirigés par génotype ciblent souvent les mutations oncogènes de gain de fonction dans les cellules cancéreuses, ayant ainsi moins d'effets secondaires sur les tissus normaux. Cependant, certaines mutations conductrices du cancer, telles que les altérations de perte de fonction dans les gènes suppresseurs de tumeurs, ne sont pas directement exploitables. Dans ce contexte, la "léthalité synthétique" est souvent utilisée pour identifier des cibles médicamenteuses alternatives dont l'inhibition est sélectivement létale pour les cellules cancéreuses hébergeant ces mutations difficiles à traiter. L'inactivation des gènes de remodelage de la chromatine SWI/SNF est connue pour provoquer des cancers (PMID: 21654818 ; 26601204). Les mutations délétères dans SMARCA4, un composant clé de SWI/SNF, sont à l'origine du cancer rare mais souvent mortel chez les jeunes femmes - le carcinome ovarien à petites cellules et hypercalcémie (SCCOHT) (PMID: 24658001 ; 24658002 ; 24658004). De même, les tumeurs tératoïdes/atypiques rhabdoïdes (AT/RT) rares mais hautement agressives affectant le système nerveux central des enfants sont attribuables à des mutations inactivatrices dans un autre membre de SWI/SNF, SMARCB1 (PMID: 9671307 ; 9892189). De plus, SMARCA4 est également fréquemment inactivé par des mutations et d'autres mécanismes dans des cancers courants tels que le CBNPC (PMID: 12566296 ; 21280140 ; 25079552). Cependant, les mécanismes sous-jacents à la perte de SWI/SNF dans la tumorigenèse sont actuellement peu clairs. Ainsi, les cancers déficients en SWI/SNF manquent toujours d'options de traitement rationalisées et ciblées. Nous avons précédemment lié plusieurs facteurs de la chromatine altérés dans les cancers à des voies oncogènes et identifié des stratégies de traitement potentielles (voir publications sélectionnées). Récemment, nous avons découvert une vulnérabilité commune et ciblable partagée par le SCCOHT déficient en SMARCA4 et le CBNPC : la perte de SMARCA4 dans ces cancers provoque une déficience en cycline D1 conduisant à une susceptibilité à l'inhibition de CDK4/6 (PMID: 30718506, 30718512). Ces résultats suggèrent que les inhibiteurs de CDK4/6 approuvés par la FDA pourraient être efficaces pour traiter ces cancers agressifs. Cela fait actuellement l'objet d'essais dans le cadre de l'étude canadienne de profilage et d'utilisation d'agents ciblés (CAPTUR) (NCT03297606) sur la base de nos découvertes. Actuellement, nous utilisons des bibliothèques de gènes familiaux druggables shRNA/CRISPR et des collections de composés pour identifier d'autres cibles synthétiquement létales de SWI/SNF dans le SCCOHT, l'AT/RT et le CBNPC. De plus, nous visons à révéler les voies conductrices de la perte de SWI/SNF en utilisant des outils complémentaires de génétique fonctionnelle et de biochimie. Notre objectif est de découvrir et de cibler les vulnérabilités de ces cancers difficiles à traiter, ce qui entraînerait un bénéfice clinique pour les patients. Targeting genetic dependencies of cancer driver mutations Genotype-directed anticancer drugs often target gain-of-function oncogenic mutations in cancer cells and thus have fewer side effects in normal tissue. However, some cancer driver mutations such as loss-of-function alterations in tumor suppressors are not directly actionable. In this context, “synthetic lethality” is often employed to identify alternative drug targets whose inhibition is selectively lethal to the cancer cells harboring these hard-to-treat mutations. Inactivation of SWI/SNF chromatin remodeling genes is known to cause cancers (PMID: 21654818; 26601204). Deleterious mutations in SMARCA4, a key SWI/SNF component, underlie the rare but often lethal cancer of young women – small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) (PMID: 24658001; 24658002; 24658004). Similarly, rare but highly aggressive atypical teratoid/rhabdoid tumors (AT/RTs) affecting the central nervous system in children are attributable to inactivating mutations in another SWI/SNF member, SMARCB1 (PMID: 9671307; 9892189). In addition, SMARCA4 is also frequently inactivated by mutations and other mechanisms in common cancers such as NSCLC (PMID: 12566296; 21280140; 25079552). However, the underlying mechanisms of SWI/SNF loss in driving tumorigenesis are currently unclear. Thus, SWI/SNF-deficient cancers still lack rationalized and targeted treatment options. We have previously linked several chromatin factors altered in cancers to oncogenic pathways and identified potential treatment strategies (see selected publications). Recently, we uncovered a common druggable vulnerability shared by SMARCA4-deficient SCCOHT and NSCLC: SMARCA4-loss in these cancers causes cyclin D1 deficiency leading to susceptibility to CDK4/6 inhibition (PMID: 30718506, 30718512). These results suggest that FDA-approved CDK4/6 inhibitors could be effective to treat these aggressive cancers. This is currently being tested as a part of the Canadian Profiling and Targeted Agent Utilization Trial (CAPTUR) (NCT03297606) based on our findings. Currently, we are using druggable gene-family shRNA/CRISPR libraries and compound collections to identify other SWI/SNF synthetic lethal targets in SCCOHT, AT/RT, and NSCLC. Furthermore, we aim to reveal the driver pathways of SWI/SNF loss using complementary functional genetics and biochemical tools. Our goal is to uncover and target vulnerabilities of these hard-to-treat cancers, resulting in clinical benefit for patients.
Surmonter la résistance médicamenteuse aux thérapies ciblées contre le cancer La résistance médicamenteuse demeure un défi clinique majeur pour la thérapie anticancéreuse. Tous les patients ne répondent pas aux mêmes traitements, et beaucoup de patients qui répondent initialement aux thérapies développent une résistance aux médicaments. Ceci est vrai non seulement pour les chimiothérapies conventionnelles et les médicaments dirigés par génotype ciblant les composants cellulaires modifiés dans les cancers, mais également pour les immunothérapies qui exploitent le système immunitaire pour cibler les cellules tumorales. Ainsi, une meilleure compréhension des mécanismes de résistance est essentielle pour permettre le développement rationnel d'options de traitement visant à surmonter ce défi clinique. Des criblages génétiques fonctionnels impartiaux se sont révélés puissants pour découvrir de nouveaux gènes et interactions de réseaux qui modulent la réponse aux thérapies anticancéreuses (PMID: 24657533). En utilisant cette approche systématique, nous avons précédemment découvert de nouveaux mécanismes de résistance aux inhibiteurs ciblant les récepteurs des kinases tyrosine (RTKs) et la voie de la protéine kinase activée par les mitogènes (MAPK) dans les cancers du poumon non à petites cellules (NSCLC), le mélanome et le cancer colorectal (voir Publications). La compréhension mécanistique de ces études nous a également permis d'identifier des stratégies de traitement potentielles pour surmonter la résistance médicamenteuse, dont l'une a été validée dans des essais cliniques (NCT01719380, NCT02164916, NCT02928224) et récemment approuvée par la FDA. Actuellement, nous étudions les mécanismes de résistance aux médicaments tels que ceux ciblant les kinases cycline-dépendantes (CDK) 4/6, approuvés par la FDA pour le traitement du cancer du sein. Nous étudions également les mécanismes sous-jacents de la résistance au traitement dans les cancers déficients en SWI/SNF. Notre objectif est d'identifier des stratégies de traitement efficaces pour surmonter la résistance médicamenteuse et d'améliorer l'utilité clinique de ces thérapies anticancéreuses. Overcoming drug resistance to targeted cancer therapeutics Drug resistance remains a major clinical challenge for cancer therapy. Not all patients respond to the same treatments and many patients who initially respond to the therapies develop drug resistance. This is true not only for the conventional chemotherapies and genotype-directed drugs targeting cellular components altered in cancers but also for the immunotherapies which harness the immune system to target tumor cells. Thus, a better understanding of resistance mechanisms is essential to enable the rational development of treatment options to overcome this clinical challenge. Unbiased functional genetic screens have been proven to be powerful in uncovering novel genes and network interactions that modulate response to cancer therapeutics (PMID: 24657533). Using this systematic approach, we have previously discovered novel resistance mechanisms to inhibitors targeting receptor tyrosine kinases (RTKs) and the mitogen-activated protein kinase (MAPK) pathway in non-small cell lung cancer (NSCLC), melanoma and colorectal cancer (see Publications). The mechanistic insight of these studies also allowed us to identify potential treatment strategies to overcome drug resistance, one of which has been validated in clinical trials (NCT01719380, NCT02164916, NCT02928224) and recently approved by the FDA. Currently, we are investigating drug resistance mechanisms to inhibitors such as those targeting cyclin-dependent kinases (CDK) 4/6, which have been approved by FDA to treat breast cancer. We are also studying the mechanisms underlying the treatment resistance in SWI/SNF-deficient cancers. Our goal is to identify effective treatment strategies to overcome drug resistance and enhance the clinical utilities of these cancer therapeutics.

Affiliations
Awards, honours, and fellowships

Professor
Rosalind & Morris Goodman Cancer Institute
Department of Biochemistry
Canada Research Chair in Functional Genomics
Scientific director of the McGill Platform for Cellular Perturbation.

Our team

Giulio Aceto Étudiant.e au doctorat PhD Student
Azadeh Arabzadeh Associé.e de recherche Research Associate / MPCP Platform Manager
Zheng Fu Étudiant.e au doctorat PhD Student
Andy Garnier Étudiant.e à la maîtrise MSc Student
Hannah Hosein Étudiant.e à la maîtrise MSc Student
Jialin (Paco) Jiang Assistant.e de recherche Research Assistant (previously MSc Student)
Minyan Liao Maîtrise en sciences MSc Student
Kexin (Judy) Liu Étudiant.e de premier cycle Undergraduate Student
Racim Sansal Étudiant.e de premier cycle (Étudiant.e à la maîtrise en Septembre 2023) BSc (MSc Student as of Sept 2023)
Jutta Steinberger Associé.e de recherche Research Associate/ MPCP Platform Manager
Xianbing Zhu Étudiant.e au doctorat PhD Student