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:
- Understanding the molecular mechanisms that underpin pro-inflammatory hematopoiesis and how this can be targeted to reduce systemic inflammation and cancer progression
- Unravelling the impact of estrogen signaling on hematopoiesis and how estrogen deficiency (menopause) leads to chronic inflammation
Inflammation is a hallmark of cancer: tumours hijack blood cell development (haematopoiesis), skewing bone marrow output towards the myeloid lineage leading to tumour-supporting chronic systemic inflammation. Conversely, chronic inflammatory conditions can also predispose individuals to developing tumours, leading to a bidirectional relationship between inflammation and cancer.
Myeloid cells, including monocytes, neutrophils, and their bone marrow progenitors, are highly plastic, rapidly integrating local and systemic cues such as pro-inflammatory mediators. Chronic systemic inflammation functionally reprogrammes these cells towards a tumour-supporting state and this “education” occurs on multiple levels: during their development in the bone marrow; within primary tumours; and in shaping the (pre-)metastatic niche.
Using spontaneous pre-clinical mouse models that closely mimic human breast and ovarian cancer progression, combined with patient samples, we aim to uncover the molecular and cellular mechanisms driving chronic inflammatory myeloid cell education. By understanding how these processes promote tumour- and metastasis-supporting inflammation, we aim to identify novel therapeutic strategies for breast and ovarian cancer patients.
What we are
currently
working on
It is increasingly recognised that the tumour macroenvironment – extending beyond the tumour microenvironment and incorporating systemic components such as the immune system - plays a critical role in tumour initiation, progression and metastatic spread. Inflammation is involved in every stage of cancer progression from initiation to metastatic spread. All circulating blood cells, including inflammatory cells develop from rare, self-renewing haematopoietic stem cells (HSCs) that differentiate through a series of steps. This system is a highly dynamic and adapts quickly to inflammatory signals, boosting the production of myeloid cells during inflammation or injury to meet demand. In cancer, primary tumours release inflammatory signals that affect distant tissues including the bone marrow (BM). These signals drive expansion and polarisation of myeloid cells, shifting their roles to support tumour progression, in addition, persistent tumour-driven inflammation can also lead to premature release of immature myeloid cells from the BM into the circulation. Causally, systemic accumulation and polarisation of myeloid cells has been shown to play many roles in disease progression from suppression of anti-tumour immune responses to contributing to the development of a pre-metastatic niche.
Our aims are to understand how different pro-inflammatory signals change haematopoiesis at a molecular, cellular and spatial level and how this bone marrow education changes the functionality of myeloid cells in the periphery.
- 1) Understanding and disrupting primary tumour induced skewing of haematopoiesis to reduce metastatic spread Different tumours produce different pro-inflammatory mediators which can lead to different lineage fate decisions. We are working to investigate how different inflammatory signals influence bone marrow output, with a particular focus on the transcription factors that control lineage specification within the myeloid compartment. Using genetically modified mouse models (GEMMs) of breast and ovarian cancer, we aim to understand how primary tumours influence local bone marrow cues that organise and control myelopoiesis. By deepening our understanding of how primary tumours alter control of myelopoiesis, we aim to uncover novel targets for normalising haematopoietic output in tumour-bearing hosts to reduce tumour-induced systemic inflammation and metastatic spread and potentially improve response to immune checkpoint blockade.
- 2) Oestrogen signalling in haematopoiesis Sex differences in the immune system are well documented with females exhibiting stronger immune responses and oestrogen is widely considered to have a “protective” effect in pre-menopausal women against chronic inflammatory conditions. However, this advantage diminishes after menopause, suggesting that hormonal signalling plays an important role. Haematopoietic stem cells (HSCs) express oestrogen receptors (ERs) and oestrogen influences their proliferation, differentiation, and survival of HSCs and progenitor cells. We are working to understand how normal, physiological variations in oestrogen levels impact haematopoiesis, lineage fate decisions and myeloid cell function during an adult biological female’s lifespan. Combining analysis of mouse models and human blood samples, we are exploring how oestrogen-deficiency reshapes immune cell development and can drive tumour-promoting chronic, systemic inflammation. In the future, we will expand our analysis to understand how targeted hormone therapies for ER+ breast cancer (such as aromatase inhibitors) impact the immune system, in particular myeloid cells. This work will provide insights into the intersection of hormonal signalling, immune regulation and cancer progression.
- 3) Long term consequences of myelosuppressive chemotherapy Chemotherapy is widely used to treat breast and ovarian cancer targeting rapidly dividing cells. However, this includes immune progenitors making them highly sensitive to killing by chemotherapeutics. Specifically, myeloid progenitors which continually replenish inflammatory cells such as monocytes and neutrophils are heavily suppressed by many chemotherapeutic agents. In the short-term this myelosuppression can lead to increased risk of bacterial infection. In the long term, immune cell numbers broadly recover, however there is limited data on the long-term functional consequences of this therapy-induced myelosuppression. Emerging evidence suggests that myelosuppressive chemotherapy can induce somatic mutations in hematopoietic stem and progenitor cells (HSPCs) resulting in clonal haematopoiesis (CH). CH is increasingly recognized not only for its association with haematological malignancies but also for its link with immune dysfunction, particularly in the context of inflammatory diseases. However, CH may not be the only mechanism by which myeloablative chemotherapy leads to immune dysfunction. Our research focuses on understanding chemotherapy-induced genetic and epigenetic changes in HSPCs and mammary gland macrophages that lead to breast cancer-promoting local and systemic chronic inflammation. Deeper, mechanistic understanding of the consequences of chemotherapy on inflammatory cells will provide insight to how chemotherapy-induced changes lead to immune dysfunction and provide insight into whether immune dysfunction contributes to resistance to immune checkpoint blockade in heavily pre-treated patients.
- Member, Rosalind and Morris Goodman Cancer Institute (2024-present)
- Assistant Professor, Department of Microbiology and Immunology (2024-present)
Our team
- Elan Behar Étudiant.e de premier cycle Undergraduate Student
- Lucie Droin Étudiant.e de premier cycle Undergraduate Student
Research Partners
Get in touch
1160 ave des Pins O
Montreal, Quebec
Office: 415
Lab:
T. 514 396 2850
T.
F.
hannah.garner@mcgill.ca
Contact us for any questions about
our recruitment process
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