Hannah Garner
Assistant Professor, Department of Microbiology and Immunology
Principal Investigator, Goodman Cancer Institute
- 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 鈥渆ducation鈥� 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.
