Our Focus

Inflammation is a hallmark of cancer: tumors hijack blood cell development (hematopoiesis), skewing bone marrow output towards the myeloid lineage leading to tumor-supporting chronic systemic inflammation. Conversely, chronic inflammatory conditions can also predispose individuals to developing tumors, 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 reprograms these cells towards a tumor-supporting state and this “education” occurs on multiple levels: during their development in the bone marrow; within primary tumors; 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 tumor- and metastasis-supporting inflammation, we aim to identify novel therapeutic strategies for breast and ovarian cancer patients.

Our Goals

To understand the molecular mechanisms that underpin pro-inflammatory hematopoiesis and how this can be targeted to reduce systemic inflammation and cancer progression

To unravel the impact of estrogen signaling on hematopoiesis and how estrogen deficiency (menopause) leads to chronic inflammation

Currently working on…

Estrogen signaling in hematopoiesis

Understanding and disrupting primary tumor induced skewing of hematopoiesis to reduce metastatic spread

Long term consequences of myelosuppressive chemotherapy