Our Work
In carcinogenesis, cancer cell fitness depends on interactions with the microenvironment. Neoplastic cells develop into overt disease when they are able to evade immune system surveillance within a permissive environment.
Emerging evidence demonstrates two critical findings:
- Inflammation supports the proliferation of mutated clones while suppressing normal cell function.
- Cancer cells and inflammatory cells create a self-reinforcing cycle that promotes both immunosuppression and cancer growth.
While studies in solid tumors have shown how immune cells contribute to tumor growth, less is known about the role of immune cells and inflammatory factors in hematological malignancies (blood cancers.)
Our Research Focus
The Melo-Cardenas Lab at Northwestern University Feinberg School of Medicine investigates the molecular mechanisms behind immune cell-mediated inflammation and examines relationships between the immune microenvironment and malignant clones in myeloid disease, with specific focus on myeloproliferative neoplasms.
Key Research Questions:
- Which intrinsic pathways maintain inflammatory signaling during:
- Normal blood cell production (hematopoiesis)
- Myeloproliferative neoplasms
- What is the functional role of immune cell-derived inflammation in disease progression?
- What is the spatial organization and nature of cell-cell interactions within inflammatory niches in the bone marrow?