Sufi Thomas, PhD

My research has extensively involved understanding the role of the tumor microenvironment in facilitating head and neck squamous cell carcinoma (HNSCC) progression and to develop effective therapeutic interventions. The tumor microenvironment consists of cellular and acellular or matrix components. Several non-malignant cells constitute the cellular stromal environment surrounding the tumor including fibroblasts, immune cells, cells that form blood vessels (endothelial cells and pericytes) and neuronal cells. Fibroblasts are the most abundant stromal type in HNSCC. My laboratory has isolated and characterized several primary cancer-associated fibroblast (CAF) lines from HNSCC tissue. My group has demonstrated that the molecular cross talk between HNSCC and CAFs that increase tumor growth, local invasion and metastasis. Further, we delineated aspects of the molecular mechanisms involved in tumor-CAF metabolic symbiosis, and HNSCC-mediated CAF secretory autophagy.

With NIH R01 funding support, Dr. Thomas is currently delineating the mechanism whereby cells in the tumor microenvironment facilitate head and neck cancer progression and response to therapy. Several types of normal cells surround the cancer. These include blood vessels, immune cells and fibroblasts. Dr. Thomas demonstrated that normal fibroblasts in contact with the tumor facilitate tumor growth and metastasis. Her laboratory is currently identifying the factors secreted by the fibroblasts involved in tumor progression. Characterizing molecules involved in tumor-fibroblast communication are critical in developing more effective therapeutic strategies. In addition to supporting tumor growth, fibroblasts are a major component of fibrotic reactions that result in scar tissue formation. Dr. Thomas is in the process of identifying targets in order to reduce fibrosis and the ability of the fibroblasts to facilitate tumor growth. The finding from these studies has tremendous potential in not only target identification and therapeutic development, but also in developing ways to reduce scar tissue formation from fibrosis.

Autophagy-dependent secretion: mechanism, factors secreted, and disease implications.

Role of tumor associated fibroblast autophagy in head and neck cancer