Neveen Said

Dr. Said’s career is grounded in extensive medical and scientific training at Cairo University, followed by postdoctoral research training at Tufts University and MCG, and faculty positions at UVA and WFUSM. As an educator, Dr. Said bridges basic science and clinical practice through a dynamic, case-based teaching approach that strengthens students' real-world clinical reasoning. This commitment to active learning is fueled by cutting-edge laboratory research into the mechanisms of cancer progression, metastasis, and therapeutic response. This discovery-driven approach directly informs Dr. Said's mission to prepare the next generation of medical researchers and clinicians; ultimately, empowering students to master the complexities of modern medical practice in an inclusive, collaborative environment.

Dr. Said’s research program investigates tumor suppressors and oncogenic pathways in bladder and ovarian cancers, with pioneering contributions that define the multifaceted roles of SPARC in tumor progression, metastasis, immune-metabolic modulation, and therapeutic response. In addition, Dr. Said provides broad institutional and national leadership through service on institutional committees, advisory groups, and major grant review panels.

Dr. Said’s research centers on understanding how tumor suppressors and oncoproteins govern the multistep cascade of urothelial and ovarian carcinogenesis, progression, and metastasis. He investigates how cellular and non-cellular components of the tumor microenvironment, including inflammatory cues, stromal interactions, and metabolic programming, shape cancer cell behavior. A major focus of his work is the tumor-suppressive role of SPARC, which we have shown to exert multifaceted tumor-suppressor effects across bladder and ovarian cancers. Using integrated preclinical systems with patients’ specimens and data, his laboratory dissects SPARC-regulated pathways in cancer and stromal cells, defining how SPARC modulates the immune and metabolic landscapes to identify diagnostic, prognostic, and therapeutic targets that can restore tumor suppressor activity or inhibit oncogenic signaling.