Advancing CAR T cell Therapies
SOPHIE HANINA | PROFILE
Innovating
Next-Generation Treatments
My academic path has been guided by a commitment to developing new treatments that help people. From early doctoral research focused on embryonic stem cells, I pursued medical training in hematology, and my postdoctoral research has centered on creating cellular therapies for solid tumors.
Translating scientific discoveries into meaningful clinical impact has always been central to my motivation. This journey is not only about making discoveries—it's about turning biological insight into effective therapies.
EDUCATION
MD
University of Oxford
PhD
University of Cambridge
BA (Hons)
University of Oxford
WORK EXPERIENCE
Associate Research Scientist
Columbia University Medical Center, 2025–Present
Senior Research Scientist
Memorial Sloan Kettering Cancer Center, 2019–2025
Hematology Fellowship
Imperial College Healthcare NHS Trust, 2017–2019
Internal Medicine Internship & Residency
University of Oxford; Imperial College Healthcare NHS Trust, 2013–2017
Recent Research
Sensitive CAR T cells redefine targetable CD70 expression in solid tumors
Sophie A. Hanina et al. Science 391, 896-905(2026). DOI: 10.1126/science.adv7378
In this study, we used a more sensitive CAR T cell to rethink what counts as a targetable antigen in solid tumors. We found that CD70, an immunotherapeutic target, that often appears heterogeneously expressed in tumors, is actually present on all tumor cells—just at levels too low for conventional methods and standard CAR T cells to detect. By using a more sensitive receptor to detect both CD70-positive and ultralow tumor cells, we could achieve complete tumor elimination. These findings position CD70 as an excellent immunotherapeutic target, but only if a highly sensitive engineered CAR is used.
Key Findings
- Sensitive CAR T cells eradicate CD70-heterogeneous tumor models of kidney, ovarian and pancreatic cancer
- Tumor cells that appear CD70-negative within heterogeneous tumors in fact retain ultralow expression
- This ultralow expression is due to the incomplete epigenetic silencing of CD70, mediated by EZH2-H3K27me3