David Solomon, MD, PhD
I am a cancer researcher at the University of California, San Francisco with a dedicated interest in the genetic alterations that drive cancer development. We have recently discovered frequent inactivating mutations of the cohesin complex gene STAG2 in glioblastoma, urothelial bladder cancer, Ewing sarcoma, and myeloid leukemia, which define molecular subgroups of these tumors with distinct clinical outcomes. The cohesin complex is responsible for sister chromatid cohesion following DNA replication and helps ensure faithful chromosome segregation during mitosis, but has also been implicated in additional cellular processes such as regulation of chromatin architecture and gene transcription. Using a newly generated conditional STAG2 knockout mouse and isogenic sets of STAG2 proficient and deficient human cell lines, we are currently working to determine the function of STAG2 during development and tumorigenesis and to identify therapeutic vulnerabilities in the many cancers harboring cohesin gene alterations. Other ongoing studies in the Solomon Lab include functional genomics and epigenomics evaluation of the many different brain tumor subtypes including glioblastoma, low-grade glioneuronal tumors, and meningioma.
5/25/21 Sharpening your Mentoring Skills (SyMS)
Websites
- Soloman Lab
- UCSF Department of Pathology
- UCSF Division of Neuropathology
- UCSF Helen Diller Family Comprehensive Cancer Center
- NIH Director's Early Independence Award Program