David Solomon, MD, PhD

Member, Helen Diller Family Comprehensive Cancer Center
Assistant Professor
Division of Neuropathology
Department of Pathology
+1 415 514-9761
Research Description: 

I am a neuropathologist and 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 acute myeloid leukemia (AML), 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. Our studies in glioblastoma demonstrated that STAG2 mutations were a direct cause of chromosomal instability and aneuploidy; however, cohesin gene alterations in urothelial carcinoma and AML have been identified primarily in near-diploid tumors, suggesting alternative mechanisms by which cohesin inactivation drives oncogenesis. Using a newly generated conditional STAG2 knockout mouse and isogenic sets of STAG2 proficient and deficient cancer cell lines, we are currently working to determine the function of STAG2 in mouse development and tumorigenesis and to identify therapeutic vulnerabilities in the many cancers harboring cohesin gene alterations. Other ongoing studies in the Solomon Lab include genomic characterization of brain tumor variants such as chordoid gliomas, choroid plexus tumors, and pineal parenchymal tumors.

Primary Thematic Area: 
Cancer Biology & Cell Signaling
Secondary Thematic Area: 
Human Genetics
Research Summary: 
Molecular mechanisms governing chromosomal instability and oncogenesis


Featured Publications: 

The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

PLoS genetics

Brohl AS, Solomon DA, Chang W, Wang J, Song Y, Sindiri S, Patidar R, Hurd L, Chen L, Shern JF, Liao H, Wen X, Gerard J, Kim JS, Lopez Guerrero JA, Machado I, Wai DH, Picci P, Triche T, Horvai AE, Miettinen M, Wei JS, Catchpool D, Llombart-Bosch A, Waldman T, Khan J

Frequent truncating mutations of STAG2 in bladder cancer.

Nature genetics

Solomon DA, Kim JS, Bondaruk J, Shariat SF, Wang ZF, Elkahloun AG, Ozawa T, Gerard J, Zhuang D, Zhang S, Navai N, Siefker-Radtke A, Phillips JJ, Robinson BD, Rubin MA, Volkmer B, Hautmann R, Küfer R, Hogendoorn PC, Netto G, Theodorescu D, James CD, Czerniak B, Miettinen M, Waldman T

Mutational inactivation of STAG2 causes aneuploidy in human cancer.

Science (New York, N.Y.)

Solomon DA, Kim T, Diaz-Martinez LA, Fair J, Elkahloun AG, Harris BT, Toretsky JA, Rosenberg SA, Shukla N, Ladanyi M, Samuels Y, James CD, Yu H, Kim JS, Waldman T

Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts.

Cancer research

Michaud K, Solomon DA, Oermann E, Kim JS, Zhong WZ, Prados MD, Ozawa T, James CD, Waldman T

Identification of p18 INK4c as a tumor suppressor gene in glioblastoma multiforme.

Cancer research

Solomon DA, Kim JS, Jenkins S, Ressom H, Huang M, Coppa N, Mabanta L, Bigner D, Yan H, Jean W, Waldman T