Cells from a variety of malignancies can escape from a primary tumor. Many of those disseminated tumor cells (DTCs) remain dormant, but those that proliferate pose a risk for metastasis, the leading cause of cancer death. Insight into the molecular mechanisms responsible for maintaining DTC dormancy is crucial for developing therapies that prevent DTCs from reactivating.

Maria Soledad Sosa, Ph.D., and colleagues have shown that the transcription factor NR2F1/COUP-TF1 induces dormancy in one population of DTCs in head and neck squamous cell carcinoma (HNSCC). The researchers also have preliminary data showing that upregulation of the gene SOX2 induces dormancy in those DTCs. Dr. Sosa has now received a five-year, $1.9 million grant from the National Cancer Institute to identify the molecular mechanisms underlying SOX2-induced dormancy and the reactivation rate of dormant DTCs controlled by SOX2. Dr. Sosa and colleagues will also investigate therapeutic strategies for preventing SOX2+ dormant DTCs from reactivating.

This year Dr. Sosa has also received two grants from private philanthropies. The Gilead Research Scholar Program has awarded Dr. Sosa a two-year, $180,000 grant to study dormancy mechanisms involved in melanoma. And the Susan G. Komen Foundation has awarded her a two-year, $160,000 ASPIRE grant to follow up on her previous finding that the protein ZFP296 induces dormant breast cancer DTCs to escape dormancy, leading to metastasis.

Dr. Sosa is an assistant professor of microbiology & immunology and of oncology at Einstein and a member of the NCI-designated Montefiore Einstein Cancer Center and its Cancer Dormancy & Tumor Microenvironment Institute