Nicholas A. Cacalano,Ph.D.
Associate Professor Experimental Radiation Oncology
The broad focus of his laboratory is basic mechanisms of signal transduction, how normal signaling becomes corrupted in cancer, and how knowledge of signaling pathways can be exploited for the identification of novel biomarkers of radiation resistance, and targets for molecular therapies.
Specifically, his lab is interested in the role of epigenetic silencing (methylation) of tumor suppressor (Ts) genes in the development of cancer and the acquisition of radiation resistance, determining the mechanism of gene silencing and identifying therapeutics that can re-activate the genes to sensitize cells to radiotherapy.
His team has also identified a novel pathway that regulates the DNA damage response. They have shown that Suppressor of Cytokine Signaling (SOCS)-3 has a radioprotective effect in normal cells and tumors, and that in cells lacking SOCS3, the DNA damage response is defective. We are interested in identifying the molecular basis of SOCS3-mediated radioprotection and determining if human tumors that silence SOCS3 epigenetically are radiosensitive due to defects in the DNA damage response.
Thus, it is possible that SOCS3 is a biomarker of radiation resistance in solid tumors, and a potential target of molecular therapeutics.