Fabiola Velazquez

imageResearch Scientist and Research Assistant Professor

Education:
Licenciada en Bioquímica Clínica (Degree in Clinical Biochemistry) at Chemical Science Faculty (FCQ) - National University of Córdoba (UNC), Argentina. 2007
Doctorado en Ciencias Químcias (PhD in Chemical Science) at Chemical Science Faculty (FCQ) - National University of Córdoba (UNC), Argentina. 2015

Contact info:
Fabiola.Velazquez@stonybrookmedicine.edu
Department of Medicine
Stony Brook University
MART Bldg., Floor 9S                                                  
Stony Brook, NY 11794-7294

Research interest:
My project is to define the role of sphingosine kinase 1 (SK1) as a novel and critical downstream target for the tumor suppressive action of p53, and to establish SK1 as a potential target for cancer therapy, particularly in tumors with loss of p53 or mutant p53.

SK1 is a highly regulated enzyme with a central role in tumor biology by regulating the levels of the bioactive sphingolipids: shingosine 1 phosphate (S1P) (a tumor promoting sphingolipid) and ceramide (a tumor suppressor lipid). Previous work shows that the induction of p53 results in loss of SK1 through proteolysis. Moreover, recent studies using the combined p53/SK1 knockout (KO) mice demonstrated that the loss of SK1 is critical for the suppression of thymic lymphoma, osteosarcoma and others cancers in the absence of p53. Since a lot of time p53 and components of the p53 pathway have emerged as key tumor suppressor, however, targeting this pathway has been difficult due to the nature and function of the proteins involved. The recent and ongoing results provide a novel and solid connection between p53, SK1 and bioactive sphingolipids, and led us to the hypothesis that SK1 is a candidate target for therapeutic development especially in the context of mutant p53.

To test this hypothesis we will utilize different animals’ models (p53 null and mutant mice) in which the SK1 expression could be controlled. These studies raise novel and fundamental questions as to the role of SK1 as a druggable target in p53 null and mutant cancers. Addressing this specific aim opens up the door for developing novel chemotherapeutic approaches to many human cancers in which p53 is deregulated or mutated.