About Me:
I obtained my Bachelor’s Degree in Science, Major in Biology, from the University of Puerto Rico in 1994. After completing my Bs. Sc., I started working on my Ph. D. degree in Developmental Neurobiology, also in the University of Puerto Rico. My Ph. D. thesis research was focused on the characterization of genes involved in tissue morphogenesis in echinoderm model systems. After completing my Ph. D. degree in 2001, I relocated to Boston, Massachusetts, to pursue postdoctoral training in molecular cancer biology, first at Harvard Medical School, and then at the New England Medical Center. My postdoctoral research was centered on the characterization of cellular pathways by which the retinoblastoma protein exerts its tumor suppressive actions. I returned to Puerto Rico in 2005, and I am currently an Assistant Professor at the Biochemistry Department at Ponce School of Medicine, where I am actively involved in both teaching and cancer research.
Project Info:
Cancer progression involves the acquisition of mutations that result in both a loss of cell cycle regulation as well as in the acquisition of the capacity to escape from the primary tumor site and metastasize to distant tissues. One of the central issues in cancer biology is whether the same mutations that disrupt cell cycle control during early tumorigenesis can also compel tumor cells to metastasize at later stages of tumor progression by disrupting cell-to-cell interactions, or alternatively, if the disruption of cell cycle control and the acquisition metastatic potential are genetically distinct events. Within the context of this issue, my research project is focused on the characterization of a novel role for the retinoblastoma tumor suppressor protein (RB), a nuclear cell cycle repressor commonly inactivated in human cancers, as a regulator of cell-to-cell adhesion. Our studies using conditional RB knockout mice show that a functional RB is necessary for proper cell-to-cell adhesion to occur. Our ongoing investigations employ several biochemical and cellular and molecular biology strategies aimed at the identification of proteins that could serve as mediators through which RB could regulate cell-to-cell adhesion. Some of the candidates under study are the Cyclin-dependent Kinase 5 (CDK5), the small Rho GTPase Rac1, and the membrane-associated tumor suppressor protein merlin. A dual role for RB as a regulator of both cell cycle progression and of cell-to-cell adhesion raises the extremely exciting prospect that, in at least some human cancers, RB inactivation can play a significant role not only during initial tumor formation by providing targeted cells with a replicative advantage over normal cells, but also during later stages of tumorigenesis by disrupting cell-to-cell adhesion consequently leading to spreading of cancer cells to other tissues. In broader terms, this project could contribute to the characterization of a signaling pathway that may be involved in the orchestration between cell proliferation itself and the mechanisms that regulate cell proliferation in response to extracellular cues such as cell-to-cell interactions. A disruption of RB´s tumor suppressive capacity with a concomitant breakdown of this orchestration could be at the core of the molecular etiology of some cancer types.