• Ph.D. in Biology, University of Puerto Rico
   
• Postdoctoral Training: Pathology Department, Harvard Medical School, Molecular Oncology Research Institute, Tufts Medical center

• Assistant Professor, Department of Biochemistry, Ponce School of
  Medicine, Ponce, Puerto Rico
   

• Co-Director of the RCMI Molecular Biology Core, Ponce School of Medicine
• M.D. Program Curriculum Committee, PSM
• Ph.D. Program in Biomedical Sciences Curriculum Committee, PSM
• Distance Learning Committee, PSM
• Internal Advisory Committee for the RISE Program at PSM
• M.D. Program Admission Committee, PSM
• Internal Advisory Committee for the RCMI Program, PSM

• Medical Biochemistry (MD Program)
• The Cellular and Molecular Basis of Cancer (Ph.D. Prog. in Biomedical Sciences)
   

• American Association for Cancer Research

1. The Retinoblastoma Protein in Osteogenesis and Osteosarcoma Formation. (2012). Pedro G. Santiago-Cardona. Osteogenesis (Yunfeng Lin, Ed.), Chapter 10, pp. 253-286. InTech. ISBN: 978-953-51-0030-0. http://www.intechopen.com/articles/show/title/-the-retinoblastoma-protein-in-osteogenesis-and-osteosarcoma-formation-.
    
2. A Novel Role for the Retinoblastoma Tumor Suppressor Protein as a Regulator of Cell Adhesion: Implications for Osteogenic Differentiation and Osteosarcoma Formation. Bernadette Sosa, Volkan Gunduz, Viviana Vázquez-Rivera, W. Douglas Cress, Gabriela Wright, Haikuo Bian, Philip W. Hinds and Pedro G. Santiago-Cardona. (2010). PLoS ONE 5(11): e13954. doi:10.1371/journal.pone.0013954. PMID: 21085651.
    
3. Yang H.-S., Alexander K., Santiago P., and Hinds P. W. (2003). ERM proteins and Cdk5 in cellular senescence. Cell Cycle, 2(6): 517-520. PMID: 14504464.
   
   
   
   
   Other (Funding)
   
   1. American Cancer Society Grant 93-032-13
   2. NIH NCI U56 CA118809 (PSMHS and H. Lee Moffitt Cancer Center Consortium)
   3. NIH NCI 3 U56 CA118809-04-S1 (ARRA Supplement)
    

Research in our laboratory is focused on the characterization of novel mechanisms of tumor suppression engendered by the retinoblastoma protein (pRb), a cell cycle repressor commonly inactivated in human cancers. Although pRb is predominantly known as a cell cycle regulator, our investigations point to an additional pRb function in cell adhesion. We have shown that pRb regulates the expression of a wide repertoire of cell adhesion genes and regulates the assembly of the membrane-associated adherens junctions required for cell adhesion. We also have evidence suggesting that the de-regulation in cell adhesion-related gene expression due to pRb loss is strongly related to some cancer types such as lung cancer. We propose that promoting cell-to-cell attachments may be an additional pRb-related tumor suppressive mechanism, and that pRb inactivation in cancer cells not only results in the expected loss of cell cycle control, but also contributes to tumor metastasis at later stages of tumorigenesis. Our current projects are aimed at elucidating the detailed molecular mechanisms linking pRb function to cell adhesion and metastasis. Specifically, we are studying a functional link between pRb and known regulators of cell adhesion such as the small Rho GTPases Rac1 and Cdc42 and their effector Pak1. We are characterizing the cellular pathways and molecular mechanisms by which pRb controls the activities of these GTPases, including possible transcriptional, post-transcriptional, translations or posttranslational controls.