Daniel Diaz, Mauricio A. Salinas Santander and Jesus A. Morlett Chavez
Posters: J Cancer Sci Ther
The carcinogenic potential of HPV infections is based on the integration and constitutive expression of the E6 and E7 genes which inhibit the p53 and Rb tumor suppressor proteins. In normal cells, Mdm2 regulates p53 in a negative feedback loop and although Mdm2 is apparently functional in HPV-infected cells, the E6 protein replaces Mdm2 in repressing p53 function in these cells. The role of Mdm2 in HPV-positive cells is still elusive. Therefore,in this study Mdm2 was knocked down in an HPV-positive cervical cancer cell line; as a result, we found expression downregulation of the E6 and E7 oncogenes as well asupregulation of p53.
Daniel Diaz got his B.Sc. in Biology at the Universidad Juarez del Estado de Durango (Mexico), he then obtained his PhD diploma at the Universidad Autonoma de Nuevo Leon where he was awarded with an AcademicExcellence fellowship from the National Board for Science and Technology (CONACyT) and a fellowship granted by the Science and Technology Research Support Program (PAICyT). He had the opportunity of undergoing extensive training in the Medical Center (Houston, TX) under the tutelage of several researchers in the University of Texas and M.D. Anderson Cancer Center and in the Institute of Biotechnology in Madrid, Spain. Currently, he is dedicated to the analysis and reprogramming of Stem Cells for tissue engineering research.
Cancer Science & Therapy received 3968 citations as per Google Scholar report
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