Andres is originally from Medellin, Colombia and migrated to the United States in 2004. In college, he pursued a BS in Biomedical Sciences and a BS in Biotechnology at the University of Central Florida, Orlando. Here he conducted neuroregeneration research focused on glial scar formation and inhibition of axonal regeneration mediated by ECM proteoglycans and glycosaminoglycans. After his undergraduate education, he pursued an MS in Cellular and Molecular Biology at Tulane University, New Orleans. At Tulane, his research work was focused on Neural Growth Factor Receptor amplification and its association with increased metastatic and recurrence potential in colorectal cancer. Andres is currently an MD/PhD candidate at the University of Arizona College of Medicine, Tucson and aspires to become a pediatric oncologist.
Andres is interested in the role of the bone marrow tumor microenvironment (TME) in the progression and recurrence of pediatric cancers. His current project explores cancer-associated adipocytes (CAAs) in the bone marrow and their interaction with metastatic neuroblastoma. He is particularly intrigued by neuroblastoma-induced phenotypic changes among resident bone marrow adipocytes, their eventual transformation into the CCA phenotype, and the subsequent changes that result in enhanced bone marrow metastases and tumor cell survival. Supported by recent literature in breast cancer, multiple myeloma, and prostate cancer, these changes may include:
- A metabolic change in the TME induced by increased fatty-acid oxidation and shift in tumor metabolism towards fat metabolism (Anti-Warburg effect). This includes modulation of HIF-1 and increased angiogenesis.
- Improved metastatic potential in bone marrow from the release of metastasis modulators, pro-inflammatory markers, and pro-migration molecules.
- CAA-derived pharmacological resistance to chemotherapy and decreased efficacy of bone marrow transplantation.