Associate Professor, Translational Molecular Pathology, Co-Director, Metastasis Research Center, Center for Stem Cell & Developmental Biology, UT MD Anderson Cancer Center
Despite the advent of advanced diagnosis and treatment options, metastasis remain accounts for more than 90 percent of deaths among cancer patients. Unfortunately, there are no treatments available for patients with metastasis. We and others have demonstrated that the carcinoma cells, which are initially confined to the primary tumor site by the continued expression of cell-cell adhesion molecules, acquires mesenchymal morphology, increased migration, invasion and metastatic properties by activating a latent embryonic program, known as epithelial-mesenchymal transition (EMT). In addition, during metastasis, cancer cells leaving the primary site recreate tumor histopathologically similar to their tissue of origin at the metastatic site. Therefore, we hypothesized and demonstrated that the cancer cells also acquire stem cell properties via EMT in addition to migratory and invasive capacities. Because both cancer stem cells (CSCs) and the EMT program are independently shown to be responsible for promoting metastasis and the acquisition of resistance to standard of care therapies and we have found that these two are indeed intertwined, we put forward the notion that the EMT-signaling pathways may offer a diagnostic and therapeutic window for detecting and treating metastasis. At present, our laboratory is investigating the biology of metastasis at the molecular level and developing ways to diagnose and treat metastasis.
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