clinics in us

Oncotarget published "Llgl1 prevents metaplastic survival driven by epidermal growth factor dependent migration" which reported that We have previously demonstrated that Llgl1 loss results in a gain of mesenchymal phenotypes and a loss of apicobasal and planar polarity. Cells lacking Llgl1 form mammospheres, where survival and transplantability is dependent upon the Epidermal Growth Factor Receptor. Additionally, Llgl1 loss allows cells to grow in soft-agar and maintain prolonged survival as orthotopic transplants in NOD-SCIDmice. The loss of Llgl1 drives EGFR mislocalization and an EGFR mislocalization point mutation drives these same phenotypes, including activation of AKT and TAZ nuclear translocation. Together, these data in this Oncotarget study indicate that the loss of Llgl1 results in EGFR mislocalization, promoting pre-neoplastic changes. Dr. Joyce Schroeder from The University of Arizona said, "Epithelial cells are regulated by apicobasal polarity complexes that provide an asymmetric cell structure, regulate growth and survival, migration and invasion, and differentiation." Advanced metastatic disease is frequently associated with stem cell characteristics, in that both stem cells and highly metastatic cancers exhibit drug resistance, migratory capacity, self-renewal, and the ability to survive and differentiate into new tissues. In fact, autocrine loops between the EGFR pathway and YAP activation have been identified in ovarian cancer and breast epithelium.

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