Magyar onkologia
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The phosphatidylinositol-3-kinase/AKT (PI3K/AKT) pathway is commonly deregulated in breast cancer through several mechanisms, including PI3K catalytic subunit alpha (PIK3CA) mutations and loss of phosphatase and tensin homolog (PTEN). The hiperactivated PI3K/AKT signaling can be associated with endocrine or trastuzumab therapy resistance and underscore the impact of targeting the pathway. Our aim was to identify PIK3CA mutations and the mechanisms of PTEN loss and assess their therapeutic consequences in breast cancer patients. ⋯ The PTEN-deficient MCF10A cell line showed increased expression of certain members of the fibroblast growth factor 2 (FGF2)/FGFR1 pathway. We suppose that loss of PTEN enhances the autocrine FGF signaling promoting cell proliferation. FGF-2 and FGFR1 can be potential targets in PTEN deficient breast cancers.