Endometrial cancer
Core of basic research: Decipher the molecular differences between estrogen-dependent (ER/PR-positive) and independent subtypes, focusing on PI3K-Akt pathway activation by PTEN inactivation, the oncogenic role of FGFR2 mutations, and the carcinogenic mechanisms of metabolic factors (e.g., obesity, diabetes) on endometrial epithelial cells.
Core key proteins: ERα/PR (mediate estrogen-dependent proliferation), PTEN (negative regulator of PI3K pathway, frequent inactivation), PI3K/Akt/mTOR (signaling pathway regulating proliferation and metabolism), FGFR2 (receptor tyrosine kinase, promotes proliferation upon mutation), TP53 (frequent mutation in independent subtypes), CTNNB1 (β-Catenin, activates Wnt pathway).
Core key proteins: ERα/PR (mediate estrogen-dependent proliferation), PTEN (negative regulator of PI3K pathway, frequent inactivation), PI3K/Akt/mTOR (signaling pathway regulating proliferation and metabolism), FGFR2 (receptor tyrosine kinase, promotes proliferation upon mutation), TP53 (frequent mutation in independent subtypes), CTNNB1 (β-Catenin, activates Wnt pathway).
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