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Pancreatic cancer
Core of basic research: Focus on KRAS mutations (incidence > 90%)-driven abnormal activation of Hedgehog and PI3K-Akt pathways, explore the "multi-step carcinogenesis" mechanism of pancreatic ductal epithelial cell transformation into cancer cells, and the impact of the tumor microenvironment (fibrosis, immune suppression) on chemoresistance.
Core key proteins: KRAS (driver mutation activating proliferation/survival signals), TP53 (tumor suppressor gene, inactivation by mutation), SMAD4 (TGF-β pathway, inactivation promotes invasion), PI3K/Akt/mTOR (core of signaling pathway), EGFR (enhances proliferation signals), VEGF (angiogenesis), PD-L1 (immune escape), Hedgehog pathway proteins (SMO, Gli, promoting cancer).
Core key proteins: KRAS (driver mutation activating proliferation/survival signals), TP53 (tumor suppressor gene, inactivation by mutation), SMAD4 (TGF-β pathway, inactivation promotes invasion), PI3K/Akt/mTOR (core of signaling pathway), EGFR (enhances proliferation signals), VEGF (angiogenesis), PD-L1 (immune escape), Hedgehog pathway proteins (SMO, Gli, promoting cancer).
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