Chronic myeloid leukemia
Core of basic research: Focus on the BCR-ABL fusion protein generated by the Philadelphia chromosome (t(9;22)), investigating its constitutive tyrosine kinase activity-mediated activation mechanisms of pathways such as STAT5 and PI3K-Akt, as well as the targets and resistance mechanisms (e.g., BCR-ABL mutations) of tyrosine kinase inhibitors (TKIs).
Core key proteins: BCR-ABL fusion protein (sustained activation of proliferation/survival signals), c-KIT (synergistically drives abnormal proliferation of hematopoietic cells), PDGFRα (receptor tyrosine kinase involved in signal crosstalk), SRC (kinase family enhancing signal transduction), STAT5 (transcription factor regulating proliferation-related genes), PI3K (core of signaling pathway mediating survival signals).
Core key proteins: BCR-ABL fusion protein (sustained activation of proliferation/survival signals), c-KIT (synergistically drives abnormal proliferation of hematopoietic cells), PDGFRα (receptor tyrosine kinase involved in signal crosstalk), SRC (kinase family enhancing signal transduction), STAT5 (transcription factor regulating proliferation-related genes), PI3K (core of signaling pathway mediating survival signals).
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