Acute myeloid leukemia
Core of basic research: Focus on the molecular mechanisms underlying the malignant transformation of myeloid hematopoietic stem/progenitor cells, with key drivers being differentiation arrest and uncontrolled proliferation induced by genetic variations. Core research directions include the function of fusion proteins generated by chromosomal translocations (e.g., t(15;17)), the signal activation mechanism of kinase mutations (e.g., FLT3-ITD), and the development of targeted drugs against these abnormal molecules.
Core key proteins: FLT3 (sustained activation of proliferation signals upon mutation), PML-RARα fusion protein (blocks myeloid differentiation), RUNX1 (key transcription factor for hematopoietic differentiation), CEBPA (regulates myeloid cell maturation), c-KIT (stem cell factor receptor, enhanced survival signals upon mutation), TP53 (tumor suppressor gene, inactivation promotes tumor progression).
Core key proteins: FLT3 (sustained activation of proliferation signals upon mutation), PML-RARα fusion protein (blocks myeloid differentiation), RUNX1 (key transcription factor for hematopoietic differentiation), CEBPA (regulates myeloid cell maturation), c-KIT (stem cell factor receptor, enhanced survival signals upon mutation), TP53 (tumor suppressor gene, inactivation promotes tumor progression).
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