Special Issue "Pathology of Acute Myeloid Leukemia (AML)"
Deadline for manuscript submissions: 25 April 2024 | Viewed by 193
Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy characterized by the uncontrolled proliferation of myeloid precursor cells in the bone marrow. This Special Issue will address various topics in the pathogenesis of AML, encompassing the underlying genetic and epigenetic alterations that contribute to disease development and progression.
AML arises from the acquisition of somatic mutations affecting key regulatory genes involved in hematopoietic cell differentiation, self-renewal, and apoptosis. The most frequently mutated genes include FLT3, NPM1, DNMT3A, IDH1/2, and TP53. These mutations disrupt normal cellular signaling pathways, leading to dysregulated proliferation and impaired differentiation of myeloid progenitor cells. In addition, chromosomal aberrations, such as translocations, inversions, and deletions, further contribute to leukemogenesis by disrupting important genes involved in hematopoiesis.
Epigenetic alterations also play a crucial role in AML pathogenesis. Aberrant DNA methylation patterns and histone modifications lead to the silencing of tumor suppressor genes and the activation of oncogenes, promoting leukemic transformation. Furthermore, alterations in microRNA expression profiles can affect critical signaling pathways and contribute to leukemogenesis.
The interaction between leukemic cells and the bone marrow microenvironment is another significant factor in AML pathogenesis. Abnormalities in the bone marrow niche, including changes in cytokine signaling, stromal cell interactions, and angiogenesis, create a supportive environment for leukemic cell survival, proliferation, and chemoresistance.
Understanding the intricate molecular mechanisms underlying AML pathogenesis is crucial for the development of targeted therapies and personalized treatment approaches. Advances in genomic profiling techniques and functional studies are rapidly unraveling the complexities of AML biology, providing opportunities for novel therapeutic strategies that may improve patient outcomes in the future.
Dr. Olga K. Weinberg
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