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NEOPLASTIC PROLIFERATIONS IN WHITE CELLS - Coggle Diagram

- - - - accumulation of immature myeloid
        blasts in the marrow
        
        marrow failure and complications related to anemia, thrombocytopenia and neutropenia
        (weakness, bleeding and infections)
  - - - transcription factor fusion protein that interferes with nromal myeloid differentiation
        
        t(8;21)
        
        inv(16)
        
        disruption of RUNX1 and CBFB genes,
        required for normal hematopoiesis
      - acute promyelocytic leukemia is a distinctive subtype of AML associated with the t(15;17)
        
        fusion gene encoding a chimeric protein consisting of the retinoic acid receptor-α (RARα) and a portion of a protein called PML
        
        interferance with the terminal differentiation of granulocytes
      - mutation of signalling proteins that result in constitutive activation of pro-growth/survival pathways
        
        AMLs with the t(15;17) also frequently have activating mutations in FLT3
        
        increasing cellular proliferation and survival
    - - with prior MDS
        
        AML with multilineage dysplasia
        
        AML with MDS-like cytogenetic aberrations (5q-, 7q-, 20q-)
    - - following alkylator therapy or radiation therapy, a 2- to 8-year latency period could have MDS-like cytogenetic aberrations (e.g., 5q-, 7q-)
      - following topoisomerase II inhibitor (e.g., etoposide) therapy, a 1- to 3-year latency can lead to translocations involving KMT2A (11q23)
    - - classified based on the degree of differentiation and the lineage of the leukemic blasts
      - AML- minimally differentiated: negative for myeloid biomarkers and myeloid antigens
        
        AML without maturation: >3% of blasts positive for myeloid markers
        
        AML with myelocytic maturation: full range of myelocytic maturation
        
        AML with myelomonocytic maturation
        
        AML with monocytic maturation: nonspecific esterase-positive monoblasts and promonocytes predominate in marrow, monoblasts or mature monocytes in the blood may be seen
        
        AML with erythroid maturation: erythroid/myeloid subtype defined by >50% dysplastic maturing erythroid precursors and >20% myeloblasts or in the form of pure erythroid subtype defined by >80% erythroid precursors without myeloblasts
        
        AML with megakaryocytic maturation: blasts of megakaryocytic lineage predominate
  - - - diagnosis of AML is based on the presence of at least 20% myeloid blasts in the bone marrow
        
        several types of myeloid blasts
        
        MYELOBLASTS
        
        delicate nuclear chromatin
        
        2-4 nucleoli
        
        more voluminous cytoplasm than lymphoblasts
        
        often, fine, peroxidase+ azulophilic granules
        
        MONOBLASTS
        
        folded or lobulated nuclei
        
        better recognizable with the bone marrow smears
        
        with the bone marrpw biopsy it is difficult to differentiate between blasts
        
        sometimes, megakaryocytic differentiation, often accompanied by marrow fibrosis caused by the release of fibrogenic cytokines
  - - - fatigue, fever, infections, spontaneous mucosal and cutaneous bleeding
    - - myeloblastoma, myeloid sarcoma or chloroma
  - - - about 60% of pts achieve complete remission with CT
      - only 15% to 30% remain free
        of disease for 5 years
      - “high-risk” forms of AML (as well as relapsed AML of all types) are treated with HSC transplantation