Acute monocytic leukemia (AMoL, or AML-M5)[2] is a type of acute myeloid leukemia. In AML-M5 >80% of the leukemic cells are of monocytic lineage.[3] This cancer is characterized by a dominance of monocytes in the bone marrow. There is an overproduction of monocytes that the body does not need in the periphery. These overproduced monocytes interfere with normal immune cell production which causes many health complications for the affected individual.
Acute monocytic leukemia
Acute monocytic leukemia with its cytochemical profile
The pathology of AML involves abnormal proliferation and differentiation of a population of myeloid stem cells. Genetic mutations are identified in the majority of cases. A common genetic mutation identified in these cases are characterized as chromosomal translocations where information from one chromosome is exchanged to a non-homologous chromosome creating an unusual rearrangement of chromosomes. This translocation is often abbreviated as t(#of one chromosome involved, #of other chromosome involved). M5 is associated with characteristic chromosomal abnormalities, often involving chromosome 11, such as t(9;11), affecting the MLL (KMTA2) locus at 11q23; however MLL translocations are also found in other leukemia subtypes. The t(8;16) translocation in AMoL is associated with hemophagocytosis. These translocations yield the formation of chimeric proteins (RUNX1-RUNX1T1 and PML-RARA, respectively) which disrupt normal myeloid precursor development.
Secondary leukaemia, which may include AML-M5, has been associated with exposure to epipodophyllotoxins, such as etoposide.[4]
Many cases of AML-M5 are seen to have enhanced phosphorylation of the STAT3 protein due to increased induction of cytokines thus increasing cell proliferation and survival.[5] Finally, genetic mutations involved in epigenetic regulation are associated with this leukemia, as they have downstream effects on cell differentiation and proliferation. Excessive cytokine release could be a byproduct of skewed epigenetic regulation.
Diagnosisedit
In order to fulfill World Health Organization (WHO) criteria for AML-5, a patient must have greater than 20% blasts in the bone marrow, and of these, greater than 80% must be of the monocytic lineage. A further subclassification (M5a versus M5b) is made depending on whether the monocytic cells are predominantly monoblasts (>80%) (acute monoblastic leukemia) or a mixture of monoblasts and promonocytes (<80% blasts). Monoblasts can be distinguished by having a roughly circular nucleus, delicate lacy chromatin, and abundant, often basophilic cytoplasm. These cells may also have pseudopods. By contrast, promonocytes have a more convoluted nucleus, and their cytoplasm may contain metachromatic granules. Monoblasts are typically MPO-negative and promonocytes are MPO variable. Both monoblasts and promonocytes stain positive for non-specific esterase (NSE), however NSE may often be negative.
Immunophenotypically, M5-AML variably express myeloid (CD13, CD33) and monocytic (CD11b, CD11c) markers. Cells may aberrantly express B-cell marker CD20 and the NK marker CD56. Monoblasts may be positive for CD34.
Treatmentedit
AML-M5 is treated with intensive chemotherapy (such as anthracyclines) or with bone marrow transplantation. Tyrosine kinase receptor inhibitors are a prominent treatment developed to combat the over activation of cell proliferation proteins induced by AML-5. Inhibiting the STAT3 protein is another useful form of treatment.[5]
^Kollmannsberger, C.; et al. (Oct 1998). "Secondary leukemia following high cumulative doses of etoposide in patients treated for advanced germ cell tumors". J. Clin. Oncol. 16 (10): 3386–91. doi:10.1200/JCO.1998.16.10.3386. PMID 9779717.
^ abDe Kouchkovsky, I.; Abdul-Hay, M. (July 2016). "'Acute myeloid leukemia: a comprehensive review and 2016 update'". Blood Cancer Journal. 6 (7): e441. doi:10.1038/bcj.2016.50. ISSN 2044-5385. PMC5030376. PMID 27367478.
External linksedit
at hmds.org.uk
October 31, 2023
acute, monocytic, leukemia, amol, type, acute, myeloid, leukemia, leukemic, cells, monocytic, lineage, this, cancer, characterized, dominance, monocytes, bone, marrow, there, overproduction, monocytes, that, body, does, need, periphery, these, overproduced, mo. Acute monocytic leukemia AMoL or AML M5 2 is a type of acute myeloid leukemia In AML M5 gt 80 of the leukemic cells are of monocytic lineage 3 This cancer is characterized by a dominance of monocytes in the bone marrow There is an overproduction of monocytes that the body does not need in the periphery These overproduced monocytes interfere with normal immune cell production which causes many health complications for the affected individual Acute monocytic leukemiaAcute monocytic leukemia with its cytochemical profileSpecialtyHematology oncologyPrognosisFive year survival rate 23 7 1 Contents 1 Causes 2 Diagnosis 3 Treatment 4 References 5 External linksCauses editThe pathology of AML involves abnormal proliferation and differentiation of a population of myeloid stem cells Genetic mutations are identified in the majority of cases A common genetic mutation identified in these cases are characterized as chromosomal translocations where information from one chromosome is exchanged to a non homologous chromosome creating an unusual rearrangement of chromosomes This translocation is often abbreviated as t of one chromosome involved of other chromosome involved M5 is associated with characteristic chromosomal abnormalities often involving chromosome 11 such as t 9 11 affecting the MLL KMTA2 locus at 11q23 however MLL translocations are also found in other leukemia subtypes The t 8 16 translocation in AMoL is associated with hemophagocytosis These translocations yield the formation of chimeric proteins RUNX1 RUNX1T1 and PML RARA respectively which disrupt normal myeloid precursor development Secondary leukaemia which may include AML M5 has been associated with exposure to epipodophyllotoxins such as etoposide 4 Many cases of AML M5 are seen to have enhanced phosphorylation of the STAT3 protein due to increased induction of cytokines thus increasing cell proliferation and survival 5 Finally genetic mutations involved in epigenetic regulation are associated with this leukemia as they have downstream effects on cell differentiation and proliferation Excessive cytokine release could be a byproduct of skewed epigenetic regulation Diagnosis editIn order to fulfill World Health Organization WHO criteria for AML 5 a patient must have greater than 20 blasts in the bone marrow and of these greater than 80 must be of the monocytic lineage A further subclassification M5a versus M5b is made depending on whether the monocytic cells are predominantly monoblasts gt 80 acute monoblastic leukemia or a mixture of monoblasts and promonocytes lt 80 blasts Monoblasts can be distinguished by having a roughly circular nucleus delicate lacy chromatin and abundant often basophilic cytoplasm These cells may also have pseudopods By contrast promonocytes have a more convoluted nucleus and their cytoplasm may contain metachromatic granules Monoblasts are typically MPO negative and promonocytes are MPO variable Both monoblasts and promonocytes stain positive for non specific esterase NSE however NSE may often be negative Immunophenotypically M5 AML variably express myeloid CD13 CD33 and monocytic CD11b CD11c markers Cells may aberrantly express B cell marker CD20 and the NK marker CD56 Monoblasts may be positive for CD34 Treatment editAML M5 is treated with intensive chemotherapy such as anthracyclines or with bone marrow transplantation Tyrosine kinase receptor inhibitors are a prominent treatment developed to combat the over activation of cell proliferation proteins induced by AML 5 Inhibiting the STAT3 protein is another useful form of treatment 5 References edit Leukemia Survival Rates Roswell Park Comprehensive Cancer Center Retrieved March 9 2023 Acute Myeloid Leukemia Signs and Symptoms Acute Monocytic Leukemia an overview ScienceDirect Topics www sciencedirect com Retrieved 2021 03 06 Kollmannsberger C et al Oct 1998 Secondary leukemia following high cumulative doses of etoposide in patients treated for advanced germ cell tumors J Clin Oncol 16 10 3386 91 doi 10 1200 JCO 1998 16 10 3386 PMID 9779717 a b De Kouchkovsky I Abdul Hay M July 2016 Acute myeloid leukemia a comprehensive review and 2016 update Blood Cancer Journal 6 7 e441 doi 10 1038 bcj 2016 50 ISSN 2044 5385 PMC 5030376 PMID 27367478 External links editImage at hmds org uk Retrieved from https en wikipedia org w index php title Acute monocytic leukemia amp oldid 1178776406, wikipedia, wiki, book, books, library,
