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Haematology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
The bone marrow in myelomonocytic leukaemia (Fig. 11.17) shows a mixture of myeloblasts and monocytes (French–US–UK classification, AMLM4 subtype). Figure11.18 shows the features of monocytic leukaemia (AML-M5) (monomorphic population of monoblasts). A significant proportion of the neonatal leukaemias have 11q23 chromosomal abnormalities.
M
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Monocytic Leukemia [Greek: monos, alone + kytos, cell + leukos, white + haima, blood] Described by Hamburg physician Hassan Reschad and V. Schiling-Torgau in 1913. Until 1930 only 16 cases were identified in the literature and William Dameshek (1900–1969) recorded two cases. A critical review with a complete bibliography was given by Otto Naegeli (1871–1938) in 1931.
Benzene Hematotoxicity
Published in Muzaffer Aksoy, Benzene Carcinogenicity, 2017
The findings of bone marrow were not consistent with the diagnosis of monocytic leukemia. These facts would indicate that there may be some benefit in reevaluating the relationship between monocytosis and chronic benzene toxicity, but it should also be remembered that young lymphocytes, especially in response to irritation, can resemble monocytes. We frequently encountered such lymphocytes in the peripheral blood of the workers that were exposed to benzene; we called them young or atypical lymphocytes.64 On the other hand, in their study among 100 workers exposed to benzene and its homologs, Moszczynski and Lisiewicz113 have established an increased count of monocytes compared to controls.
Importance of distinguishing the promonocyte in leukemia
Published in Baylor University Medical Center Proceedings, 2020
John R. Krause, Arthur Bredeweg
The acute monocytic leukemias are composed of a monoblastic variant and a monocytic variant.1,2 They are morphologically distinguished by the relative proportions of monoblasts and promonocytes. In acute monoblastic leukemia, ≥80% of the cells are monoblasts, whereas in acute monocytic leukemia, most cells are promonocytes or monocytes. Both types require ≥20% blasts. The promonocyte is considered a “blast equivalent.” Monoblasts have round nuclei with delicate lacy chromatin and one or more prominent nucleoli (Figure 1a).3 Promonocytes have irregular and convoluted fine lacy nucleoli with basophilic finely granulated cytoplasm and varying numbers of granules and/or vacuoles (Figure 1b).3 We report a case of acute monocytic leukemia in which the promonocytes morphologically masqueraded as promyelocytes.
Curcumin inhibited the growth and invasion of human monocytic leukaemia SHI-1 cells in vivo by altering MAPK and MMP signalling
Published in Pharmaceutical Biology, 2020
Guohua Zhu, Qun Shen, Hong Jiang, Ou Ji, Lingling Zhu, Linyang Zhang
Acute myeloid leukaemia (AML) is a heterogeneous haematologic malignancy characterized by the clonal expansion of immature myeloid cells and bone marrow failure (Saultz and Garzon 2016). The complete remission rates of acute monocytic leukaemia are relatively low in the clinic, and a considerable number of patients die due to chemotherapy drug resistance as well as intramedullary and extramedullary relapse. AML is the most common form of acute leukaemia among adults, and it accounts for the largest number of annual deaths from leukaemia in the United States. An estimated 21,450 people are expected to be diagnosed with AML, and 10,920 patients are expected to die of AML in 2019 (Siegel et al. 2019).
Hsa-circ_0003420 induces apoptosis in acute myeloid leukemia stem cells and impairs stem cell properties
Published in Immunopharmacology and Immunotoxicology, 2021
Guoqiang Lin, Yingying Fei, Yanming Zhang
Acute monocytic leukemia (AML) can spread to the gums, spleen, liver, and lymphonodus outside the marrow and is influenced by many factors. Approximately 80–90% of patients can achieve complete remission from chemotherapy, but relapses are common, and the five-year event-free survival rate is about 50% [1]. However, currently, the progression and etiology of AML are insufficiently understood. Previous studies using various experimental models have indicated that AML originates from a small population of LSCs [2].