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A tired old lady
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
The symptoms of AML are caused by the clonal expansion of malignant myeloid precursor cells in the marrow and blood, causing bone marrow failure and infiltration of other organs. AML is classified according to the morphology of the most common blast cells found on examination of the marrow.
Leukemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
AML accounts for nearly 80% of all adult acute leukemias with an annual incidence of approximately 3.55 per 100,000 adults; its incidence increases progressively with age to greater than 20 per 100,000 adults aged 80 years or older. In contrast, AML accounts for 10% of childhood leukemias with an annual incidence of less than 1 per 100,000 children.9 The median age at diagnosis is about 70 years. Some subtypes, such as APL, are more common in younger adults, with a median age of 40 years, and in the United States, appear to affect Hispanics more than any other races/ethnicities. The incidence of APL is about 0.33 per 100,000 persons. Among the risk factors for AML are ARCH/CHIP, chronic myeloproliferative diseases, MDS, paroxysmal nocturnal hemoglobinuria (PNH), and therapy-related causes, such as radiotherapy and drugs. Indeed, therapy-related AML is now recognized as a subgroup of the 2016 WHO classification of AML, classified as a therapy-related myeloid neoplasm (t-MN), which also includes therapy-related MDS (t-MDS).
Familial Acute Myeloid Leukemia
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Acute myeloid leukemia (AML) is a hematologic malignancy that results from a clonal proliferation of myeloid blasts, with extreme underlying genetic heterogeneity in the disease, involving sporadic or de novo genesis, and secondary to preexisting myelodysplastic syndromes. The latter are pre-leukemic disorders characterized by ineffective hematopoiesis, cytopenias, often with detected clonal cytogenetic abnormalities, and a propensity to progress to secondary AML [1]. A clinical history of AML affecting more than one family member is uncommon but may occur in both de novo and secondary AML, with the latter including preexisting myelodysplastic syndromes in familial cases. While families with multiple individuals affected by acute leukemia were described in the 1960s and 1970s, a genetic basis for familial AML was not identified until 1990, when germline aberrations in the TP53 gene were linked to Li–Fraumeni syndrome, wherein multiple hematopoietic and non-hematopoietic malignancies may occur, including frequently AML [2,3].
Endoplasmic reticulum stress-related signature predicts prognosis and immune infiltration analysis in acute myeloid leukemia
Published in Hematology, 2023
Lu Dong, Haili Wang, Zefeng Miao, Yanhui Yu, Dongzheng Gai, Guoxiang Zhang, Li Ge, Xuliang Shen
Acute myeloid leukemia (AML) is a malignant disease of myeloid stem/progenitor cells. The primary causes of AML are genetic and cytogenetic alterations [1]. Recent evidence indicates that the identification of novel AML biomarkers could contribute to a better understanding of the molecular basis of this disease [2]. However, some patients with relapsed and refractory AML and older patients have a poor prognosis, which is currently a challenging issue. The WHO also recently released the fifth edition of the Classification of Hematolymphoid Tumours [3], and the European Leukemia Net (ELN) recently published a revised system (ELN-2017) [4]. The authors used molecular genetic changes as risk stratification criteria, such as the presence of NPM1, FLT3-ITD, and CEBPA, to indicate a favorable prognosis and the presence of TP53, RUNX1, and ASX1, to indicate a poor prognosis. With the development of many molecularly targeted drugs, new mutated genes to modify the genetic risk stratification system and accommodate the progression of treatment strategies must be continued.
The role of autophagy in acute myeloid leukemia development
Published in Expert Review of Anticancer Therapy, 2023
Martyna Bednarczyk, Karolina Kociszewska, Olga Grosicka, Sebastian Grosicki
Acute myeloid leukemia (AML) as a most common type of acute leukemia in adults, originates from various aberrations and alterations of hematopoietic cells. The critical point is the suppression of myeloid differentiation and overproliferation of leukemia blasts [10,11]. It leads to subsequent bone marrow insufficiency [12]. AML could develop ‘de novo’ or as the consequence of previous hematological disorder or therapy (e.g. chemotherapy with alkylating agents) [10]. It is associated with poor overall survival and prognosis and high risk of relapse [12,13]. The symptoms and clinical manifestations of AML are the consequence of the bone marrow and other organs infiltration with undifferentiated myeloid cells: blood cytopenia (anemia, thrombocytopenia), weight loss, fatigue, FUO (fever of unknown origin), night sweats. The goal of the therapy is to achieve complete remission and it consists of induction and consolidation in order to eradicate any residual disease. However, progress in standard chemotherapy definitely improved the outcome of treatment, still there is a lot to uncover especially in elderly patients [10]. Simultaneously poor prognosis and clinical response are related to AML genetic background. This aspect triggered research to search for molecular targeted therapy [12]. Moreover, also other than genetic mechanism, like cellular processes – e.g. autophagy, were profoundly investigated [11,12]. Autophagy seems to be impaired in AML individuals and it could be responsible for drug resistance [12].
MiR-140 targets lncRNA FAM230B to suppress cell proliferation in acute myeloid leukemia running title: MiR-140 targets FAM230B in AML
Published in Hematology, 2022
Yan Wang, Fangfang Wang, Yang Lu, Yan Li, Haonan Ran, Feihu Yan, Yuyang Tian
As a type of malignancy originating from bone marrow, Acute myeloid leukemia (AML) is characterized by the arrested hematopoietic precursors as early developmental stages [1]. AML has been reported to be closely correlated with several risk factors, such as drug exposures, environmental exposures, familial syndromes, and antecedent hematologic disorders. However, most de novo AML patients show no identifiable risk factors [2,3], suggesting the complex molecular mechanism of this disease [4,5]. AML patients are usually treated with combined treatment of chemotherapy and radiotherapy, and bone marrow transplant is also performed in some cases [6,7]. However, even with active treatment, the overall survival of AML patients is still poor. It is estimated that only fewer than 25% of AML patients can survive 5 years after diagnosis [8]. Therefore, more therapeutic approaches are needed.