Acute myeloid leukaemia in adults

Ferrara, Felicetto; Schiffer, Charles A.

doi:10.1016/s0140-6736(12)61727-9

Cited by 473 publications

(418 citation statements)

References 133 publications

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“…AML is a heterogeneous clonal disorder in which hematopoietic progenitor cells lose their ability to differentiate normally and respond to normal regulators of proliferation and apoptosis (Ferrara and Schiffer, 2013). DNA repair systems have a key role in maintaining genome integrity and stability.…”

Section: Discussionmentioning

confidence: 99%

“…Acute myeloid leukemia (AML) is a type of cancer in which hematopoietic progenitor cells lose the ability to differentiate normally and respond to normal regulators of proliferation and apoptosis (Ferrara and Schiffer, 2013). The etiology of AML was found to be multifactorial and there are some environmental factors that may potentially play a role in susceptibility, including radiation, smoking, obesity, and exposure to chemical carcinogens (Ilhan et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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135G/C polymorphism in the RAD51 gene and acute myeloid leukemia risk: a meta-analysis

Long

Dai

2016

Genet. Mol. Res.

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ABSTRACT. Numerous studies have evaluated the association between the 135G/C polymorphism in the RAD51 gene and risk of acute myeloid leukemia (AML), but the results have been inconsistent. The aim of this study is to precisely examine the association between the 135G/C polymorphism in the RAD51 gene and AML risk through a meta-analysis. PubMed, Google Scholar, and Web of Science databases were systematically searched to identify relevant studies from their inception to June 2015. Pooled odds ratios (OR) with 95% confidence intervals (95%CI) were calculated using fixed-or random-effect models. A total of 6 case-control studies containing 1432 patients and 2750 controls were used in this meta-analysis, and our results showed no association between the 135G/C polymorphism in the RAD51 gene and AML risk (CC vs GG: OR = 1.67, 95%CI = 0.93-3.02; GC vs GG: OR = 1.24, 95%CI = 0.80-1.92; the dominant model: OR = 1.26, 95%CI = 0.83-1.91; the recessive model: OR = 1.63, 95%CI = 0.90-2.95). No publication bias was found in this study. In summary, the present meta-analysis suggests that the 135G/C polymorphism in the RAD51 gene may not be associated with AML risk. However, further studies with larger cohorts are needed to confirm this conclusion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

135G/C polymorphism in the RAD51 gene and acute myeloid leukemia risk: a meta-analysis

Long

Dai

2016

Genet. Mol. Res.

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“…AML is the most common type of acute leukemia, and accounts for ~80% of all cases of acute leukemia in adults (2). AML is a clonal disorder caused by rapid proliferation, accumulation and differentiation arrest of hematopoietic progenitors in the bone marrow and blood (3). It was predicted that in 2015, there would be 20,830 new cases and 10,460 mortalities due to AML in the United States (4).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA 217 inhibits cell proliferation and enhances chemosensitivity to doxorubicin in acute myeloid leukemia by targeting KRAS

Xiao

Deng

et al. 2017

Oncology Letters

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Abstract. Acute myeloid leukemia (AML) is a heterogeneous malignant disorder derived from the myeloid hematopoietic cells that accounts for ~80% of all adult acute leukemia. Numerous studies have shown that drug resistance not only exists against conventional chemotherapeutic drugs, but also limits the efficacy of new biological agents. Therefore, it is important to identify the mechanisms behind chemoresistance and seek therapeutic strategies to enhance efficacy in AML chemotherapy. MicroRNA (miR)-217 has been recognized as a tumor suppressor that is downregulated in various types of cancer, however the mechanisms behind the expression and function of miR-217 in AML have not yet been recognized. The expression of miR-217 was determined by quantitative polymerase chain reaction (qPCR). Following transfection with miR-217 mimics, an MTT assay, chemosensitivity assay, cell apoptosis assay and western blot analysis were performed in AML cell lines. Functional assays were also performed to explore the effects of endogenous Kirsten rat sarcoma viral oncogene homolog (KRAS) in AML. The results revealed that miR-217 was downregulated in patients with AML. Overexpression of miR-217 inhibited cellular proliferation and enhanced cell chemosensitivity to doxorubicin by the cell apoptosis pathway in AML cells. A dual-luciferase reporter assay demonstrated that KRAS was a direct target gene of miR-217 in vitro. qPCR and western blot analysis revealed that miR-217 negatively regulated KRAS protein expression, but had no impact on KRAS mRNA expression. Knockdown of KRAS expression markedly suppressed AML cellular proliferation, and enhanced cell chemosensitivity to doxorubicin via the cell apoptosis pathway. These findings indicate that miR-217 functions as a tumor suppressor in AML by directly targeting KRAS. Therefore, miR-217-based therapeutic strategies may provide a novel strategy for the enhancement of efficacy in the treatment of AML.

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“…Acute myeloid leukemia (AML) is a clonal disease characterized by the proliferation and accumulation of myeloid progenitor cells in the bone marrow, which ultimately leads to hematopoietic failure (1). Chromosome translocations are frequently present in AML and are important in leukemia development (2).…”

Section: Introductionmentioning

confidence: 99%

Macrocalyxin A inhibits proliferation and induces apoptosis of t (8;21) leukemia cells through mitochondrial signaling pathways and regulates AML-ETO mRNA expression

Wang

Xia

et al. 2015

Molecular Medicine Reports

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Abstract. Progress in the last decade has improved the treatment of acute myeloid leukemia (AML); however, the treatment of AML is also demanding and better treatments are required. The present study aimed to examine the antiproliferative and proapoptotic effects of macrocalyxin A (MA), a novel deterpenid compound, on AML cells. It was identified that MA significantly inhibits kasumi-1 cell proliferation in a time-and dose-dependent manner. Furthermore, low concentrations of MA were able to induce kasumi-1 cell differentiation; however, high concentrations of MA induced kasumi-1 cell apoptosis. MA was also able to increase the expression of mitochondrial membrane protein in a dose-dependent manner while the ∆Ψm was reduced. Additionally, Bad expression in kasumi-1 cells was increased when treated with MA, indicating that the intrinsic apoptotic pathway may be important in MA-induced kasumi-1 cell apoptosis, where the mitochondrial permeability transition pore is opened and the ΔΨm is reduced. In addition, it was demonstrated that AML-ETO mRNA may also be important in MA-induced apoptosis.

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Acute myeloid leukaemia in adults

Cited by 473 publications

References 133 publications

135G/C polymorphism in the RAD51 gene and acute myeloid leukemia risk: a meta-analysis

135G/C polymorphism in the RAD51 gene and acute myeloid leukemia risk: a meta-analysis

MicroRNA 217 inhibits cell proliferation and enhances chemosensitivity to doxorubicin in acute myeloid leukemia by targeting KRAS

Macrocalyxin A inhibits proliferation and induces apoptosis of t (8;21) leukemia cells through mitochondrial signaling pathways and regulates AML-ETO mRNA expression

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