Immunotherapy for acute myeloid leukemia (AML): a potent alternative therapy

Acheampong, Desmond Omane; Adokoh, Christian K.; Asante, Du-Bois; Asiamah, Ernest Amponsah; Barnie, Prince Amoah; Bonsu, Dan Osei Mensah; Kyei, Foster

doi:10.1016/j.biopha.2017.10.100

Cited by 36 publications

(26 citation statements)

References 92 publications

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“…However, overall effect and safety of the treatment are still debatable [85,87,88]. The chemotherapies for AML can cause serious side-effects and relapse [89,90].…”

Section: Discussionmentioning

confidence: 99%

Natural Products and Acute Myeloid Leukemia: A Review Highlighting Mechanisms of Action

et al. 2019

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Recent findings have shown great potential of alternative interventions such as immunotherapy and natural products for acute myeloid leukemia (AML). This study aims to review the anti-AML effect of various natural compounds. Natural compounds were classified into five groups: alkaloids, carotenoids, nitrogen-containing compounds, organosulfur compounds or phenolics based on each compound’s chemical properties. Fifty-eight studies were collected and reviewed in this article. Phenolics are the most abundant group to have an apoptotic effect over AML cells, while other groups have also shown significant apoptotic effects. Some compounds induced apoptosis by regulating unique mechanism like human telomerase reverse transcriptase (hTERT) or laminin receptor (67LR), while others modified caspases, poly (adp-ribose) polymerase (PARP) and p53. Further study is required to identify side-effects of potent compounds and the synergistic effects of combination of two or more natural compounds or existing conventional anti-AML drugs to treat this dreadful disease.

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“…However, overall effect and safety of the treatment are still debatable [85,87,88]. The chemotherapies for AML can cause serious side-effects and relapse [89,90].…”

Section: Discussionmentioning

confidence: 99%

Natural Products and Acute Myeloid Leukemia: A Review Highlighting Mechanisms of Action

et al. 2019

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“…The capacity of the immune system to control tumor growth and metastasis has focused attention in order to develop new strategies to treat cancer directed to stimulate the patient immune system such as checkpoint blockade or using engineered immune cells to attack cancer as it is currently used in CAR-T therapies. Thus, novel cancer immunotherapies have emerged in the last decade that are being analyzed in clinical trials in patients with hematologic and solid cancer [ 2 , 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Characterization of the DNAM-1, TIGIT and TACTILE Axis on Circulating NK, NKT-Like and T Cell Subsets in Patients with Acute Myeloid Leukemia

Valhondo

Hassouneh

López-Sejas

et al. 2020

Cancers

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Background: Acute myeloid leukemia (AML) remains a major clinical challenge due to poor overall survival, which is even more dramatic in elderly patients. TIGIT, an inhibitory receptor that interacts with CD155 and CD112 molecules, is considered as a checkpoint in T and NK cell activation. This receptor shares ligands with the co-stimulatory receptor DNAM-1 and with TACTILE. The aim of this work was to analyze the expression of DNAM-1, TIGIT and TACTILE in NK cells and T cell subsets in AML patients. Methods: We have studied 36 patients at the time of diagnosis of AML and 20 healthy volunteers. The expression of DNAM-1, TIGIT and TACTILE in NK cells and T cells, according to the expression of CD3 and CD56, was performed by flow cytometry. Results: NK cells, CD56− T cells and CD56+ T (NKT-like) cells from AML patients presented a reduced expression of DNAM-1 compared with healthy volunteers. An increased expression of TIGIT was observed in mainstream CD56− T cells. No differences were observed in the expression of TACTILE. Simplified presentation of incredibly complex evaluations (SPICE) analysis of the co-expression of DNAM-1, TIGIT and TACTILE showed an increase in NK and T cells lacking DNAM-1 and co-expressing TIGIT and TACTILE. Low percentages of DNAM-1−TIGIT+TACTILE+ NK cells and DNAM-1− TIGIT+TACTILE+ CD56− T cells were associated with a better survival of AML patients. Conclusions: The expression of DNAM-1 is reduced in NK cells and in CD4+ and CD8+ T cells from AML patients compared with those from healthy volunteers. An increased percentage of NK and T cells lacking DNAM-1 and co-expressing TIGIT and TACTILE is associated with patient survival, supporting the role of TIGIT as a novel candidate for checkpoint blockade.

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“…Currently, the management of AML is divided into induction phase and consolidation phase [4,5]. Chemotherapy is a standard treatment option applied in both induction and consolidation phases to destroy leukemic cells [6].…”

Section: Introductionmentioning

confidence: 99%

TRIM31 promotes acute myeloid leukemia progression and sensitivity to daunorubicin through the Wnt/β-catenin signaling

Xiao

Deng

et al. 2020

Bioscience Reports

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Tripartite motif (TRIM) 31 is a member of TRIM family and exerts oncogenic role in the progression and drug resistance of several cancers. However, little is known about the relevance of TRIM31 in acute myeloid leukemia (AML). Herein, we investigated the role of TRIM31 in AML. We examined the expression levels of TRIM31 in the blood samples from 34 patients with AML and 34 healthy volunteers using qRT-PCR. The mRNA levels of TRIM31 in human bone marrow stromal cells (HS-5) and five AML cell lines were also detected. Loss/gain-of-function assays were performed to assess the role of TRIM31 in AML cells proliferation, apoptosis and sensitivity to daunorubicin. The expression levels of pro-caspase 3, cleaved caspase 3, Wnt3a, β-catenin, cyclin D1 and c-Myc were measured using Western blot. TRIM31 expression levels were significantly up-regulated in AML patients and cell lines. Knockdown of TRIM31 suppressed cell proliferation and promoted apoptosis in AML-5 and U937 cells. The IC50 of daunorubicin was significantly decreased in TRIM31 siRNA (si-TRIM31) transfected cells. Oppositely, induced cell proliferation and decreased cell apoptosis were observed in pcDNA-3.1-TRIM31 transfected cells. Furthermore, knockdown of TRIM31 suppressed the activation of Wnt/β-catenin pathway in AML cells. Activation of Wnt/β-catenin pathway by LiCl abolished the effects of si-TRIM31 on cell proliferation, apoptosis and sensitivity to daunorubicin in AML cells. In conclusion, the results indicated that TRIM31 promoted leukemogenesis and chemoresistance to daunorubicin in AML. The oncogenic role of TRIM31 in AML was mediated by the Wnt/β-catenin pathway. Thus, TRIM31 might serve as a therapeutic target for the AML treatment.

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Immunotherapy for acute myeloid leukemia (AML): a potent alternative therapy

Cited by 36 publications

References 92 publications

Natural Products and Acute Myeloid Leukemia: A Review Highlighting Mechanisms of Action

Natural Products and Acute Myeloid Leukemia: A Review Highlighting Mechanisms of Action

Characterization of the DNAM-1, TIGIT and TACTILE Axis on Circulating NK, NKT-Like and T Cell Subsets in Patients with Acute Myeloid Leukemia

TRIM31 promotes acute myeloid leukemia progression and sensitivity to daunorubicin through the Wnt/β-catenin signaling

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