Study of T-cell immunoglobulin and mucin domain-3 expression profile in peripheral blood and bone marrow of human acute lymphoblastic leukemia patients

Balajam, Narges Zargar; Shabani, Mahdi; Aghaei, Mahmoud; Haghighi, Mansoureh; Kompani, Farzad

doi:10.4103/jrms.jrms_759_19

Cited by 5 publications

(2 citation statements)

References 29 publications

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“…In a primary study, we examined the expression of TIM-3 and mucin-domain 3 as one of the molecules present in the ALL pathway. Our results indicated that TIM-3 expression was increased in the peripheral blood and bone marrow of these patients ( 18 ). Therefore, in the extension of our previous study here we aimed to investigate the effects of galectin-9 (as a TIM-3 ligand) on the proliferation and apoptosis on ALL cell lines.…”

Section: Introductionsupporting

confidence: 50%

Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation

Balajam

Shabani

Aghaei

2021

Research in Pharmaceutical Sciences

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Background and purpose: Acute lymphoblastic leukemia (ALL) is a type of cancer of blood and bone marrow characterized by abnormal proliferation of lymphoid progenitor cells. Galectin-9 is a tandem-repeat type galectin expressed in various tumor cells. It seems that the connection between galectin-9 and T cell immunoglobulin mucin-3 receptor acts as a negative regulator of cancer cells proliferation. Experimental approach: In this research, the effects of galectin-9 were investigated using MTS cell proliferation colorimetric, colony-forming, annexin V-FITC/PI, and caspase-3 assays in the Jurkat and KE-37 cell lines of ALL. Furthermore, the western blotting technique was used to evaluate the levels of apoptotic proteins such as Bax and Bcl-2 in these cell lines. Findings/Results: Our results indicated that galectin-9 can considerably reduce the cell growth and colony formation ability of both Jurkat and KE-37 cell lines in a concentration-dependent manner. Besides, galectin-9 induced apoptosis in a concentration-dependent manner in ALL cells by a mechanism associated with Bax/Bcl-2 expression and activation of the caspase-3 activation. Conclusion and implications: Galectin-9 inhibited the growth and proliferation of cell lines with increased programmed cell death, therefore it can be considered as a potential factor in the progression of ALL therapeutics that needs more research in this context.

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Section: Introductionsupporting

confidence: 50%

Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation

Balajam

Shabani

Aghaei

2021

Research in Pharmaceutical Sciences

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“…In a more recent study, Balajam et al. included both B-ALL and T-ALL cases and documented TIM-3 overexpression in bone marrow and peripheral blood mononuclear cells (PBMCs) in ALL patients compared to control individuals ( 69 ) ( Table 1 ). Thus, more studies regarding the possible diagnostic and/or prognostic value of TIM-3 in ALL are recommended.…”

Section: Alterations In Tim-3 Expression In Patients With Leukemiamentioning

confidence: 99%

TIM-3 in Leukemia; Immune Response and Beyond

et al. 2021

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T cell immunoglobulin and mucin domain 3 (TIM-3) expression on malignant cells has been reported in some leukemias. In myelodysplastic syndrome (MDS), increased TIM-3 expression on TH1 cells, regulatory T cells, CD8+ T cells, and hematopoietic stem cells (HSCs), which play a role in the proliferation of blasts and induction of immune escape, has been reported. In AML, several studies have reported overexpression of TIM-3 on leukemia stem cells (LSCs) but not on healthy HSCs. Overexpression of TIM-3 on exhausted CD4+ and CD8+ T cells and leukemic cells in CML, ALL, and CLL patients could be a prognostic risk factor for poor therapeutic response and relapse in patients. Currently, several TIM-3 inhibitors are used in clinical trials for leukemias, and some have shown encouraging response rates for MDS and AML treatment. For AML immunotherapy, blockade TIM-3 may have dual effects: directly inhibiting AML cell proliferation and restoring T cell function. However, blockade of PD-1 and TIM-3 fails to restore the function of exhausted CD8+ T cells in the early clinical stages of CLL, indicating that the effects of TIM-3 blockade may be different in AML and other leukemias. Thus, further studies are required to evaluate the efficacy of TIM-3 inhibitors in different types and stages of leukemia. In this review, we summarize the biological functions of TIM-3 and its contribution as it relates to leukemias. We also discuss the effects of TIM-3 blockade in hematological malignancies and clinical trials of TIM-3 for leukemia therapy.

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Unraveling the Esophageal Cancer Tumor Microenvironment: Insights and Novel Immunotherapeutic Strategies

Khan

Ali

Hashem

et al. 2023

Interdisciplinary Cancer Research

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Study of T-cell immunoglobulin and mucin domain-3 expression profile in peripheral blood and bone marrow of human acute lymphoblastic leukemia patients

Cited by 5 publications

References 29 publications

Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation

Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation

TIM-3 in Leukemia; Immune Response and Beyond

Unraveling the Esophageal Cancer Tumor Microenvironment: Insights and Novel Immunotherapeutic Strategies

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