Despite recent advancements in the therapeutic landscape of acute myeloid leukemia (AML), the prognosis of patients remains poor. Immune check point inhibitors have been investigated in hematological malignancies, including AML; however, the role of T-cell immunoglobulin and mucin domain 3 (TIM-3) in AML has not yet been fully elucidated. Thus, the present study aimed to investigate TIM-3 gene expression in patients with AML and determine its associations with prognostic variables and clinical outcome. A total of 60 patients newly diagnosed with AML and 15 healthy matching individuals were recruited in the present study, and reverse transcription-quantitative PCR analysis was performed to detect TIM-3 expression. The results demonstrated that TIM-3 expression was significantly upregulated in patients with AML compared with that in healthy individuals (P<0.001). In addition, patients with extramedullary disease (EMD) exhibited significantly lower median TIM-3 expression levels compared with those without EMD (P=0.001). Furthermore, patients with high TIM-3 expression had significantly lower complete remission rates following induction chemotherapy compared with those with low TIM-3 expression (P=0.004). High TIM-3 expression was significantly associated with lower overall survival rates during the 1-year follow-up (P=0.001). Taken together, the results of the present study suggest that TIM-3 may act as a biomarker of a poor prognosis in patients with AML, and be used as a therapeutic target.
The mechanism of the well observed hypercoagulability and high incidence of Thromboembolic Events (TE) in β- thalassemia patients has not been fully elucidated. This study aimed to evaluate evaluate the endothelial dysfunction and monocyte activation among adult Egyptian β-thalassemic patients and assess their role in the hypercoagulability and development of TE. A total of 40 adults patients with bthalassemics and 20 healthy age and sex-matched controls were assessed for endothelial dysfunction using serum Von Willebrand Factor Antigen (VWFAg) and for monocytic activation using flow cytometric assessment of CD14 monocyte microparticles and CD11b activated monocytes. The VWF:Ag level was significantly higher among thalassemic patients (P<0.001) and was positively correlated to development of TE (P<0.05). There was no significance difference for CD14 between patients and controls (P>0.5) and CD11b was higher in controls (P=0.004) with no significant correlation between both and TE development (P>0.05). VWF:Ag is increased in thalassemic patients and could be used as a risk factor for thrombosis in these patients, while no identified role of activated monocytes in thrombotic tendency in such patients.
One of the fundamental hallmarks of cancer is the incapacity of the immune system to eliminate malignancy. Cytotoxic T‐lymphocyte antigen‐4 (CTLA‐4) and lymphocyte activation gene‐3 (LAG‐3) are considered major inhibitory immune checkpoints expressed on T cells. In this study, we investigated mRNA expression of CTLA‐4 and LAG‐3, as well as their diagnostic and prognostic value in acute myeloid leukemia (AML) patients. The study involved 60 AML patients and 15 controls. Significantly up‐regulated CTLA‐4 (P = .005) and LAG‐3 (P = .02) mRNA expressions were found in AML patients as compared with the healthy control group. AML patients with unfavorable prognosis also showed significant up‐regulation of CTLA‐4 (P = .006) and LAG‐3 (P = .001) mRNA expressions as compared with those with favorable prognosis. Moreover, multiple stepwise linear regression analysis confirmed that patients prognosis was an independent predictor of both CTLA‐4 (P = .003) and LAG‐3 (P < .001) expression levels. Receiver‐operating characteristic (ROC) curve using combined CTLA‐4 and LAG‐3 expression showed good diagnostic value for AML (area under the curve [AUC] = 0.80, sensitivity = 80%, specificity = 80% for a cut‐off probability >.619) as well as moderate predictive value for unfavorable prognosis (AUC = 0.760, sensitivity = 70%, specificity =100% for a cut‐off probability >.617). It is clear from this current study that both CTLA‐4 and LAG‐3 may be promising prognostic markers in AML patients.
Background One of the crucial functions of the immune system is to prevent tumorigenesis, yet cancer occurs when malignant cells manage to evade immune surveillance via multiple strategies. Accordingly, this study aimed at assessing the potential significance of the novel immune checkpoint B and T lymphocyte attenuator (BTLA) as a prognostic marker in acute myeloid leukemia (AML), in addition to how it relates to response to treatment and patients’ survival. Thus, mRNA expression of BTLA was investigated on peripheral blood in 60 AML patients and 15 healthy controls. Results BTLA expression was found to be significantly elevated (p = 0.024) in the tested AML cases in comparison with healthy controls. Moreover, BTLA was over-expressed in the CD13, CD33, and HLA-DR positive cases as compared to their negative counterparts (p = 0.003; p < 0.001, and p = 0.001, respectively), and cases showing BTLA over-expression had significantly poorer overall survival times (p = 0.001) as confirmed by Kaplan–Meier survival analysis. Conclusion These observations suggest that BTLA over-expression may be associated with reduced immunity against tumors and could be recommended as a promising biomarker for unfavorable prognosis in AML.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.