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Peripheral blood mRNA expression of IL37, IL1F10, and C17orf99 genes is altered in patients with B-acute lymphoblastic leukemia: a case-control study

  • Noor T. Kadhim,
  • Reema M. Abed

摘要

Background

Acute lymphoblastic leukemia (ALL) is a hematological malignancy of two main types, B-ALL and T-ALL, with B-ALL being the most common. Growing evidence suggests that B-ALL pathophysiology is linked to immune system dysfunction in which cytokines play a pivotal role. Interleukin (IL)-37, IL-38, and IL-40, encoded by IL37, IL1F10, and C17orf99 genes, respectively, are novel cytokines involved in regulating immune functions and are proposed to influence cancer pathogenesis. However, these cytokines have not been studied in B-ALL, either genetically or phenotypically. Therefore, this research aimed to evaluate gene expression of IL37, IL1F10, and C17orf99 to explore their association with B-ALL.

Methods

A case-control study was conducted on 114 B-ALL patients and 100 controls. A quantitative analysis based on real-time PCR was performed to measure IL37, IL1F10, and C17orf99 mRNA expression levels in peripheral blood.

Results

IL37 (probability < 0.001) and C17orf99 (probability < 0.001) expression levels were significantly lower, while IL1F10 expression levels (probability < 0.001) were significantly higher in B-ALL patients compared to controls. Multiple binary logistic regression analysis demonstrated that mRNA expression of these genes was significantly associated with B-ALL. However, the estimated area under the curve (AUC) indicated that the discriminatory performance (B-ALL versus controls) was fair for IL37 (AUC = 0.77), poor for IL1F10 (AUC = 0.69), and considerable for C17orf99 (AUC = 0.82).

Conclusions

IL37 and C17orf99 genes showed downregulated expression, while IL1F10 gene showed upregulated expression in B-ALL. Dysregulated expression of these genes was associated with B-ALL and may be of significance in disease identification. However, further research is warranted to understand these molecular vulnerabilities in B-ALL.