ARID5B gene polymorphisms and the risk of childhood acute lymphoblastic leukemia: a meta-analysis

Yang, Jule; Liu, Yini; Bi, Yang; Wang, Hong

doi:10.1007/s12185-019-02658-2

Cited by 10 publications

(7 citation statements)

References 33 publications

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“…It is a co-activator that binds to the 5′-AATA(CT)-3′ sequence [ 43 ]. The rs10821936 is a variant located in intron 3, and variants present in this intron are the most associated with susceptibility to ALL [ 44 , 45 , 46 , 47 ]. Although its role in leukemogenesis is not fully understood, SNPs in intron 3 of ARID5B may alter the transcription network involving normal hematopoiesis, thus, altering cell growth and differentiation [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia

Pantoja

Azevedo²,

Carvalho

et al. 2022

Genes

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Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm derived from the balanced reciprocal translocation of chromosomes 9 and 22 t (9q34 and 22q11), which leads to the formation of the Philadelphia chromosome and fusion of the BCR-ABL genes. The first-line treatment for CML is imatinib, a tyrosine kinase inhibitor that acts on the BCR-ABL protein. However, even though it is a target-specific drug, about 25% of patients do not respond to this treatment. The resistance mechanisms involved in this process have been investigated and studies have shown that germinal alterations can influence this mechanism. The aim of this work was to investigate 32 polymorphisms in 24 genes of carcinogenic pathway to verify the influence of these genetic variants on the response to treatment with imatinib. Our results demonstrated that individuals with the recessive GG genotype for the rs2372536 variant in the ATIC gene are approximately three times more likely to experience treatment failure with imatinib (p = 0.045, HR = 2.726, 95% CI = 0.9986–7.441), as well as individuals with the TT genotype for the rs10821936 variant in the ARID5B gene, who also have a higher risk for treatment failure with imatinib over time (p = 0.02, HR = 0.4053, IC 95% = 0.1802–0.911). In conclusion, we show that variants in the ATIC and ARIDB5 gene, never screened in previous studies, could potentially influence the therapeutic response to imatinib in patients treated for CML.

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Section: Discussionmentioning

confidence: 99%

Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia

Pantoja

Azevedo²,

Carvalho

et al. 2022

Genes

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“…In addition, Wang et al indicated that the ARID5B SNPs were associated with higher MTX-PGs levels in B lymphocytes, which provides a possible explanation for the stronger response of B-ALL to MTX ( Wang et al, 2020 ).Csordas et al found that the ARID5B rs4948502, rs4948496, and rs4948487 were associated with MTX serum levels and there were significant associations between hepatotoxicity and the ARID5B rs4948502 in patients who received 5 g/m 2 MTX ( Csordas et al, 2014 ). Further, a meta-analysis indicated that the ARID5B variants rs10821936, rs10994982, and rs7089424 were significantly related to the increased risk of childhood ALL ( Yang et al, 2019 ). Collectively, the ARID5B variants were related to MTX serum levels and the increased risk of childhood ALL.…”

Section: Gene Polymorphisms In the Folate Pathwaymentioning

confidence: 99%

Association between high-dose methotrexate-induced toxicity and polymorphisms within methotrexate pathway genes in acute lymphoblastic leukemia

Wang

et al. 2022

Front. Pharmacol.

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Methotrexate (MTX) is a folic acid antagonist, the mechanism of action is to inhibit DNA synthesis, repair and cell proliferation by decreasing the activities of several folate-dependent enzymes. It is widely used as a chemotherapy drug for children and adults with malignant tumors. High-dose methotrexate (HD-MTX) is an effective treatment for extramedullary infiltration and systemic consolidation in children with acute lymphoblastic leukemia (ALL). However, significant toxicity results in most patients treated with HD-MTX, which limits its use. HD-MTX-induced toxicity is heterogeneous, and this heterogeneity may be related to gene polymorphisms in related enzymes of the MTX intracellular metabolic pathway. To gain a deeper understanding of the differences in toxicity induced by HD-MTX in individuals, the present review examines the correlation between HD-MTX-induced toxicity and the gene polymorphisms of related enzymes in the MTX metabolic pathway in ALL. In this review, we conclude that only the association of SLCO1B1 and ARID5B gene polymorphisms with plasma levels of MTX and MTX-related toxicity is clearly described. These results suggest that SLCO1B1 and ARID5B gene polymorphisms should be evaluated before HD-MTX treatment. In addition, considering factors such as age and race, the other exact predictor of MTX induced toxicity in ALL needs to be further determined.

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“…Several meta-analyses systematically reviewing the independent association studies also highlighted the strong impact of ARID5B SNPs on the enhanced risk of childhood ALL (Guo et al, 2014;Zeng et al, 2014;Yang et al, 2019). Collectively, it is reasonable to state that unequivocal evidence has been provided for inherited genetic background of ALL pathogenesis with ARID5B serving as one of the most critical loci.…”

Section: Impact Of Arid5b Snp Genotype On All Susceptibilitymentioning

confidence: 99%

The Role of ARID5B in Acute Lymphoblastic Leukemia and Beyond

et al. 2020

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Acute lymphoblastic leukemia (ALL) is the most common malignancy in children with distinct characteristics among different subtypes. Although the etiology of ALL has not been fully unveiled, initiation of ALL has been demonstrated to partly depend on genetic factors. As indicated by several genome wide association studies (GWASs) and candidate gene analyses, ARID5B, a member of AT-rich interactive domain (ARID) protein family, is associated with the occurrence and prognosis of ALL. However, the mechanisms by which ARID5B genotype impact on the susceptibility and treatment outcome remain vague. In this review, we outline developments in the understanding of ARID5B in the susceptibility of ALL and its therapeutic perspectives, and summarize the underlying mechanisms based on the limited functional studies, hoping to illustrate the possible mechanisms of ARID5B impact and highlight the potential treatment regimens.

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ARID5B gene polymorphisms and the risk of childhood acute lymphoblastic leukemia: a meta-analysis

Cited by 10 publications

References 33 publications

Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia

Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia

Association between high-dose methotrexate-induced toxicity and polymorphisms within methotrexate pathway genes in acute lymphoblastic leukemia

The Role of ARID5B in Acute Lymphoblastic Leukemia and Beyond

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