ArticleMolecular biology reports2026
TP53 isoform dysregulation in pediatric B-ALL: identifying markers of favorable prognosis and relapse-associated dynamic.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTP53 isoforms produced by alternate splicing and promoter usage are shown to play a role in pathogenesis, chemoresistance and relapse in various cancers. Our present study focused on analyzing the expression of different TP53 isoforms in pediatric B cell acute lymphoblastic leukemia (B-ALL).
methodsWe performed the transcriptomic analysis of TP53 isoforms expression in publicly available datasets followed by RT-qPCR in our cohort of pediatric B-ALL and correlated with various clinical and hematological parameters.
resultsTranscriptomic data on B-ALL available online showed overexpression of p53α in B-ALL cases at diagnosis while Δ40p53, p53β and Δ133p53 were downregulated in cases at relapse. In our cohort data (n = 99) at diagnosis, we found the upregulation of the long isoform p53α in 65.65% of patients and the short isoforms Δ133p53 in 61.61% patients and Δ40p53 in 27.27% of the patients, respectively. The over-expression of p53γ and p53β was noted in 19.19% and 14.14% of patients, respectively. To check if TP53 gene mutation contributed to this dysregulated isoform expression, we analysed the whole exome data of our B-ALL patients (n = 88). As expected only 3.7% of patients showed mutation in TP53 gene. Further, we analysed the correlation with various clinical parameters and found positive association of Δ133p53 with ETV6::RUNX1 gene fusion (p = 0.032) which is a known marker of good prognosis in B-ALL. To further validate this observation, we enrolled B-ALL relapse cases (n = 46) where samples at diagnosis were also available (n = 12). Analysis of TP53 isoforms expression in relapse B-ALL patients showed significant reduction in the expression of short isoforms of TP53 i.e. Δ133p53 (p = 0.0036) and Δ40p53 (p = 0.032).
conclusionOur data show that TP53 isoforms are dysregulated in B-ALL at diagnosis as well as at relapse. Short TP53 isoforms, particularly Δ133p53 is associated with better prognosis suggesting its potential role in refining risk stratification of B-ALL.
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