Global bibliometric analysis of TP53-mutated acute myeloid leukemia: research hotspots and evolution.

BACKGROUND

Acute myeloid leukemia (AML) with TP53 mutations represents a high-risk molecular subtype distinguished by genomic instability, resistance to therapy, and unfavorable clinical prognosis. This investigation sought to enhance comprehension of the worldwide research domain concerning TP53-mutated AML via bibliometric analysis.

METHODS

Articles and reviews concerning TP53 mutations in AML were gathered from the Web of Science Core Collection (WoSCC) and Scopus databases spanning from 1990 to 2025. A bibliometric analysis was conducted utilizing Microsoft Excel, CiteSpace, VOSviewer, and the bibliometrix R package was used to evaluate publication patterns, the roles of countries and institutions, authorship and collaborative networks, journals, co-cited references, and keyword evolution.

RESULTS

A total of 683 publications were analyzed in this study, consisting of 626 original articles and 57 reviews, revealing a continuous rise in research productivity concerning TP53 mutation-associated AML, notably post-2010. The United States ranked first in publication volume, citation impact, and international collaboration, followed by Japan, China, and several European countries. Washington University School of Medicine, The University of Texas MD Anderson Cancer Center, and Harvard University were identified as the most productive institutions, while Kantarjian HM, Garcia-Manero G, and Fenaux P were identified as the most influential authors. TP53-mutated AML research was predominantly published in high-impact hematology and oncology journals, notably Blood and Leukemia. Keyword and co-citation analyses indicated a progressive shift in research focus from early cytogenetic and TP53 biological studies toward integrated molecular classification, next-generation sequencing (NGS), clonal evolution, prognostic stratification, and therapeutic resistance.

CONCLUSIONS

This analysis demonstrated that research on TP53-mutated AML has progressively shifted toward molecularly driven and translational approaches, while unmet clinical needs persist. Future studies should focus on multi-omics integration and mechanism-based therapeutic strategies to support refined risk stratification and improve patient outcomes.