Evidence map›Paper›PMID 42440143›Full record

ArticleAnnals of hematology2026

The clinical relevance of RAS pathway gene mutations in childhood B-cell acute lymphoblastic leukemia.

Xiaoyu Chen, Li Gao, Yongping Zhang, Yixin Hu, Jian Pan, Zhiheng Li, Jun Lu, Yizhen Li, Shaoyan Hu

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Article in Annals of hematology, 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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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Xiaoyu ChenDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Li GaoDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Yongping ZhangDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Yixin HuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Jian PanDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Zhiheng LiDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China.
Jun Lu *Department of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China. drlujun_sz@163.com.
Yizhen Li *Department of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China. liyz@suda.edu.cn.
Shaoyan Hu *Department of Hematology and Oncology, Children's Hospital of Soochow University, No. 92, Zhongnan Street, Suzhou, China. hushaoyan@suda.edu.cn.

Funding

National Key Research and Development Program of China No. 2022YFC2502700Suzhou Key project DZXYJ202305, SZS201615, SZS2023014, SKY2022012the National Natural Science Foundation of China 82170218, 82470221, 82103917, 82400264,82470127the National Natural Science Foundation of China 82200177
6 · The paper itself

Abstract

objectiveNotably, FLT3 and RAS pathway gene mutations represent a significant proportion of childhood B-cell acute lymphoblastic leukemia (B-ALL) cases. Our study explores whether these patients have distinct clinical features and prognostic outcomes.

methodsWe retrospectively analyzed 488 pediatric B-ALL cases from the CCCG-ALL-2015 cohort using whole transcriptome sequencing to assess the clinical features of FLT3 mutations, RAS pathway alterations, and their cooperative effects.

results192 patients (39.3%) carried at least one RAS pathway alterations, while 76 patients (15.6%) had FLT3 mutations. Strikingly, 6 of 11 NF1-mutated patients harbored concurrent FLT3 mutations. A significant correlation was observed between FLT3 and NF1 mutations (Phi coefficient = 0.16, χ² = 13.0, p < 0.001), NRAS and KRAS mutations (Phi coefficient = 0.19, χ² = 17.12, p < 0.0001), NRAS and PTPN11 (Phi coefficient = 0.138, χ² = 9.54, p = 0.0042). FLT3/NF1 co-mutated patients exhibited a higher frequency of abnormal karyotypes and had significantly poorer overall survival (OS) and event-free survival (EFS) (p < 0.05), particularly when compared to those without KMT2A rearrangements (p = 0.004 and p = 0.003, respectively). Collectively, RAS pathway alterations were not significantly associated with inferior OS or EFS. Multivariable Cox regression analysis confirmed that FLT3/NF1 co‑mutations were independently associated with inferior OS (HR = 12.39, 95% CI: 1.40-109.46, p = 0.024), and multivariable logistic regression analysis showed that they were also independently associated with Day 46 MRD ≥ 0.01% (OR = 9.50, 95% CI: 1.65-54.71, p = 0.01).

conclusionOur findings suggest that FLT3/NF1 co-mutations-rather than other RAS pathway mutations, may be associated with adverse outcomes in pediatric B‑ALL, warranting further validation.

trial registrationThe study was conducted with approval from the Institutional Review Board of Children's Hospital of Soochow University (Approval number: 2019KS006).

Indexed as

fms-Like Tyrosine Kinase 3MutationPrecursor B-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins p21(ras)Signal TransductionAdolescentChildChild, PreschoolFemaleGTP PhosphohydrolasesHumansInfantMaleMembrane ProteinsNeurofibromin 1Protein Tyrosine Phosphatase, Non-Receptor Type 11FLT3 protein, humanfms-Like Tyrosine Kinase 3GTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNeurofibromin 1NF1 protein, humanNRAS protein, humanProtein Tyrosine Phosphatase, Non-Receptor Type 11Proto-Oncogene Proteins p21(ras)PTPN11 protein, humanB-cell acute lymphocytic leukemiaFLT3NF1RAS pathway gene mutation

Identifiers

PMID42440143
PMCPMC13642409

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.