Evidence map›Paper›PMID 41230692›Full record

ArticleHaematologica2026

Chromosomal rearrangement-enhanced mRNA stability drives the oncogenic potential of fusion genes in pediatric leukemia.

Xuejing Shao, Zhimei Xia, Minyi Cai, Chen Shao, Shaowei Bing, Tianrui Wang, Wenxin Du, Jiayi Liu, Diying Shen, Ji Cao and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Xuejing ShaoInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China; Nanhu Brain-computer Interface Institute, Hangzhou, 311100.
Zhimei XiaInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Minyi CaiInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Chen ShaoInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Shaowei BingInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Tianrui WangInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Wenxin DuInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Jiayi LiuInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Diying ShenDivision of Hematology-Oncology, the Children's Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang 310005.
Ji CaoInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058.
Bo YangInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China; Nanhu Brain-computer Interface Institute, Hangzhou, 311100, China; School of Medicine, Hangzhou City University, Hangzhou, Zhejiang 310015.
Qiaojun HeInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China; Nanhu Brain-computer Interface Institute, Hangzhou, 311100, China; Cancer Center, Zhejiang University, Hangzhou, 310058.
Xiaojun XuDivision of Hematology-Oncology, the Children's Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang 310005.
Jingying ZhangDivision of Hematology-Oncology, the Children's Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang 310005. zhangjy423@zju.edu.cn.
Meidan YingInstitute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China; Nanhu Brain-computer Interface Institute, Hangzhou, 311100, China; Division of Hematology-Oncology, the Children's Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang 310005, China; School of Medicine, Hangzhou City University, Hangzhou, Zhejiang 310015, China; Cancer Center, Zhejiang University, Hangzhou, 310058. mying@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL), the most common type of pediatric leukemia, is frequently driven by fusion genes generated by chromosomal rearrangements. Compared with wild-type genes, many oncogenic fusions show increased expression and sustained functional activity that drives tumorigenesis. However, the mechanisms by which chromosomal rearrangements lead to functional enhancement remain largely elusive. In addition, although large-scale sequencing has identified numerous fusion events, the functional significance of most remains unclear. Here, we demonstrate that enhanced mRNA stability represents an important tumorigenic mechanism for oncogenic fusions, including classical PAX5 fusions. Based on this mechanism, we characterize a novel oncogenic fusion, STK38-PXT1, which exhibits upregulated STK38 mRNA levels and drives the development of ALL. Mechanistically, the increased mRNA stability results primarily from enhanced N6-methyladenosine modification of oncogenic fusions, which is attributable to "gene truncation" (as in PAX5 fusions) and "partner collaboration" (as in STK38-PXT1). Furthermore, the m6A reader IGF2BP3 is crucial for maintaining the high mRNA stability of oncogenic fusions. We further propose venetoclax as an innovative and clinically available therapy for ALL driven by these oncogenic fusions characterized by high mRNA stability. Our study not only highlights mRNA stabilization as a crucial mechanism by which oncogenic fusions drive tumorigenesis, but also presents a promising therapeutic strategy for patients with ALL.

Indexed as

Chromosome AberrationsGene RearrangementOncogene Proteins, FusionPrecursor Cell Lymphoblastic Leukemia-LymphomaRNA StabilityAnimalsCell Line, TumorGene Expression Regulation, LeukemicHumansRNA, MessengerOncogene Proteins, FusionRNA, Messenger

Identifiers

PMID41230692
PMCPMC13317875

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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 OpenQuestion graph.