Evidence map›Paper›PMID 42533362›Full record

ArticleExperimental hematology & oncology2026

Arsenic trioxide promotes a glue‑like interaction to drive STUB1-mediated NPM-ALK degradation in ALK

Guiming Li, Jun Wang, Shiguang Ye, Lixin Zhou, Yanli Sun, Bowen Li, Yunshuo Zhao, Yi Ding, Yu Zeng, Bin Xue and 8 more

Abstract readLetter
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental hematology & oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Guiming Li *Department of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Jun Wang *Lingang Laboratory, Shanghai, 200031, China.
Shiguang Ye *Department of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Lixin ZhouDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Yanli SunLingang Laboratory, Shanghai, 200031, China.
Bowen LiDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Yunshuo ZhaoDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Yi DingDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Yu ZengDepartment of Pathology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Bin XueDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Guangming WangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Fangce WangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Xiu LuoDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Aibin LiangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Ellen L WeisbergDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Wenjun ZhangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. zhangwenjun@tongji.edu.cn.
Wenchao LuLingang Laboratory, Shanghai, 200031, China. luwenchao@lglab.ac.cn.
Jing YangDepartment of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. jingy@tongji.edu.cn.

Funding

Fundamental Research Funds for the Central Universities 22120250374National Key Research and Development Program of China 2021YFA1100800National Natural Science Foundation of China 82370158National Natural Science Foundation of China 82373937Youth Innovation Promotion Association of the Chinese Academy of Sciences 2022453
6 · The paper itself

Abstract

The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion constitutively activates ALK tyrosine kinase, driving oncogenesis in anaplastic large cell lymphoma (ALCL). While arsenic trioxide (ATO) exhibits therapeutic potential, its precise mechanism remains elusive, limiting clinical application. Here, we used a combined approach of E3 ligase library screening, ATO chemical proteomics, and NPM-ALK immunoprecipitation-mass spectrometry to reveal that ATO regulates NPM-ALK stability via the E3 ligase STUB1. Clinically, high STUB1 expression correlates with improved survival, identifying it as a candidate favorable prognostic biomarker in NPM-ALK

Indexed as

ATOGlue-like interactionNPM-ALK+ ALCLSTUB1Synergistic therapy

Identifiers

PMID42533362
PMCPMC13421824

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.