Evidence map›Paper›PMID 39560864›Full record

ArticleStem cell reviews and reports2025

LNK/SH2B3 Loss Exacerbates the Development of Myeloproliferative Neoplasms in CBL-deficient Mice.

Yafei Chen, Shangyu Gong, Juan Tang, Xinying Wang, Yudan Gao, Hanying Yang, Wanze Chen, Hailiang Hu, Wei Tong, Kaosheng Lv

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PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reviews and reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Review
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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

10 authors.

Yafei ChenDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Shangyu GongDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Juan TangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Xinying WangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Yudan GaoDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Hanying YangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China.
Wanze ChenKey Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Hailiang HuDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, 518071, China. huhl@sustech.edu.cn.
Wei TongDivision of Hematology, Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA. tongw@chop.edu.
Kaosheng LvHunan Provincial Key Laboratory of Animal Models and Molecular Medicine, School of Biomedical Sciences, Hunan University, Changsha, 410013, China. lvks@hnu.edu.cn.ORCID 0000-0001-7998-2753

Funding

Novel Regulation of Oncogenic NRAS Signaling in Myeloid MalignanciesR01CA271523 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI Wei Tong · 2022 to 2026
$2.7M
Regulation of FLT3 Signaling in LeukemiaR01CA282668 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI Wei Tong · 2023 to 2026
$2.5M
Regulation of protein ubiquitination in hematopoietic cytokine signalingR01HL133828 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI TONG, WEI · 2017 to 2020
$2.2M
National Natural Science Foundation of China 82173131National Natural Science Foundation of China 82370110NCI NIH HHS R01 CA271523NCI NIH HHS R01 CA282668NHLBI NIH HHS R01 HL133828Shenzhen Medical Academy of Research and Translation B2302017
6 · The paper itself

Abstract

Genetic variations of signaling modulator protein LNK (also called SH2B3) are associated with relatively mild myeloproliferative phenotypes in patients with myeloproliferative neoplasms (MPN). However, these variations can induce more severe MPN disease and even leukemic transformation when co-existing with other driver mutations. In addition to the most prevalent driver mutation JAK2V617F, LNK mutations have been clinically identified in patients harboring CBL inactivation mutations, but its significance remains unclear. Here, using a transgenic mouse model, we demonstrated that mice with the loss of both Lnk and Cbl exhibited severe splenomegaly, extramedullary hematopoiesis and exacerbated myeloproliferative characteristics. Moreover, a population of Mac1

Indexed as

Intracellular Signaling Peptides and ProteinsMyeloproliferative DisordersProto-Oncogene Proteins c-cblAdaptor Proteins, Signal TransducingAnimalsDisease Models, AnimalHumansMiceMice, KnockoutMice, TransgenicMyeloid CellsProteasome Endopeptidase ComplexSignal TransductionAdaptor Proteins, Signal TransducingCbl protein, mouseIntracellular Signaling Peptides and ProteinsLnk protein, mouseProteasome Endopeptidase ComplexProto-Oncogene Proteins c-cblCBLLeukemiaMPNProteasomeSH2B3

Identifiers

PMID39560864
PMCPMC11976319

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.