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Article

CD69 blockade restores the bone marrow niche and delays leukemogenesis in a mouse model of Nras G12D-driven chronic myelomonocytic leukemia.

Cancer biology & therapy - 31 Dec 2026

Li Yuchen, Jiang Xu, Gu Yinfeng, Zha Xianfeng, Wu Jie, Wu Xiuli, Qi Chunli, Chen Shaohua, Li Yangqiu, Jin Zhenyi, Xia Chengxiang, Xu Ling

Abstract excerpt

BACKGROUND: A subset of patients with chronic myelomonocytic leukemia (CMML) carries NRAS mutations, which are associated with shorter overall survival and an increased risk of transformation to acute myeloid leukemia. However, the effects of NRAS mutations on the bone marrow microenvironment (BME) remain unclear. METHODS: We used a CMML mouse model driven by a single Nras G12D allele mutation to investigate...

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Topics

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Share to Antigens, CD
Share to Antigens, Differentiation, T-Lymphocyte

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Bone Marrow

Share to Lectins, C-Type

Share to Leukemia, Myelomonocytic, Chronic

Share to Monomeric GTP-Binding Proteins

Share to T-Lymphocytes, Regulatory

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Source

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Identifiers

PMID: 42330053
DOI: 10.1080/15384047.2026.2692184
PMCID: PMC13290085

Genes

CD69
NRAS

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

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Research trail→

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CD69 blockade restores the bone marrow niche and delays leukemogenesis in a mouse model of Nras G12D-driven chronic myelomonocytic leukemia.PMID 42330053Read ↗

CD69 Blockade Restores the Bone Marrow Niche and Delays Leukemogenesis in a Mouse Model of NrasG12D-driven Chronic Myelomonocytic LeukemiaSemantic proximity Read ↗

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