What does this research mean for the field?

The Srsf2 P95H mutation alters hematopoietic lineage composition and induces systemic immune dysregulation in the bone marrow microenvironment, contributing to the early-stage progression of myelodysplastic syndromes and chronic myelomonocytic leukemia. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine how somatic SRSF2 P95H mutations alter the bone marrow microenvironment and contribute to early-stage myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) pathogenesis.

August 22, 2026Cell Death and DiseaseOpen Access

SRSF2 mutations contribute to bone marrow immune microenvironment alterations

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Authors

CTChangrui Tao WLWei Li YJYu Jiang

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Overview

Preclinical mouse models reveal that SRSF2 mutations remodel bone marrow immune cell composition and RNA splicing, suggesting early microenvironment disruption in leukemia progression.

Key Points

To determine how somatic SRSF2 P95H mutations alter the bone marrow microenvironment and contribute to early-stage myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) pathogenesis.
Generated two mouse models without overt disease phenotypes: a cell-derived xenograft (CDX) via tail-vein injection of BA/F3-KRAS G12C-SRSF2 P95H cells and a heterozygous Vav1-Cre conditional knock-in model (Srsf2 P95H/WT).
Characterized bone marrow cellular composition and transcriptional alterations using bulk RNA-seq, single-cell RNA-seq (scRNA-seq), flow cytometry, and Sanger sequencing.
SRSF2 P95H expression induced systemic immune dysregulation, manifested by depleted hematopoietic stem and progenitor cells (HSPCs), natural killer (NK) cells, and effector T cells, alongside an expansion of neutrophil precursors.
Identified a marked B-cell lineage shift toward mature, antibody-secreting states and extensive alternative mis-splicing across key epigenetic, spliceosomal, and cytoskeletal genes, notably Hnrnpa2b1.

Cite This Study

Tao et al. (2026) studied this question.

synapsesocial.com/papers/6a895effca7ade938187d47c https://doi.org/10.1038/s41419-026-09205-y

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August 22, 2026Cell Death and DiseaseOpen Access

SRSF2 mutations contribute to bone marrow immune microenvironment alterations

View Full Paper

Ask AI

Bookmark

Authors

CTChangrui Tao WLWei Li YJYu Jiang

Discussion

Member takes

Overview

Preclinical mouse models reveal that SRSF2 mutations remodel bone marrow immune cell composition and RNA splicing, suggesting early microenvironment disruption in leukemia progression.

Key Points

To determine how somatic SRSF2 P95H mutations alter the bone marrow microenvironment and contribute to early-stage myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) pathogenesis.
Generated two mouse models without overt disease phenotypes: a cell-derived xenograft (CDX) via tail-vein injection of BA/F3-KRAS G12C-SRSF2 P95H cells and a heterozygous Vav1-Cre conditional knock-in model (Srsf2 P95H/WT).
Characterized bone marrow cellular composition and transcriptional alterations using bulk RNA-seq, single-cell RNA-seq (scRNA-seq), flow cytometry, and Sanger sequencing.
SRSF2 P95H expression induced systemic immune dysregulation, manifested by depleted hematopoietic stem and progenitor cells (HSPCs), natural killer (NK) cells, and effector T cells, alongside an expansion of neutrophil precursors.
Identified a marked B-cell lineage shift toward mature, antibody-secreting states and extensive alternative mis-splicing across key epigenetic, spliceosomal, and cytoskeletal genes, notably Hnrnpa2b1.

Cite This Study

Tao et al. (2026) studied this question.

synapsesocial.com/papers/6a895effca7ade938187d47c https://doi.org/10.1038/s41419-026-09205-y

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