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A 30-gene classifier distinguishes low-risk MDS HSPCs from healthy HSPCs.

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Experimental hematology 📖 저널 OA 50% 2025: 1/2 OA 2026: 11/22 OA 2025~2026 2025 Vol.152() p. 105252
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PICO 자동 추출 (휴리스틱, conf 2/4)

유사 논문
P · Population 대상 환자/모집단
환자: IPSS-M moderate low risk, low risk, and very low risk patients and have a limited median survival of 3 to 10 years
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
The genes in our score suggest dysfunction in vesicular trafficking, which we further resolve across the myeloid differentiation axis. The gene products of vesicular trafficking-related pathways may be suitable translational targets for LR-MDS.

Bhat P, Van Amburg JC, Potts CR, Gracie TJ, Cartailler JA, Parker AC

📝 환자 설명용 한 줄

Myelodysplastic syndromes (MDS) are a group of malignant clonal disorders that are characterized by functional impairment of hematopoiesis, morphologic dysplasia, and genetic heterogeneity.

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↓ .bib ↓ .ris
APA Bhat P, Van Amburg JC, et al. (2025). A 30-gene classifier distinguishes low-risk MDS HSPCs from healthy HSPCs.. Experimental hematology, 152, 105252. https://doi.org/10.1016/j.exphem.2025.105252
MLA Bhat P, et al.. "A 30-gene classifier distinguishes low-risk MDS HSPCs from healthy HSPCs.." Experimental hematology, vol. 152, 2025, pp. 105252.
PMID 40972808 ↗

Abstract

Myelodysplastic syndromes (MDS) are a group of malignant clonal disorders that are characterized by functional impairment of hematopoiesis, morphologic dysplasia, and genetic heterogeneity. While less likely to transform to acute leukemia, lower-risk MDS (LR-MDS) include patients with IPSS-M moderate low risk, low risk, and very low risk patients and have a limited median survival of 3 to 10 years. Further, there is growing interest in discovering translational targets of LR-MDS pathophysiology. Clonal populations within the hematopoietic stem and progenitor (HSPC) to myeloid differentiation spectrum are widely considered to be a major contributor to MDS pathophysiology. A granular assessment of cell-type and lineage-specific states that contribute to LR-MDS pathophysiology remains to be elucidated. Here, we leverage single-cell transcriptomics to characterize cell states across the HSPC-myeloid differentiation landscape in LR-MDS. We develop a 30-gene score to classify LR-MDS HSPCs and identify novel molecular features of LR-MDS. The genes in our score suggest dysfunction in vesicular trafficking, which we further resolve across the myeloid differentiation axis. The gene products of vesicular trafficking-related pathways may be suitable translational targets for LR-MDS.

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