ArticleBlood2016
KIT D816V-mutated bone marrow mesenchymal stem cells in indolent systemic mastocytosis are associated with disease progression.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- KIT mutation and AHN-associated oncogenic profiles in systemic mastocytosis with an associated hematological neoplasm.Blood advances · 2026Article
- Article
- Development of a High-Sensitivity Multiplex mRNA-Based KIT D816V Droplet Digital PCR Assay and Correlation with Tumor Load in Systemic Mastocytosis.International journal of molecular sciences · 2026Article
- Chronic Anaphylaxis With Indolent Systemic Mastocytosis: A Case Report.Case reports in hematology · 2025Article
- Unraveling the Rare Entity ofJournal of hematology · 2024Article
- Indolent systemic mastocytosis and aleukemic mast cell leukemia: Subtle diagnostic differences with distinct management approaches.JAAD case reports · 2023Article
- Avapritinib for the treatment of KIT mutation-negative systemic mastocytosis.Proceedings (Baylor University. Medical Center) · 2023Article
- Remission of indolent systemic mastocytosis in the absence of targeted therapy.The journal of allergy and clinical immunology. In practice · 2022Article
- Article
- Comprehensive Analysis of Acquired Genetic Variants and Their Prognostic Impact in Systemic Mastocytosis.Cancers · 2022Review
- Molecular quantification of tissue disease burden is a new biomarker and independent predictor of survival in mastocytosis.Haematologica · 2020Article
- Detection of AML-specific TP53 mutations in bone marrow-derived mesenchymal stromal cells cultured under hypoxia conditions.Annals of hematology · 2019Article
- Impact of somatic and germline mutations on the outcome of systemic mastocytosis.Blood advances · 2018Article
- CD44 is a RAS/STAT5-regulated invasion receptor that triggers disease expansion in advanced mastocytosis.Blood · 2018Article
- Deciphering the differentiation trajectory from hematopoietic stem cells to mast cells.Blood advances · 2018Review
- Analysis of the function of microRNA-375 in humans using bioinformatics.Biomedical reports · 2017Article
- Advances in the Classification and Treatment of Mastocytosis: Current Status and Outlook toward the Future.Cancer research · 2017Review
- Altered neutrophil immunophenotypes in childhood B‑cell precursor acute lymphoblastic leukemia.Oncotarget · 2016Article
- Beyond the Niche: Myelodysplastic Syndrome Topobiology in the Laboratory and in the Clinic.International journal of molecular sciences · 2016Review
- Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multilineage involvement of bone marrow (BM) hematopoiesis by the somatic KIT D816V mutation is present in a subset of adult indolent systemic mastocytosis (ISM) patients in association with a poorer prognosis. Here, we investigated the potential involvement of BM mesenchymal stem cells (MSCs) from ISM patients by the KIT D816V mutation and its potential impact on disease progression and outcome. This mutation was investigated in highly purified BM MSCs and other BM cell populations from 83 ISM patients followed for a median of 116 months. KIT D816V-mutated MSCs were detected in 22 of 83 cases. All MSC-mutated patients had multilineage KIT mutation (100% vs 30%, P = .0001) and they more frequently showed involvement of lymphoid plus myeloid BM cells (59% vs 22%; P = .03) and a polyclonal pattern of inactivation of the X-chromosome of KIT-mutated BM mast cells (64% vs 0%; P = .01) vs other multilineage ISM cases. Moreover, presence of KIT-mutated MSCs was associated with more advanced disease features, a greater rate of disease progression (50% vs 17%; P = .04), and a shorter progression-free survival (P ≤ .003). Overall, these results support the notion that ISM patients with mutated MSCs may have acquired the KIT mutation in a common pluripotent progenitor cell, prior to differentiation into MSCs and hematopoietic precursor cells, before the X-chromosome inactivation process occurs. From a clinical point of view, acquisition of the KIT mutation in an earlier BM precursor cell confers a significantly greater risk for disease progression and a poorer outcome.
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