ArticleBlood advances2020
Role of lncRNA Morrbid in PTPN11(Shp2)E76K-driven juvenile myelomonocytic leukemia.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Computational insights into synergistic mechanisms of PD-901 and 5-azacitidine targeting PTPN11 (SHP2) E76K mutation in juvenile myelomonocytic leukemia.Frontiers in bioinformatics · 2026Article
- Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice.Disease models & mechanisms · 2025Article
- The Emerging Role of LncRNA AWPPH in Multiple Cancers: A Review Study.Current molecular medicine · 2025Review
- Review
- Transcription regulation by long non-coding RNAs: mechanisms and disease relevance.Nature reviews. Molecular cell biology · 2024Review
- Potential clinical use of azacitidine and MEK inhibitor combination therapy in PTPN11-mutated juvenile myelomonocytic leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Behind the scenes: How RNA orchestrates the epigenetic regulation of gene expression.Frontiers in cell and developmental biology · 2023Review
- Analysis of the clinical characteristics and prognosis of adultOpen medicine (Warsaw, Poland) · 2023Article
- Long Noncoding RNA MIR4435-2HG Suppresses Colorectal Cancer Initiation and Progression By Reprogramming Neutrophils.Cancer immunology research · 2022Article
- Prioritizing risk genes as novel stratification biomarkers for acute monocytic leukemia by integrative analysis.Discover oncology · 2022Article
- KRAS-related long noncoding RNAs in human cancers.Cancer gene therapy · 2022Review
- Article
- Hyperglycemia cooperates with Tet2 heterozygosity to induce leukemia driven by proinflammatory cytokine-induced lncRNA Morrbid.The Journal of clinical investigation · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations in PTPN11, which encodes the protein tyrosine phosphatase SHP2, contribute to ∼35% of cases of juvenile myelomonocytic leukemia (JMML). A common clinical picture in children with JMML is that it presents as a constitutive hyperinflammatory syndrome, partially reminiscent of chronic myelomonocytic leukemia in adults. Thus, a component of JMML is associated with a hyperinflammatory state and abundant innate immune cells such as neutrophils and monocytes. Recently, we showed that the evolutionarily conserved mouse lncRNA Morrbid is specifically expressed in myeloid cells and uniquely represses the expression of the proapoptotic gene Bim to regulate the lifespan of myeloid cells. However, its role in JMML has not been investigated. In this study, we characterized the role of Morrbid and its target Bim, which are significantly dysregulated in Shp2E76K/+-bearing myeloid cells, in driving JMML. Loss of Morrbid in a mouse model of JMML driven by the Shp2E76K/+ mutation resulted in a significant correction of myeloid and erythroid cell abnormalities associated with JMML, including overall survival. Consistently, patients with JMML who had PTPN11, KRAS, and NRAS mutations and high expression of MORRBID manifested poor overall survival. Our results suggest that Morrbid contributes to JMML pathogenesis.
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