ArticleNature communications2015
Whole-exome and targeted sequencing identify ROBO1 and ROBO2 mutations as progression-related drivers in myelodysplastic syndromes.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- The efficacy and toxicity of the CHG priming regimen (low-dose cytarabine, homoharringtonine, and G-CSF) in higher risk MDS patients relapsed or refractory to decitabine.Journal of cancer research and clinical oncology · 2019Trial
- ROBO1 is required for postnatal growth and survival.Genes & genomics · 2026Article
- CD47 stabilizes ROBO2 to regulate glioblastoma progression by preventing ITCH-mediated ubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Significance of Mutation Spots and Concurrent Gene Mutations on Prognosis and Clinical Outcomes in Myelodysplastic Syndromes With SF3B1 Mutation.Cancer medicine · 2025Article
- Article
- DHX9-mediated pathway contributes to the malignant phenotype of myelodysplastic syndromes.iScience · 2023Article
- Somatic mutations of activating signalling, transcription factor, and tumour suppressor are a precondition for leukaemia transformation in myelodysplastic syndromes.Journal of cellular and molecular medicine · 2022Article
- Article
- DNA methylation-mediated differential expression of DLX4 isoforms has opposing roles in leukemogenesis.Cellular & molecular biology letters · 2022Article
- A somatic mutation in moesin drives progression into acute myeloid leukemia.Science advances · 2022Article
- ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment.Blood cancer discovery · 2021Article
- Article
- Structural insights and evaluation of the potential impact of missense variants on the interactions of SLIT2 with ROBO1/4 in cancer progression.Scientific reports · 2020Article
- The evolution of relapse of adult T cell acute lymphoblastic leukemia.Genome biology · 2020Article
- Genome-wide methylation sequencing identifies progression-related epigenetic drivers in myelodysplastic syndromes.Cell death & disease · 2020Article
- IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway.Oncology reports · 2020Article
- Identification and validation of prognosis-related DLX5 methylation as an epigenetic driver in myeloid neoplasms.Clinical and translational medicine · 2020Article
- Article
- Tracking longitudinal genetic changes of circulating tumor DNA (ctDNA) in advanced Lung adenocarcinoma treated with chemotherapy.Journal of translational medicine · 2019Article
- The Expression of the SLIT-ROBO Family in Adult Patients with Acute Myeloid Leukemia.Archivum immunologiae et therapiae experimentalis · 2019Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progressive mechanism underlying myelodysplastic syndrome remains unknown. Here we identify ROBO1 and ROBO2 as novel progression-related somatic mutations using whole-exome and targeted sequencing in 6 of 16 (37.5%) paired MDS patients with disease progression. Further deep sequencing detects 20 (10.4%) patients with ROBO mutations in a cohort of 193 MDS patients. In addition, copy number loss and loss of heterogeneity (LOH) of ROBO1 and ROBO2 are frequently observed in patients with progression or carrying ROBO mutations. In in vitro experiments, overexpression of ROBO1 or ROBO2 produces anti-proliferative and pro-apoptotic effects in leukaemia cells. However, this effect was lost in ROBO mutants and ROBO-SLIT2 signalling is impaired. Multivariate analysis shows that ROBO mutations are independent factors for predicting poor survival. These findings demonstrate a novel contribution of ROBO mutations to the pathogenesis of MDS and highlight a key role for ROBO-SLIT2 signalling in MDS disease progression.
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