ArticleEMBO molecular medicine2019
An autocrine ActivinB mechanism drives TGFβ/Activin signaling in Group 3 medulloblastoma.
Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Modeling medulloblastoma pathogenesis and treatment in human cerebellar organoids.Genes & development · 2026Article
- The MYC-dependent lncRNA MB3 inhibits apoptosis in Group 3 Medulloblastoma by regulating the TGF-β pathway via HMGN5.Cell death & disease · 2025Article
- Carbon minibeam radiation therapy results in tumor growth delay in an osteosarcoma murine model.Scientific reports · 2025Article
- Circular extrachromosomal DNA promotes tumor heterogeneity in high-risk medulloblastoma.Nature genetics · 2023Article
- The mitochondrial NADH shuttle system is a targetable vulnerability for Group 3 medulloblastoma in a hypoxic microenvironment.Cell death & disease · 2023Article
- Article
- Spatially resolved transcriptomic profiling of degraded and challenging fresh frozen samples.Nature communications · 2023Article
- Coming in from the cold: overcoming the hostile immune microenvironment of medulloblastoma.Genes & development · 2022Review
- The multilayer community structure of medulloblastoma.iScience · 2021Article
- Medulloblastomics revisited: biological and clinical insights from thousands of patients.Nature reviews. Cancer · 2020Review
- An autocrine ActivinB mechanism drives TGFβ/Activin signaling in Group 3 medulloblastoma.EMBO molecular medicine · 2019Article
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Authors and funding
21 authors at 6 institutions in 2 countries.
Funding
Abstract
Medulloblastoma (MB) is a pediatric tumor of the cerebellum divided into four groups. Group 3 is of bad prognosis and remains poorly characterized. While the current treatment involving surgery, radiotherapy, and chemotherapy often fails, no alternative therapy is yet available. Few recurrent genomic alterations that can be therapeutically targeted have been identified. Amplifications of receptors of the TGFβ/Activin pathway occur at very low frequency in Group 3 MB. However, neither their functional relevance nor activation of the downstream signaling pathway has been studied. We showed that this pathway is activated in Group 3 MB with some samples showing a very strong activation. Beside genetic alterations, we demonstrated that an ActivinB autocrine stimulation is responsible for pathway activation in a subset of Group 3 MB characterized by high PMEPA1 levels. Importantly, Galunisertib, a kinase inhibitor of the cognate receptors currently tested in clinical trials for Glioblastoma patients, showed efficacy on orthotopically grafted MB-PDX. Our data demonstrate that the TGFβ/Activin pathway is active in a subset of Group 3 MB and can be therapeutically targeted.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.