ArticleNature genetics2016
Recurrent mTORC1-activating RRAGC mutations in follicular lymphoma.
Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 121 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
121 citing papers in PubMed, 206 citations in OpenAlex.
- Identification of a genetic signature enriching for response to ibrutinib in relapsed/refractory follicular lymphoma in the DAWN phase 2 trial.Cancer medicine · 2022Trial
- Pan-phosphatidylinositol 3-kinase inhibition with buparlisib in patients with relapsed or refractory non-Hodgkin lymphoma.Haematologica · 2017Trial
- Integrated multiomic profiling reveals 2 distinct splenic marginal zone lymphoma subgroups with prognostic relevance.Blood advances · 2026Article
- RagC and Map4K3 deficiency in high-grade gliomas drives proliferation and modulates mTORC1-dependent cellular functions.Journal of neuropathology and experimental neurology · 2026Article
- Genomic heterogeneity in primary cutaneous follicular center lymphomas reveals different clinicopathological subgroups.HemaSphere · 2026Article
- Lysosomal phosphoinositide turnover acts upstream of RagGTPase-mTORC1 and controls muscle growth.Nature metabolism · 2026Article
- Whole Exome Sequencing in Children With Autoimmune Hepatitis Identified Mutations in Genes Involved in the mTORC1 Signaling Pathway.Gastro hep advances · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- V-ATPase-dependent induction of selective autophagy.Nature communications · 2025Article
- Recent advances in the clinical spectrum and pathomechanisms associated with X-linked myopathy with excessive autophagy and otherJournal of neuromuscular diseases · 2025Review
- Transcriptional reprogramming in oral squamous cell carcinoma.Scientific reports · 2025Article
- Follicular lymphoma: contemporary clinical management with a focus on recent therapeutic advances.The Korean journal of internal medicine · 2025Review
- Audit of B-cell cancer genes.Blood advances · 2025Review
- STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in follicular lymphoma.Leukemia · 2025Article
- mTORC1, the maestro of cell metabolism and growth.Genes & development · 2025Review
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Follicular lymphoma research: an open dialogue for a collaborative roadmap.Histopathology · 2025Review
- Clinicopathological characteristics and genomic profiling in patients with transformed lymphoma: a monocentric retrospective study.Annals of medicine · 2024Article
- Big1 is a newly identified autophagy regulator that is critical for a fully functional V-ATPase.Molecular biology of the cell · 2024Article
- Identification of genetic subtypes in follicular lymphoma.Blood cancer journal · 2024Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
35 authors at 11 institutions in 4 countries.
Funding
Abstract
Follicular lymphoma is an incurable B cell malignancy characterized by the t(14;18) translocation and mutations affecting the epigenome. Although frequent gene mutations in key signaling pathways, including JAK-STAT, NOTCH and NF-κB, have also been defined, the spectrum of these mutations typically overlaps with that in the closely related diffuse large B cell lymphoma (DLBCL). Using a combination of discovery exome and extended targeted sequencing, we identified recurrent somatic mutations in RRAGC uniquely enriched in patients with follicular lymphoma (17%). More than half of the mutations preferentially co-occurred with mutations in ATP6V1B2 and ATP6AP1, which encode components of the vacuolar H(+)-ATP ATPase (V-ATPase) known to be necessary for amino acid-induced activation of mTORC1. The RagC variants increased raptor binding while rendering mTORC1 signaling resistant to amino acid deprivation. The activating nature of the RRAGC mutations, their existence in the dominant clone and their stability during disease progression support their potential as an excellent candidate for therapeutic targeting.
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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.