ArticleNature communications2017
MAX inactivation is an early event in GIST development that regulates p16 and cell proliferation.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Precision therapeutic strategies for advanced gastrointestinal stromal tumors.Cancer metastasis reviews · 2026Review
- Multiomic Landscape of Gastrointestinal Stromal Tumors in a Real-World Patient Cohort of 1,427 Cases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Establishment and genomic validation of novel patient-derived xenograft models for drug discovery in gastrointestinal stromal tumor.BMC cancer · 2026Article
- Clinical significance of comprehensive genomic profiling in unresectable or recurrent gastrointestinal stromal tumors: a multicenter retrospective cohort study.Journal of gastroenterology · 2026Article
- MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues.Science advances · 2025Article
- Genome-Wide DNA Methylation and Copy Number Alterations in Gastrointestinal Stromal Tumors.Genes, chromosomes & cancer · 2025Article
- Genomic and transcriptomic landscape of human gastrointestinal stromal tumors.Nature communications · 2024Article
- Circadian clock-related genome-wide mendelian randomization identifies putatively genes for ulcerative colitis and its comorbidity.BMC genomics · 2024Article
- Pathologic diagnosis and molecular features of gastrointestinal stromal tumors: a mini-review.Frontiers in oncology · 2024Review
- Novel Genomic Risk Stratification Model for Primary Gastrointestinal Stromal Tumors (GIST) in the Adjuvant Therapy Era.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Whole-genome and Epigenomic Landscapes of Malignant Gastrointestinal Stromal Tumors HarboringCancer research communications · 2023Article
- Primary Hyperparathyroidism in a Patient With Bilateral Pheochromocytoma and a Mutation in the Tumor SuppressorJCEM case reports · 2023Article
- Concurrent inhibition of CDK2 adds to the anti-tumour activity of CDK4/6 inhibition in GIST.British journal of cancer · 2022Article
- Clinical sequencing of soft tissue and bone sarcomas delineates diverse genomic landscapes and potential therapeutic targets.Nature communications · 2022Article
- Risk stratification of gastrointestinal stromal tumors by Nanostring gene expression profiling.Journal of cancer research and clinical oncology · 2022Article
- The GIST of Advances in Treatment of Advanced Gastrointestinal Stromal Tumor.American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting · 2022Review
- Neuroprotective Gene Therapy by Overexpression of the Transcription Factor MAX in Rat Models of Glaucomatous Neurodegeneration.Investigative ophthalmology & visual science · 2022Article
- Risk-Related Genes and Associated Signaling Pathways of Gastrointestinal Stromal Tumors.International journal of general medicine · 2022Article
- Gastrointestinal stromal tumours.Nature reviews. Disease primers · 2021Review
- Update on Molecular Genetics of Gastrointestinal Stromal Tumors.Diagnostics (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
24 authors at 7 institutions in 3 countries.
Funding
Abstract
KIT, PDGFRA, NF1 and SDH mutations are alternate initiating events, fostering hyperplasia in gastrointestinal stromal tumours (GISTs), and additional genetic alterations are required for progression to malignancy. The most frequent secondary alteration, demonstrated in ∼70% of GISTs, is chromosome 14q deletion. Here we report hemizygous or homozygous inactivating mutations of the chromosome 14q MAX gene in 16 of 76 GISTs (21%). We find MAX mutations in 17% and 50% of sporadic and NF1-syndromic GISTs, respectively, and we find loss of MAX protein expression in 48% and 90% of sporadic and NF1-syndromic GISTs, respectively, and in three of eight micro-GISTs, which are early GISTs. MAX genomic inactivation is associated with p16 silencing in the absence of p16 coding sequence deletion and MAX induction restores p16 expression and inhibits GIST proliferation. Hence, MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs.
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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.