ArticleNature communications2018
Regulation of mutant TERT by BRAF V600E/MAP kinase pathway through FOS/GABP in human cancer.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
126 citing papers in PubMed, 3 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- Genetic drivers of etiologic heterogeneity in thyroid cancer.Nature communications · 2026Pooled it
- Melanoma of unknown primary: a comprehensive review of immune-mediated pathogenesis and therapies.The oncologist · 2025Pooled it
- The Coexistence of Genetic Mutations in Thyroid Carcinoma Predicts Histopathological Factors Associated With a Poor Prognosis: A Systematic Review and Network Meta-Analysis.Frontiers in oncology · 2020Pooled it
- The impact of RET fusions on radioiodine avidity and prognosis in patients with distant metastatic papillary thyroid cancer.Endocrine · 2026Article
- ERK Signaling in Thyroid Cancer: Lineage Suppression, Epigenetic Reprogramming, and Theranostic Reversal.Cancers · 2026Review
- Recent Advances in Neoadjuvant Treatment of Anaplastic Thyroid Carcinoma: A Narrative Review.Current treatment options in oncology · 2026Review
- Preoperative Co-Mutation of BRAFCancer medicine · 2026Article
- Role of the ETV5/p38 Signaling Axis in Aggressive Thyroid Cancer Cells.Molecular cancer therapeutics · 2026Article
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- Correction: Multi-gene co-mutations of BRAF with TERT, PIK3CA, or TP53 are powerful predictors of central lymph node metastasis in papillary thyroid carcinoma.Frontiers in endocrinology · 2026Article
- Immunophenotypic Panel for Comprehensive Characterization of Aggressive Thyroid Carcinomas.Cells · 2025Article
- Genetic modification of the AJCC classification of papillary thyroid cancer: an international, multicentre, retrospective cohort study.The Lancet. Oncology · 2025Article
- AURKB and PI3K/AKT/mTOR pathways converge to regulateiScience · 2025Article
- TERT Promoter C228T and C250T Hotspot Mutations Are Absent in BRAF V600E-Positive Langerhans Cell Histiocytosis.Cancer medicine · 2025Article
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
- BRAF-induced EHF Expression Affects TERT in Aggressive Papillary Thyroid Cancer.The Journal of clinical endocrinology and metabolism · 2025Article
- Multi-gene co-mutations ofFrontiers in endocrinology · 2025Article
- Viral infection and thyroid disorders: a narrative review.Frontiers in microbiology · 2025Review
- Application and recent advances in conventional biomarkers for the prognosis of papillary thyroid carcinoma.Frontiers in oncology · 2025Review
- Blocking interplay between TERT and c-Myc: a new therapeutic strategy forInternational journal of biological sciences · 2025Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The unique oncogene duet of coexisting BRAF V600E and TERT promoter mutations are widely found to be a robust genetic background promoting human cancer aggressiveness, but the mechanism is unclear. Here, we demonstrate that the BRAF V600E/MAP kinase pathway phosphorylates and activates FOS, which in turn acts as a transcription factor to bind and activate the GABPB promoter, increasing GABPB expression and driving formation of GABPA-GABPB complex; the latter selectively binds and activates mutant TERT promoter, upregulating TERT expression. Elevated TERT functions as a strong oncoprotein, robustly promoting aggressive behaviors of cancer cells and tumor development. We thus identify a molecular mechanism for the activation of mutant TERT by the BRAF V600E/MAP kinase pathway, in which FOS as a transcriptional factor of GABPB promoter plays a key role in functionally bridging the two oncogenes in cooperatively promoting oncogenesis, providing important cancer biological and clinical implications.
Indexed as
Identifiers
What OpenQuestion holds
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.