ArticleCancer discovery2015
NF2 Loss Promotes Oncogenic RAS-Induced Thyroid Cancers via YAP-Dependent Transactivation of RAS Proteins and Sensitizes Them to MEK Inhibition.
Article in Cancer discovery, 2015. 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 90 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
90 citing papers in PubMed, 150 citations in OpenAlex.
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.Research square · 2026Article
- Stereotactic radiosurgery for NF2-related schwannomatosis and schwannomatosis-associated spinal tumors: a single-institution cohort.Journal of spine surgery (Hong Kong) · 2026Article
- Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.bioRxiv : the preprint server for biology · 2026Article
- Sp1 mechanotransduction regulates breast cancer cell invasion in engineered viscoelastic extracellular matrices.Biomaterials · 2026Article
- Article
- Dedifferentiation and Redifferentiation of Follicular-Cell-Derived Thyroid Carcinoma: Mechanisms and Therapeutic Implications.Biomedicines · 2025Review
- Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.European thyroid journal · 2025Review
- Alterations in gene expression associated with invasion of RAS-mutant thyroid tumors and their potential diagnostic and therapeutic utility.European thyroid journal · 2025Article
- RBM10 loss promotes metastases by aberrant splicing of cytoskeletal and extracellular matrix mRNAs.The Journal of experimental medicine · 2025Article
- Review
- Somatic copy number deletion of chromosome 22q in papillary thyroid carcinoma.European thyroid journal · 2025Article
- Development of animal models to study aggressive thyroid cancers.European thyroid journal · 2025Review
- Role ofCancers · 2024Review
- NF2: An underestimated player in cancer metabolic reprogramming and tumor immunity.NPJ precision oncology · 2024Review
- NF2-Related Schwannomatosis (NF2): Molecular Insights and Therapeutic Avenues.International journal of molecular sciences · 2024Review
- Columnar Cell Thyroid Carcinoma: A Heterogeneous Entity Demonstrating Overlap Between Papillary Thyroid Carcinoma and Follicular Neoplasms.Head and neck pathology · 2024Article
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- Genetic alterations in thyroid cancer mediating both resistance to BRAF inhibition and anaplastic transformation.Oncotarget · 2024Article
- Case report of selumetinib as a novel therapy in a neurofibromatosis type 2-associated ependymoma.Molecular therapy. Methods & clinical development · 2023Article
- Oncofetal reprogramming in tumor development and progression: novel insights into cancer therapy.MedComm · 2023Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrection:2019
Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledCh22q LOH is preferentially associated with RAS mutations in papillary and in poorly differentiated thyroid cancer (PDTC). The 22q tumor suppressor NF2, encoding merlin, is implicated in this interaction because of its frequent loss of function in human thyroid cancer cell lines. Nf2 deletion or Hras mutation is insufficient for transformation, whereas their combined disruption leads to murine PDTC with increased MAPK signaling. Merlin loss induces RAS signaling in part through inactivation of Hippo, which activates a YAP-TEAD transcriptional program. We find that the three RAS genes are themselves YAP-TEAD1 transcriptional targets, providing a novel mechanism of promotion of RAS-induced tumorigenesis. Moreover, pharmacologic disruption of YAP-TEAD with verteporfin blocks RAS transcription and signaling and inhibits cell growth. The increased MAPK output generated by NF2 loss in RAS-mutant cancers may inform therapeutic strategies, as it generates greater dependency on the MAPK pathway for viability. SIGNIFICANCE: Intensification of mutant RAS signaling through copy-number imbalances is commonly associated with transformation. We show that NF2/merlin inactivation augments mutant RAS signaling by promoting YAP/TEAD-driven transcription of oncogenic and wild-type RAS, resulting in greater MAPK output and increased sensitivity to MEK inhibitors.
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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.