ArticleOncogene2000
RAS oncogene activation induces proliferation in normal human thyroid epithelial cells without loss of differentiation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 50 citations in OpenAlex.
- RAS-Mutant Follicular Thyroid Tumors: A Continuous Challenge for Pathologists.Endocrine pathology · 2024Review
- Epigenetic Silencing of SOX15 Is Controlled by miRNAs rather than Methylation in Papillary Thyroid Cancer.Disease markers · 2021Article
- Molecular Determinants of Thyroid Nodules with Indeterminate Cytology andThyroid : official journal of the American Thyroid Association · 2021Article
- Coding Molecular Determinants of Thyroid Cancer Development and Progression.Endocrinology and metabolism clinics of North America · 2019Review
- A Review of Driver Genetic Alterations in Thyroid Cancers.Iranian journal of pathology · 2018Review
- Oncogenes, mitochondrial metabolism, and quality control in differentiated thyroid cancer.The Korean journal of internal medicine · 2017Review
- NRAS codon 61 mutation is associated with distant metastasis in patients with follicular thyroid carcinoma.Thyroid : official journal of the American Thyroid Association · 2014Article
- Molecular pathogenesis and mechanisms of thyroid cancer.Nature reviews. Cancer · 2013Review
- New treatment in advanced thyroid cancer.Journal of oncology · 2012Article
- Genetic alterations in the phosphatidylinositol-3 kinase/Akt pathway in thyroid cancer.Thyroid : official journal of the American Thyroid Association · 2010Review
- The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Current genomics · 2007Article
- Suppression of Egr-1 transcription through targeting of the serum response factor by oncogenic H-Ras.The EMBO journal · 2006Article
- Article
- RET/PTC-induced dedifferentiation of thyroid cells is mediated through Y1062 signaling through SHC-RAS-MAP kinase.Oncogene · 2003Article
- Article
- Altered gene expression in immunogenic poorly differentiated thyroid carcinomas from RET/PTC3p53-/- mice.Oncogene · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neoplastic transformation of rodent thyroid epithelial cell lines by mutant RAS genes has been widely studied as an experimental model of oncogene-induced loss of tissue-specific differentiation. However, separate evidence strongly implicates RAS mutation as an early event in human thyroid tumour development at a stage prior to loss of differentiation. To resolve this controversy we examined the short- and long-term responses of normal human thyroid epithelial cells to mutant RAS introduced by micro-injection and retroviral transduction respectively. In both cases, expression of RAS at a level sufficient to induce rapid proliferation did not lead to loss of differentiation as shown by expression of cytokeratin 18, E-cadherin, thyroglobulin, TTF-1 and Pax-8 proteins. Indeed, RAS was able to prevent, and to reverse, the loss of thyroglobulin expression which occurs normally in TSH-deficient culture medium. These responses were partially mimicked by activation of RAF, a major RAS effector, indicating involvement of the MAP Kinase signal pathway. The striking contrast between the effect of mutant RAS on differentiation in primary human, compared to immortalized rodent, epithelial cultures is most likely explained by the influence of additional co-operating abnormalities in the latter, and highlights the need for caution in extrapolating from cell line data.
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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.