ArticleOncogene2003
Senescing oral dysplasias are not immortalized by ectopic expression of hTERT alone without other molecular changes, such as loss of INK4A and/or retinoic acid receptor-beta: but p53 mutations are not necessarily required.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
- Identification of Phenotypically Distinct Cancer Stem Cell Subpopulations in Oral Squamous Cell Carcinoma.Cancers · 2025Article
- A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer.International journal of molecular sciences · 2024Review
- Escape from Cellular Senescence Is Associated with Chromosomal Instability in Oral Pre-Malignancy.Biology · 2023Review
- Article
- Desmoglein-3 induces YAP phosphorylation and inactivation during collective migration of oral carcinoma cells.Molecular oncology · 2022Article
- Article
- Article
- Analysis of head and neck carcinoma progression reveals novel and relevant stage-specific changes associated with immortalisation and malignancy.Scientific reports · 2019Article
- The secreted protein S100A7 (psoriasin) is induced by telomere dysfunction in human keratinocytes independently of a DNA damage response and cell cycle regulators.Longevity & healthspan · 2014Article
- MAPK/ERK-dependent translation factor hyperactivation and dysregulated laminin γ2 expression in oral dysplasia and squamous cell carcinoma.The American journal of pathology · 2012Article
- Antitumor effect of retinoic acid receptor-beta2 associated with suppression of cyclooxygenase-2.Cancer prevention research (Philadelphia, Pa.) · 2009Article
- Tumor-suppressive activity of retinoic acid receptor-beta in cancer.Cancer letters · 2007Review
- Expression of hTERT immortalises normal human urothelial cells without inactivation of the p16/Rb pathway.Oncogene · 2006Article
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous work showed that acquisition of immortality at the dysplasia stage of oral cancer progression was consistently associated with four changes: loss of retinoic acid receptor (RAR)-beta and p16INK4A expression, p53 mutations and activation of telomerase. One atypical dysplasia (D17) that underwent delayed senescence after an extended lifespan showed loss of RAR-beta and p16INK4A/p14ARF expression, but retained functional wild-type p53 and telomerase was not activated. We now demonstrate that retroviral delivery of hTERT results in telomere lengthening and immortalization of D17 without loss of functional wild-type p53 activity. In contrast, the expression of hTERT in two other typical mortal dyplasia cultures (that retain RAR-beta and p16INK4A expression) does not extend their lifespan, even though telomeres are lengthened.
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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.