ArticleMund-, Kiefer- und Gesichtschirurgie : MKG2007
[Exploration of tumor suppressors p16INK4a and p14ARF in oral leukoplakias].
Article in Mund-, Kiefer- und Gesichtschirurgie : MKG, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 1 citations in OpenAlex.
- Ultrasonically assisted anchoring of biodegradable implants for chevron osteotomies - clinical evaluation of a novel fixation method.The open orthopaedics journal · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inactivation of p16 and p14ARF is considered to be an important step in the carcinogenesis of oropharygeal carcinomas. This consideration is supported by the observation of multiple allelic losses in the coding loci of chromosome 9p21 in squamous cell carcinomas and in dysplastic premalignant lesions. The present study hypothesized that comparable alterations already occur in leukoplakia, which are seen as potential predecessors of oral squamous cell carcinomas and that it is possible to differ leukoplakia with from leukoplakia without further malignant transformation. Furthermore we evaluated, whether such leukoplakia show sequence alterations in the genes p16 and p14ARF, which are capable to cause a limitation in gene function. The results show that the LOH pattern in genes p16 and p14ARF occur as well in leuplakia with malignant transformation as in leukoplakia, that do not show clinical alterations. The rate of allelic loss did not differ significantly. Overall, the incidence of allelic loss was lower in leuplakia compared to succeeding squamous-cell carcinomas (p<0,05). The results further illustrated an increase in LOH patterns in dyplastic leukoplakia, without reaching statistical significance. Significant increases in allelic losses were found in heavy smokers, (p < 0,05). PCR analysis of the exons 1-alpha, exon 1-beta and exon 2 in leukoplakia, containing LOH patterns did not show genetic alterations. Thus we concluded, that gene deletion and gene mutation have a minor role in the inactivation process of p16 and p14ARF in oral leukoplakia. Representing an early process in carcinogenesis, gene deletion and mutation occur in leukoplakia with and without malignant transformation. Therefore, taken as a singular parameter they represent an uncertain criteria to assess the potential of malignant transformation. However they could provide information in combination with other genetic factors like chromosomal methylation patterns and histology.
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