Tobacco and alcohol related to the anatomical site of oral squamous cell carcinoma

Jovanovic, Andreas; Schulten, E.A.J.M.; Kostense, Pieter J.; Snow, Gordon B.; Waal, I. van der

doi:10.1111/j.1600-0714.1993.tb00125.x

Cited by 100 publications

(82 citation statements)

References 23 publications

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“…Alcohol and tobacco exposure have been identi®ed as important risk factors for this disease (Jovanovic et al, 1993). However, little is known regarding the molecular changes underlying this disease.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the FHIT gene and its product in squamous cell carcinomas of the head and neck

et al. 1998

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The FHIT gene has been implicated as a tumor suppressor gene in human malignancies. To determine if FHIT alterations play a role in human squamous cell carcinogenesis of the head and neck (HNSCC), we examined the gene and its product by RT ± PCR, SSCP, Northern, Southern, and Western blot analysis in primary HNSCC and/or HNSCC cell lines. Three of 32 tumor samples lacked detectable expression of FHIT by RT ± PCR but showed ampli®cation of a control gene of similar size. One of 29 primary tumors and 2/9 HNSCC cell lines exhibited aberrant transcripts generated by RT ± PCR methods using one set of 40 cycles of ampli®cation. FHIT mRNA expression was absent in seven HNSCC cell lines but detectable in primary keratinocytes by Northern analysis. Using speci®c polyclonal antiserum to the full-length FHIT protein in immunoblot analyses, 4/9 cell lines analysed showed no expression of pFhit, two exhibited low levels of expression, and three expressed a putative truncated pFhit. One of 15 tumors analysed also exhibited an overexpressed truncated protein. PCR/SSCP and Southern analysis of one cell line DNA that expressed a truncated protein indicated that it sustained homozygous loss of FHIT exon 5. Our results suggest that alterations in FHIT at the DNA, RNA, and protein levels exist at a low but signi®cant frequency in HNSCCs. Further studies regarding the potential biological activity of FHIT are needed to clarify the role of this gene in HNSCC tumorigenesis.

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Section: Introductionmentioning

confidence: 99%

Analysis of the FHIT gene and its product in squamous cell carcinomas of the head and neck

et al. 1998

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“…The most common sites for oral squamous cell carcinoma (SCC) are tongue, floor of the mouth and lip. High biological and prognostic diversity has been seen between SCCHN tumours originating from different sites (3)(4)(5). Tumours of the tongue are reported to have a unique gene expression pattern making it possible to separate them from other tumours in the oral cavity (6), emphasizing the need for site-specific studies.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of archival tongue squamous cell carcinomas provides sub-classification based on DNA repair genes

Rentoft

Laurell²,

Coates³

et al. 2009

Int J Oncol

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Abstract.A subgroup of patients with squamous cell carcinoma of the head and neck (SCCHN) comprise young persons under the age of 40, who have not been heavily exposed to the classical risk factors, smoking and alcohol. The number of SCCHN in young adults, particularly tongue tumours, is increasing in several parts of the world. Here we employed a novel gene expression array methodology specifically developed for analysis of degraded RNA and investigated the expression of 502 cancer-related genes in archival paraffin-embedded SCCHN of the tongue from young (≤40) and elderly patients (≥50). Genes detected as de-regulated in tumours compared to non-malignant controls were in concordance with results from earlier studies of fresh frozen material. No genes were detected as significantly differentially expressed between young and old patients suggesting that the overall pathobiology of SCCHN is similar in young and old. Unsupervised clustering divided tumours into three groups, irrespective of age, where several differentially expressed DNA repair genes were a prominent separation factor. High levels of DNA repair genes associated with impaired therapeutic response to radiation, suggesting that DNA repair genes play a role in clinical outcome after radiotherapy.

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“…The development of oral SCC shows a positive correlation with exposure to tobacco and alcohol. Multiple genetic changes are thought to contribute to the development of SCCs of oral cavity (2)(3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

p53 Transgenic Mice Are Highly Susceptible to 4-Nitroquinoline-1-Oxide-Induced Oral Cancer

Zhang

Wang

Yao

et al. 2006

Molecular Cancer Research

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In this study, we did a bioassay employing mice with a dominant-negative p53 mutation (p53 Val135/WT ) to assess whether a germ-line p53 mutation predisposed mice toward the development of squamous cell carcinomas (SCC) in the oral cavity. Treatment of the mouse oral cavity with 4-nitroquinoline-1-oxide produced a 66%, 91%, and 20% tumor incidence in the oral cavity, esophagus, and forestomach/stomach, respectively, in p53 Val135/WT mice. In contrast, only a 25%, 58%, and 4% tumor incidence was observed in oral cavity, esophagus, and forestomach/stomach, respectively, in wild-type littermates (p53 WT/WT ). The most striking difference between p53 Val135/WT and p53 WT/WT mice following the carcinogen treatment was the higher prevalence and more rapid development of SSC in p53 Val135/WT mice than in wild-type mice. To identify the precise genes or pathways involved in these differences during tumor development, we examined gene expression profiles of 4-nitroquinoline-1-oxide-treated normal tongues as well as tongue SCC in p53 Val135/WT and p53 WT/WT mice. Microarray and GenMAPP analysis revealed that dominant-negative p53 ( 135 Valp53) affects several cellular processes involved in SCC development. Affected processes included apoptosis and cell cycle arrest pathways, which were modulated in both tumor and normal epithelium. These results showed that reduction of p53-dependent apoptosis and increases in cell proliferation might contribute to the observed increase in oral cavity and gastroesophageal malignancies in p53 Val135/WT mice as well as to the more rapid growth and progression of tumors.

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Tobacco and alcohol related to the anatomical site of oral squamous cell carcinoma

Cited by 100 publications

References 23 publications

Analysis of the FHIT gene and its product in squamous cell carcinomas of the head and neck

Analysis of the FHIT gene and its product in squamous cell carcinomas of the head and neck

Gene expression profiling of archival tongue squamous cell carcinomas provides sub-classification based on DNA repair genes

p53 Transgenic Mice Are Highly Susceptible to 4-Nitroquinoline-1-Oxide-Induced Oral Cancer

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