Understanding Carcinogenesis for Fighting Oral Cancer

Tanaka, Takuji; Ishigamori, Rikako

doi:10.1155/2011/603740

Cited by 135 publications

(150 citation statements)

References 81 publications

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“…The biological basis for the concept of oral premalignancy has been established by carcinogenesis studies [7,[28][29][30].…”

Section: Leukoplakiamentioning

confidence: 99%

“…The rat tongue mucosa SCC induced by the oral administration of 4-nitroquinoline 1-oxide (4-NQO) in drinking water is also a good model for human oral cancer [28,30,58]. When 20 ppm 4-NQO in drinking water was administered orally to rats for eight weeks, followed by the administration of normal tap water without 4-NQO for 24 weeks, gross changes including leukoplakia, erosions, ulcers and papillary tumors on the dorsum of the posterior tongue developed (Figure 6).…”

Section: Animal Models Of Oral Carcinogenesismentioning

confidence: 99%

“…The findings of genetic alterations in defined premalignant lesions, as well as in the non-malignant epithelium, have indicated that oral carcinogenesis is a multistep process associated with the accumulation of genetic insults over time [28,30,78]. Given the readily accessible means for objectively assessing premalignant lesions in the oral cavity, the concept of chemoprevention, whereby the use of a pharmacological or natural agent is intended to halt this process, has been an attractive topic in oral SCC.…”

Section: Chemopreventionmentioning

confidence: 99%

“…Since oral cancer is an aggressive malignancy, more work is needed to improve our understanding of the natural history of the disease and to identify key molecular alterations that render transformation irreversible. Over the past few decades, many chemopreventive agents have been studied for cancers in a variety of tissues, including the oral cavity [28,30,[78][79][80][81]. Candidate agents include retinoids, cyclooxygenase inhibitors, green tea polyphenols, p53-targeted agents, thiazolidinediones and epidermal growth factor receptor (EGFR) inhibitors have all been evaluated [80,81].…”

Section: Chemopreventionmentioning

confidence: 99%

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Preneoplasia and carcinogenesis of the oral cavity

Watanabe¹,

Ohkubo²,

Shimizu³

et al. 2015

Oncol Discov

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Oral cancer, ranking sixth in the cancer incidence worldwide, is one of the most common neoplasms. Preneoplastic or premalignant (precancerous) lesions are lesions that can potentially transform into malignancy in a variety of tissues, including the oral cavity. Such oral lesions may be caused by tobacco use, exposure to the human papillomavirus and chewing of the betel nut. These substances contain carcinogens and/or tumor promoters. The mucosa of the oral cavity is covered with squamous epithelium and is relatively resistant to injury. However, exposure to these substances can cause the mucosa to undergo changes. The changes are usually initiated by a leukoplakic patch. While some leukoplakic patches recover and resolve, others progress to squamous cell carcinoma with or without invasion. Other premalignant lesions include oral submucous fibrosis, which is a potentially malignant condition caused by the abuse of the betel nut. Understanding the histology, premalignant states and molecular mechanisms of oral carcinogenesis may facilitate the development of novel strategies for the prevention and treatment of oral cancer. In addition, early detection is of critical importance to improve the survival rates of patients with oral cancer. In this review, we will summarize these aspects of oral cancer development, beginning from the histology of the oral cavity.

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“…The biological basis for the concept of oral premalignancy has been established by carcinogenesis studies [7,[28][29][30].…”

Section: Leukoplakiamentioning

confidence: 99%

Section: Animal Models Of Oral Carcinogenesismentioning

confidence: 99%

Section: Chemopreventionmentioning

confidence: 99%

Section: Chemopreventionmentioning

confidence: 99%

See 2 more Smart Citations

Preneoplasia and carcinogenesis of the oral cavity

Watanabe¹,

Ohkubo²,

Shimizu³

et al. 2015

Oncol Discov

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“…It is one of the major global threats to public health [16]. Oral cancers have been reported as the 6 th most common cancer worldwide [17,18].…”

Section: Epidemiology Of Oral Cancer In Nigeriamentioning

confidence: 99%

Oral Cancer- The Nigerian Perspective

Okoh¹,

Okoh²

2017

J Mol Biomark Diagn

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Study background: In our environment, oral cancer is one of the most common lethal diseases encountered in dental practice. It is frequently diagnosed in the late stages because most patients present late in the course of the disease. This may be attributed to their low socioeconomic status, illiteracy, and some traditional beliefs in alternative native therapies. Some authors have reported on oral cancers specifically in their individual geographic settings; however, there is a paucity of reviews on Oral cancers generally in our environment. This study aims to review the prevalence, awareness and clinicopathologic patterns of oral cancers across the different geographic zones in Nigeria.Methods: Information was sourced from journals, electronic data base such as Medline, Pubmed, Elsevier ScienceDirect and personal research work.Result: Several prevalence rates have been reported in different geopolitical locations in our environment. Orofacial carcinomas were reported mostly in the older age groups while the Orofacial sarcomas were found in the slightly younger age groups. Squamous cell carcinoma was the predominant histopathological type. There is a low level of awareness of these lesions among the low socio-economic groups which makes them present late in our health care facilities hence a poor prognosis. Conclusion:There is a need for increased awareness, advocacy and preventive care and early detection.

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Promotion of cell proliferation by the proto‐oncogene DEK enhances oral squamous cell carcinogenesis through field cancerization

et al. 2017

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Oral squamous cell carcinoma (OSCC) develops through a multistep carcinogenic process involving field cancerization. The DEK gene is a proto‐oncogene with functions in genetic and epigenetic modifications, and has oncogenic functions, including cellular proliferation, differentiation, and senescence. DEK overexpression is associated with malignancies; however, the functional roles of DEK overexpression are unclear. We demonstrated that DEK‐expressing cells were significantly increased in human dysplasia/carcinoma in situ and OSCC. Furthermore, we generated ubiquitous and squamous cell‐specific doxycycline (DOX)‐inducible Dek mice (iDek and iDek‐e mice respectively). Both DOX+ iDek and iDek‐e mice did not show differences in the oral mucosa compared with DOX‐ mice. In the environment exposed to carcinogen, DOX‐treated (DOX+) iDek mice showed field cancerization and OSCC development. Microarray analysis revealed that DEK overexpression was mediated by the upregulation of DNA replication‐ and cell cycle‐related genes, particularly those related to the G 1/S transition. Tongue tumors overexpressing DEK showed increased proliferating cell nuclear antigen and elongator complex protein 3 expression. Our data suggest that DEK overexpression enhanced carcinogenesis, including field cancerization, in OSCC by stimulating the G 1/S phase transition and promoting DNA replication, providing important insights into the potential applications of DEK as a target in the treatment and prevention of OSCC.

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Understanding Carcinogenesis for Fighting Oral Cancer

Cited by 135 publications

References 81 publications

Preneoplasia and carcinogenesis of the oral cavity

Preneoplasia and carcinogenesis of the oral cavity

Oral Cancer- The Nigerian Perspective

Promotion of cell proliferation by the proto‐oncogene DEK enhances oral squamous cell carcinogenesis through field cancerization

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