Oral leukoplakias: to treat or not?

Tradati, Nicoletta; Grigolat, R.; Calabrese, Luca; Costa, Luigi; Giugliano, Gioacchino; Morelli, F.; Scully, Crispian; Boyle, Peter; Chiesa, Fausto

doi:10.1016/s1368-8375(97)00016-x

Cited by 46 publications

(24 citation statements)

References 45 publications

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“…Besides elimination of risk factors, medical therapy or surgery is usually undertaken 25 .The general treatment policy towards oral PM lesions at the investigating department is to perform a biopsy first. If a carcinoma is present, the patient is referred to an oncology department.…”

Section: Discussionmentioning

confidence: 99%

The effect of quitting smoking on the risk of unfavorable events after surgical treatment of oral potentially malignant lesions

Vladimirov

Schiødt

2009

International Journal of Oral and Maxillofacial Surgery

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Section: Discussionmentioning

confidence: 99%

The effect of quitting smoking on the risk of unfavorable events after surgical treatment of oral potentially malignant lesions

Vladimirov

Schiødt

2009

International Journal of Oral and Maxillofacial Surgery

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“…2 In India, oral leukoplakias have been reported to show a significant tendency to malignant transformation from 0.13 to 6% and rising to 14% or higher in cases of dysplasia. 3,4 Epidemiological studies reveal the betel quid and tobacco chewing habit as an important risk factor in the etiology of oral cancer in India. Since carcinogenesis is a multi-step process, therefore, in addition to insult by tobacco-associated intra oral carcinogens, several additional factors, such as genetic susceptibility of individuals and external agents, such as dietary factors and viruses (human papillomavirus, HPV, and Epstein-Baar virus, EBV), may play a synergetic role in oral tumorigenesis.…”

Section: Abstract: P53 Polymorphism; Hpv; Oral Cancermentioning

confidence: 99%

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Nagpal

Patnaik

Das

2001

Intl Journal of Cancer

136

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Key words: p53 polymorphism; HPV; oral cancerOral squamous cell carcinoma (OSCC) is the sixth most common malignancy and is a major cause of cancer morbidity and mortality worldwide. The overall survival percentage has not changed in recent years, despite extensive research on the biological and molecular aspects of oral SCC. Among the more pressing problems in clinical management are the lack of early detection and the high incidence of local-regional recurrence, even with aggressive surgical therapy. OSCC incidence accounts for up to 40% of all malignancies in India and South East Asia. 1 Moreover differences have been observed in the clinico-pathological and molecular pathological profile in the tobacco smoking and alcoholassociated oral cancers in the USA, UK, France, Japan, etc. and the chewing tobacco-associated oral cancers, particularly in the Indian sub-continent. 2 In India, oral leukoplakias have been reported to show a significant tendency to malignant transformation from 0.13 to 6% and rising to 14% or higher in cases of dysplasia. 3,4 Epidemiological studies reveal the betel quid and tobacco chewing habit as an important risk factor in the etiology of oral cancer in India. Since carcinogenesis is a multi-step process, therefore, in addition to insult by tobacco-associated intra oral carcinogens, several additional factors, such as genetic susceptibility of individuals and external agents, such as dietary factors and viruses (human papillomavirus, HPV, and Epstein-Baar virus, EBV), may play a synergetic role in oral tumorigenesis. [5][6][7][8] HPVs are a very heterogenous group of DNA viruses. Almost 90 HPV types have been described; 30 of these types are associated with anogenital cancers, forming either the high-risk types (HPV16 and HPV18) that are associated with anogenital invasive tumour and their precursor lesions or the low-risk types (HPV6 and HPV11) that rarely progress to malignancy. Analysis of viral genome has revealed that 2 early genes, E6 and E7, of high risk HPVs (16/18) are transforming genes that are responsible for maintenance of tumorigenic phenotype. 6,9,10 Genetic polymorphism at the genes involved in tumorigenesis may determine individual susceptibility of cancer. The genotype distribution of p53 codon 72 polymorphism is significantly different among ethnic groups. 11 Storey et al. 12 recently reported the probable correlation between p53 polymorphism and HPV associated cervical tumorigenesis. They showed that population homozygous for Arg-72 (arginine) is about 7 times more susceptible to development of cervical cancer than heterozygotes. However, this has been subject of much debate. Makni et al. 13 recently showed the substantial inter-laboratory variation in the proportion of Arg/Arg, Arg/Pro (proline) and Pro/Pro.In spite of its great relevance, so far only 2 contradictory reports have been proposed on the status of HPV in oral cancer on Indian population. The work on South Indian population has indicated 42% HPV-16 infection and 47% of HPV-18 infection, 7 whereas the r...

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“…Tradati et al [84] suggest surgical excision of all persistent leukoplakias because of poor patient compliance with follow-up. Other authors [55] recommend active treatment for lesions showing moderate or severe dysplasia, with oral sub-site being the deciding factor in whether or not to treat mild dysplasia.…”

Section: Potentially Malignant Oral Lesionsmentioning

confidence: 99%

Oral cancer in the UK: to screen or not to screen

1998

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Although oral squamous cell carcinoma accounts for only a small proportion of malignant neoplasms in the UK, oral cancer incidence and mortality rates have been rising in recent years. The natural history of oral cancer is not adequately understood at present and there is very little information about the epidemiology of precancerous lesions in the UK. There are also insucient data to provide ®rm evidence that the percentage of cases arising de novo is greater in the UK and the Western world as compared to the Indian subcontinent. Screening for oral cancer by visual examination is simple, inexpensive and causes little discomfort; however, there is no evidence for the eectiveness of screening for oral cancer either in reducing mortality from the disease or in reducing the incidence of invasive disease by detection and treatment of precancerous lesions. There is currently insucient evidence to recommend population screening for oral cancer in the UK. Measures aimed at primary prevention of the disease may be a more feasible method of disease control at present. #

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Oral leukoplakias: to treat or not?

Cited by 46 publications

References 45 publications

The effect of quitting smoking on the risk of unfavorable events after surgical treatment of oral potentially malignant lesions

The effect of quitting smoking on the risk of unfavorable events after surgical treatment of oral potentially malignant lesions

Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Oral cancer in the UK: to screen or not to screen

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