European journal of cancer. Part B, Oral oncology最新文献

The aetiology of oral premalignant lesions is generally accepted to be multifactorial. Tobacco and alcohol are established as important cofactors in malignant development in the oral cavity, but in addition microorganisms, such as human papillomavirus (HPV), have gained much interest over the past decade. For many years, HPV has been accepted as an important cofactor in the development of cervical cancer, originating from a mucous membrane with similarities to the oral mucosa. 49 patients with oral premalignant lesions and 20 control patients with normal oral mucosa and no history of HPV infection were examined for the presence of HPV by immune histochemical staining using the peroxidase anti-peroxidase technique (PAP), DNA-DNA in situ hybridisation (ISH), and polymerase chain reaction (PCR) analysed by Southern blot hybridisation with an HPV 16 specific probe. The investigations revealed that HPV was found in 62.5% of the verrucous leucoplakias, 50.0% of the erythroplakias, 45.5% of the homogeneous leucoplakias, 33.3% of erythroleucoplakias and in 12.5% of the nodular leucoplakias. An overall HPV detection rate in the examined premalignant lesions was 40.8% and no patients in the control sample were positive. Concerning oral cancer development, it seems likely that HPV may be a cofactor, as 100% of patients who developed oral cancers within 4–12 years were all positive for HPV, one being positive for HPV 16.

Surgical specimens from 65 patients with squamous cell carcinoma (SCC) of the oral cavity were examined immunohistochemically. The clinicopathological significance of the expression of epidermal growth factor receptor (EGFR) and matrix metalloproteinase-3 (MMP-3) was assessed. Among the 65 tumours, 20 (30.8%) and 37 (56.9%) tested positively for EGFR and MMP-3, respectively. A positive correlation between the expression of EGFR and MMP-3 was found. The expression of EGFR in oral SCCs was associated with an advanced T stage of the primary tumour, an advanced pathological stage, and a high incidence of neck metastasis. In addition, MMP-3 was primarily expressed at the advancing front of cancer with a diffuse invasive mode. Thus, overexpression of MMP-3 was associated with an advanced pathological stage, a diffuse invasive mode, and a high incidence of neck metastasis. The analysis of MMP-3 expression is useful to evaluate the pathological status of tumours. Because EGFR-overexpressed tumour should produce larger amounts of MMP-3 in vivo, a close examination of oral SCC for expression of EGFR and MMP-3 should be helpful to predict their malignant potential.

As a tumour suppressor gene, the inactivation of p53 induces the development of numerous human cancers. Mutations of p53 have been implicated in the pathogenesis of head and neck squamous cell carcinoma (HN-SCC) at a high incidence. In premalignant lesions and in situ carcinomas, p53 overexpression is not exclusively restricted to neoplastic cells, but frequently affects the normal appearing keratinocytes adjacent to p53 positive neoplasms or present in dysplastic areas. These results suggest that as contributors to the early phases of HN-SCC development, p53 alterations may be excellent biomarkers that indicate the predisposition of a particular oral cavity premalignant lesion toward malignancy. In most cases, the p53 overexpression status of a tumour metastasis is identical to that of a primary tumour, indicating that a p53 mutation precedes metastatic spread. In patients with multiple primary tumours, multiple foci of p53 overexpression are observed in epithelia distant from the tumour. So the expression of p53 in normal epithelium would indicate an increased risk for transformation to second or third primary cancers. Distinct p53 mutations in different primary tumours of the same patient indicate that these cancers arise as independent events; these results support the existence of multifocal polyclonal processes. Regardless of the aforementioned results that support p53 as a valid tumour biomarker, most studies have shown no relationship between the expression of p53 and clinical and histopathological parameters. The role played by p53 mutations in the progression and vital prognosis of HN-SCC has not yet been demonstrated.

The area, perimeter and diameter of basal cell nuclei of rat palatal epithelium were measured and the deviation of the basal cell nuclear profile from the form of a sphere was assessed after the application of the carcinogen 4-nitroquinoline-1-oxide (4NQO). After a 24-week treatment-free period, designed to eliminate the irritant effect of the carcinogen, the rats were killed, the palatal mucosa was recovered and processed and the nuclear histometry was assessed with image analysis techniques. The basal cell nuclear area increased as the epithelium became dysplastic and then decreased as carcinoma developed, but there were significant variations in this parameter in the control groups. Basal cell nuclei from moderately or severely dysplastic epithelium, and from epithelium adjacent to areas of invasive carcinoma, were significantly less regular in profile by comparison with control nuclei. Variations in nuclear profile, but not nuclear area, perimeter or diameter, might reflect fundamental nuclear alterations of significance during the process of carcinogenesis.

Between 1985 and 1990, 99 head and neck cancer patients were treated at Mount Vernon Centre for Cancer Treatment in a CHART pilot study. The aims of this retrospective review were to obtain baseline data for this population on their pretreatment dental status and to determine the extent to which our conservative policy of teeth preservation is being realised. This is of particular interest because of the believed sparing of late normal tissue effects by CHART compared with conventional fractionation. Prior to treatment, 40% of patients were edentulous, and prophylactic dental clearance was avoided in 59% of the remaining (dentate) patients. Following radiotherapy, only 21% of dentate patients subsequently lost all their remaining teeth. The proportion of patients with full or partial upper dentures increased from 61% pretreatment to 76% post-treatment; the corresponding increase in lower dentures was 46% to 66%. However, actual usage of dentures decreased somewhat. There was only one documented case of (minor) osteo-radionecrosis of the mandible which resolved with conservative care. The greater use in our patients of prophylactic measures, in particular, chlorhexidine and fluoride mouthwashes seemed indicated.

Multiple basal cell carcinomas and odontogenic keratocysts of the jaws are a feature of the inherited naevoid basal cell carcinoma syndrome (NBCCS), although both occur more commonly as single, sporadic cases. The NBCCS gene has been mapped to chromosome 9q22.3-q31 and loss of heterozygosity for DNA markers from this region has been observed in familial and sporadic basal cell carcinomas. Based on these observations, we undertook a pilot study to determine if a similar pattern of chromosome loss occurs in odontogenic keratocysts. DNA extracted from microdissected odontogenic keratocyst epithelium was examined for loss of heterozygosity for six polymorphic DNA markers mapping to human chromosome 9q22.3-q31. Allelotype loss was detected in epithelium from three, single, sporadic odontogenic keratocysts. These results implicate homozygous inactivation of the NBCCS gene in the initiation and progression of the odontogenic keratocyst.

The aim of the present study is to characterise the cell kinetics of pleomorphic adenoma of the parotid gland by assessing DNA content and proliferating cell nuclear antigen (PCNA) positivity. In 22 parotid adenomas, DNA content was measured by densitometry in histological serial sections stained with Feulgen's method and PCNA positivity was determined by immunohistochemistry with the monoclonal antibody PC10. To assess the proliferative activity, DNA index and PCNA index were evaluated. It was possible to distinguish two types of adenoma. In Group I there was a prevalence of diploid cells with a low PCNA index. Group II is represented by adenomas with a large percentage of triploid cells and a PCNA index significantly higher than that of Group I. Our findings suggest that the possibility of recurrence or malignant transformation depends on intrinsic biological properties of each adenoma.

Oral manifestations are present in about 3–5% of cases of non-Hodgkin's lymphoma (NHL) and oral lesions are only rarely the initial manifestations of NHL. A case is presented of an 80-year-old patient with a NHL of the tongue, without visceral or lymph node involvement. The diagnosis of NHL can be made only by biopsy. The prognosis of NHL seems to be related to the tumour stage, tumour aggressiveness and response to treatment: the oral lesions appear to respond quite well to irradiation.