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

Hybrid tumours are very rare tumour entities which are composed of two different tumour entities, each of which conforms with an exactly defined tumour category. The tumour entities of a hybrid tumour are not separated but have an identical origin within the same topographical area. In contrast, biphasically differentiated tumours are a mixture of two cellular patterns with a corresponding term in the tumour classification. Examples of a biphasic differentiation are: basaloid-squamous carcinoma, adeno-squamous carcinoma or sarcomatoid carcinoma, and epithelial-myoepithelial carcinoma, mucoepidermoid carcinoma or adenoid cystic carcinoma. Hybrid tumours must also be distinguished from the multiple occurrence of salivary gland tumours which can develop syn- or metachronously. In the tissue samples of more than 6600 salivary gland tumours covered by the Salivary Gland Register (Institute of Pathology, University of Hamburg, Germany) only 5 cases of hybrid tumours were recorded between 1965 and 1994. This means less than 0.1% of all registered tumours. Case 1 was a very rare example of a hybrid adenoma with differentiation as a basal cell adenoma and a canalicular adenoma of the parotid gland. The similar cellular origin of both types of adenoma may be an explanation for its development into a hybrid adenoma. Case 2 is a hybrid tumour with a composition of basal cell adenoma and a glandular type of adenoid cystic carcinoma. In both types of tumours the two cell types (duct-lining cells and modified myoepithelial cells) have a similar histogenetic origin. Therefore, the development of both cell types in a hybrid tumour with two trends of differentiation is possible. Case 3 represents a hybrid adenoma as a mixture of a Warthin tumour and a sebaceous adenoma. Although inclusions of sebaceous cells are observed in Warthin tumours, this hybrid tumour shows a composition of two different epithelial structures in a varied mixture. Case 4 is a very rare and unique hybrid carcinoma with two absolutely different components: acinic cell carcinoma and salivary duct carcinoma. The poor prognosis of this hybrid carcinoma is determined by the salivary duct carcinoma. Case 5 represents a hybrid carcinoma whose two components have a similar histogenetical basis: epithelial-myoepithelial carcinoma and a glandular type of adenoid cystic carcinoma. Both carcinomas are composed of variable proportions of ductlining cells and myoepithelial cells.

A rare, minor salivary gland tumour of the hard palate in a middle-aged woman was presented. The small (1.0 × 0.5 cm in diameter) hemispherical tumour was well circumscribed with a fine papillomatous surface. Histopathologically, tumour cells with eosinophilic cytoplasm and a large nucleus were single-strand cuboidal and columnar cells, which showed intraductal growth exhibiting a cribriform pattern. The histological features were distinct from adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma because the tumour lacked the neurotropic infiltration, cord-like proliferation and targetoid arrangement. The tumour could not be identified as a typical salivary-duct carcinoma because Roman bridging, papillary projection, and severe cell atypia were not found. Tumour cells were negative for PAS, Alcian blue, mucicarmine, p53, c-erbB-2, CEA, S-100 protein, α-smooth muscle actin, lactoferrin or vimentin. About 5% of the tumour cells were positive for proliferating cell nuclear antigen. Taking these factors into account, together with the clinical features, the name low malignant intraductal carcinoma seems appropriate.

The chemopreventive effect of oral and intraperitoneal (i.p.) administration of hexamethylene bisacetamide (HMBA) on 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced tumour formation in hamster cheek pouches was investigated. Male Syrian hamsters were treated by painting both cheek pouches with a 0.5% solution of DMBA twice weekly for 11 weeks. In addition to DMBA application, Group 1 hamsters were given 1% HMBA continuously in the drinking water and Group 2 hamsters received i.p. injection of HMBA at a dose of 500 mg/kg three times per week during the experiment. Group 3 animals received DMBA application alone. Thirteen weeks after the start of the experiment, the numbers of cheek pouch tumours and tumour volume were significantly decreased by oral but not i.p. administration of HMBA. Low levels of HMBA were detected in the plasma of the hamsters which were given 1% HMBA in drinking water. These results indicate that oral administration of HMBA can act as a chemopreventive agent against hamster cheek pouch tumorigenesis.

Recent evidence suggests that loss of heterozygosity (LOH) of the adenomatous polyposis coli (APC) gene plays a role in colorectal tumorigenesis and other cancers. However, little is known as to whether the APC gene contributes to the pathogenesis of oral squamous cell carcinoma. To assess involvement of both the APC gene and the human papillomavirus (HPV) in the development of oral pre-malignant and malignant lesions, we analysed DNA from 14 paired oral normal and pre-malignant or malignant paraffin-embedded biopsy specimens, and DNA from cultured normal and HPV 16-immortalised oral epithelial cells for the presence of LOH of APC and for HPV infection, using PCR based techniques. LOH of APC occurred in 80% of cases of oral epithelial dysplasia, 67% of carcinoma in situ, 50% of invasive squamous cell carcinoma cases, and in the HPV 16-immortalised oral epithelial cells. HPV was detected in half of the biopsy specimens, with HPV 16 as the dominant type. More than half of the carcinoma cases were found to contain both LOH of APC and HPV infection. These results suggest that LOH of APC is an early event during oral tumorigenesis. Our findings also suggest a strong correlation between HPV infection, particularly HPV 16, and LOH of the APC gene in oral squamous cell carcinomas.

p53 and bcl-2 are involved in the control of cell cycling and apoptosis. Environmental factors such as smoking and radiation can disturb p53 function and predispose a cell to malignant transformation. To investigate the role of p53 mutations, as well as p53 and bcl-2 protein expression in squamous cell carcinoma of the tongue, 39 samples were analysed. Since neck metastasis is the most important prognostic factor of this disease, samples from patients both with and without nodal disease were selected to find out whether there was any difference between the groups. Non-radioactive singlestranded conformation polymorphism (SSCP) was used to screen p53 mutations; an altered SSCP pattern indicating p53 mutation was found in 21 samples (54%). A significant correlation between tumour size, histological differentiation and p53 mutations was found (P < 0.01). Immunocytochemically, nuclear expression of p53 was moderate or strong in 18 (46%) samples. No correlation between altered p53 SSCP pattern and p53 immunoreactivity was seen, bcl-2 expression was cytoplasmic; moderate or strong staining was detected in only six of the carcinoma samples (15.5%). Interestingly, there was a significant correlation between smoking and bcl-2 expression (P < 0.01): all six samples with moderate or strong staining were taken from heavy smokers. Furthermore, all those patients died within 32 months.

Vitamin C is an essential nutrient whose protective influence in carcinogenesis has been reported frequently, suggesting that vitamin C inhibits the formation of some carcinogens and decreases the incidence and delays the neoplastic lesions. However, the mechanisms by which this occurs are unknown. In this study, the water soluble carcinogen 4-nitroquinoline-1-oxide (4NQO) has been used to induce a high yield of tumours in the oral cavity either singly or in combination with tobacco. Since the mucosa of rats is less susceptible to carcinogens than the hamster cheek pouch, the hamster cheek pouch has been used to study the influence of vitamin C on 4NQO-induced oral malignancy. The aim of this study was to determine whether topically applied vitamin C had an effect on the oral carcinogenesis induced by application of 4NQO. Similarly, an attempt was made to study the modulating effect of vitamin C on the histopathological and ultrastructural changes during the neoplastic process in the hamster. Vitamin C appeared to delay tumour induction and had other protective effects against neoplasia.

We performed a retrospective analysis on the effect of initial induction chemotherapy with two courses of cisplatin (each course 120 mg/m² cisplatin on day 1, then 20 mg/m² bleomycin (alone) per day for 5 days with 4 weeks between courses) in 75 consecutive patients with advanced cancer of the oral cavity or lip. Further local therapy consisted of surgery or radiation, depending on tumour location. In 18 resected patients adjuvant chemotherapy was added. This consisted of carboplatin, 400 mg/m² on day 1 then ftorafur alone, 500 mg/m²/day for 30 consecutive days, repeated every month for 4 consecutive months.

Among the patients treated in the neoadjuvant setting, complete response was observed in 10 out of 75 patients (13%), and partial response in a further 50 patients (67%) (partial plus complete rate 80%). Of all the patients, 43% in stage III and 26% in stage IV were long-term survivors. Improved survival was observed in surgical patients where adjuvant postoperative chemotherapy was added (P < 0.025).

The main toxic effect was vomiting, observed in 71 patients. We noted a low rate of stomatitis (4%) and an important hearing loss (12%).

Neoadjuvant and adjuvant cisplatin-based chemotherapy as part of a multidisciplinary approach have a high overall response rate and low toxicity, and should increase survival in cancer of the oral cavity or lip.

We have investigated the role of serum ferritin, in relation to disease stages, in patients with nasopharyngeal carcinoma. Patients with localised disease (Ho's stage I–IV) had levels which were not significantly different from age, sex matched normal subjects and there was no relationship between mean serum ferritin levels and stage. However, in patients with metastatic disease levels were grossly elevated with mean levels increased more than 6-fold compared to normal subjects and patients with localised disease. Furthermore, among the small group of patients with localised disease but hyperferritinaemia, the subsequent development of metastatic disease within 1 year was significantly much higher (32.4%) than in those with levels falling within the reference range (10.3%). Hyperferritinaemia is strongly associated with, and may predict, metastatic disease in patients with nasopharyngeal carcinoma.