We analyzed specimens of head and neck squamous cell carcinomas (HNSCC) from 110 patients for p53 gene mutations, and 92 of them for human papillomavirus (HPV) infection, in order to evaluate the prognostic significance of these factors by comparison with clinical follow-up data. Mutations within the exons 5 to 8 of the p53 gene were found in 48 tumors (44%). Sequencing revealed in most cases mis-sense mutations (16/21). Frequency of p53 gene mutations was not related to the tumor stage or the presence of lymph node metastases. Of the 46 tumors that were analyzed by immunohistochemistry, 26 stained positively (56%). The number of positively stained nuclei increased slightly with decreasing differentiation of the tumors, whereas no correlation was found between tumor stage and immunoreactivity. An infection with the high-risk HPV types 16 and 18 could be detected in 39/92 tumor specimens (42%). Follow-up data were obtained from 99 patients within a range of 2 to 112 months. No dependence of overall survival on the presence of p53 gene mutations or HPV infection could be observed. The absence of statistically significant correlations between p53 gene mutation and progressive disease, however, does not deny its putative relevance in early phases of tumor development.

Monoclonal antibodies which react against T‐cell subpopulations and Langerhans' cells were used to examine the phenotype of immunocompetent cells in oral lichen planus. Immunomorphologically, the stromal infiltrate of this condition considerably resembled the delayed type of immune reaction. Although all subpopulations of immunocompetent cells were present in the stromal infiltrate, Langerhans' cells (OKT‐6 positive, HLA‐DR positive) and suppressor/cytotoxic T‐lymphocytes (OKT‐3 positive, OKT‐4 negative, OKT‐8 positive, HLA‐DR positive) predominated. Our immunohistological findings support the suggestion that aggregations of T‐lymphocytes are responsible for the cytotoxic processes which occur within the squamous epithelium in oral lichen planus.

Six oral papillomas and 7 oral leukoplakias were studied with genus‐specific antibodies against detergent‐disrupted papillomaviruses. Indirect immunofluorescence staining was applied to frozen sections. Distinct nuclear staining of superficial keratinocytes was seen in 5 of 6 oral papillomas, 2 of 5 homogenous leukoplakias, and in 2 cases of nodular leukoplakia, one of these showing transition into an invasive carcinoma. Papillomavirus antibodies offer a new way to detect and localize papillomaviruses in epithelial hyperplasias. The relevance of the immunomorphological identification of papillomavirus‐associated antigens is discussed with special reference to the molecular hybridization technique.

The local immune reaction of progressive chronic periodontal disease may be particularly influenced by macrophages and macrophage‐derived factors. Among these substances the prostaglandins and lysosomal enzymes may play an important pathogenetic role. Parallel immunohistochemical and radioimmunological studies were done to investigate the relationships of the immune‐competent cells and the inflammatory mediators in gingival tissues. The radioimmunological analysis revealed that prostaglandin E increases markedly in the established gingival lesions. Immunohistochemically prostaglandin E was mainly localized within macrophage‐like cells. Cytoplasmic lysozyme could be detected in these cells, too. On the other hand, the B‐cell response is the prominent feature in established chronic periodontal disease. However, there is apparently a disturbed B‐cell reaction as indicated by the irregular IgG‐subclass pattern and by the production of mainly monomeric IgA. The possible interactions of macrophages and especially B‐cells via prostaglandin E‐mediated mechanisms are discussed.

The aim of this study was to evaluate the presence and distribution of p53 alterations in pure endometrioid adenocarcinomas (n = 120) of different grades and stages, as opposed to normal endometrium (n = 13) and various risk groups of hyperplasia (n = 39). All samples were initially analysed by immunohistochemistry with the monoclonal antibody Ab-6. Normal endometria were negative. With increasing degrees of malignancy, the number of cases with p53 accumulation rose and ranged from 9% to 18% in hyperplasia, through 25% in low-grade carcinomas (G1), to 69% in high-grade carcinomas (G3). This increase was also seen when comparing tumours by stage. Of carcinomas in stage IA, only 17% showed p53 immunostaining, in contrast with 72% in stage IC. Of this material, 34 carcinomas and 8 hyperplasias were analysed for p53 mutations in exons 5-8 by means of polymerase chain reaction and temperature-gradient gel electrophoresis (TGGE). In none of 5 hyperplasia and 6 of 12 carcinomas showing p53 accumulation by immunohistochemistry, p53 mutations were detected by TGGE. In contrast, 4 of 22 carcinomas harboured mutant p53 but were negative by immunohistochemistry. Immunohistochemical and molecular investigations revealed that p53 alterations are related to the standard prognostic markers of endometrial cancer, i.e. grading and staging. TGGE, an indirect screening procedure for p53 mutations, is used to detect the type of p53 alteration and may provide additional insight into the complex figure of p53 abnormalities in the development and progression of malignant endometrial lesions.