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Mutations in the p53 tumor suppressor gene are the most frequent genetic alterations found in human tumors. There are mainly point mutations that lead to single amino acid substitutions. The mutated proteins have a longer half-life than wild-type p53 and accumulate in the nucleus of tumor cells. Anti-p53 antibodies have been found in sera of patients with several types of cancers including breast cancer. This report describes a T cell immune response in three patients with breast tumors who had mutated p53 gene and accumulated p53 protein. All showed a humoral response to p53 protein and the T cells of these patients recognized the wild-type p53 protein and proliferated in response to it. The data reported here are relevant to the immune processes leading to autoimmunity and have a bearing on anti-p53 vaccine development in tumor immunology.

Malignant histiocytosis (MH) is a true histiocytic disorder, whose identification is still based on too broad morphologic criteria. Using routine histology, cytochemical and immunohistochemical techniques on involved lymph nodes, 15 cases of MH have been investigated. Pleomorphism and cellular atypia, phagocytosis, lack of cohesiveness between proliferating cells, sinusoidal involvement, and plasmacytic infiltrate were the most common histologic features. MGG-stained imprints from 14 cases showed a composite tumor population mainly consisting of histiocyte-appearing cells, poorly differentiated atypical cells, and multinucleated giant cells. These cells, irrespective of cytologic features, revealed a diffuse, moderately to strongly positive reaction with acid phosphatase and nonspecific esterase. Naphthol-AS-D-chloroacetate esterase, Sudan black B, alkaline phosphatase, and beta-glucuronidase reactions were completely negative. Immunoperoxidase studies in 11 cases demonstrated that tumor cells stained positively for both kappa and lambda chains. These cells were also positive for albumin. Polytypic staining for IgG was observed in two cases, and a weak staining for lysozyme was found in two other nodes. Global results confirm the value of these studies for functional profile determination of MH proliferating cells. A combined approach using a variety of cytochemical and immunohistochemical techniques should be routinely considered in MH as useful additional studies for a more precise diagnostic definition of the disease.

It has been suggested that cytokeratin 13 is a useful marker of malignancy. We examined normal squamous cell epithelia, hyperplasia, dysplasias of various grades, intraepithelial neoplasia and invasive squamous cell carcinomas of the pyriform fossa using K13 and KL1. Positive staining for K13 was seen in all normal or hyperplastic benign epithelia, was inconstant in dysplasia, and intraepithelial neoplasia and carcinoma was negative. KL1 expression is constant and non significant. These results suggest that tumour cells are unable to synthesize keratin 13 a finding which may be valuable in surgical pathology.

Cytochemical reactions were examined in lymph node imprints from a group of 53 previously untreated patients with histologically proven Hodgkin's disease. In 40 of 51 cases investigated, Reed-Sternberg (R-S) cells, irrespective of the cytologic appearances and the histologic types, showed moderate to strong reactions with acid phosphatase (ACP). In 12 cases ACP activity was present in more than 25% of the R-S cells. The reaction consisted of formation of small- to medium-sized granules, which were located close to the nuclei on a diffusely positive background or irregularly distributed throughout the cytoplasm. In three cases, a coarse granular reaction product with periodic acid-Schiff was present. R-S cells were positive to the naphthol-AS acetate esterase and beta-glucuronidase reactions in four and two cases, respectively. Alkaline phosphatase and naphthol-AS-D-chloroacetate esterase reactions were completely negative. Our results have revealed a pattern of staining in the diagnostic R-S cells similar to that in its morphologic variants; this supports the view that these cells may derive from a common primitive cell. Moreover, the quality and quantity of the ACP reaction product shows that R-S cells differ from both neoplastic histiocytes of malignant histiocytosis and neoplastic lymphocytes of T-cell lymphomas. This study confirms that R-S cells lack definite cytochemical characteristics of each of supposed progenitor cells: histiocytes and T-lymphocytes.