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Papillary adenoma of type II pneumocytes is a rare tumour. It is considered to be a benign neoplasm and is derived from immature cells in the bronchioloalveolar epithelium, however, its biological nature has not been elucidated. We report a case of an adenomatous tumour; a papillary adenoma of type II pneumocytes, which we regard as possessing malignant potential. Light microscopically, as well circumscribed, papillary tumour of predominantly cuboidal cells resembling type II pneumocytes was found, but Clara type and ciliated cells were also present. Immunohistochemically, the tumour cells reacted positively with antibodies to surfactant apoproteins (A, B), carcinoembryonic antigen, cytochrome P-450 1A1-2 and 2B1-2. Ultrastructurally, many osmiophilic lamellar bodies and electron-dense granules were demonstrated. Semi-serial sections revealed signs of transbronchial dissemination and vascular invasion. Morphometry using 12-dimensional cluster analysis disclosed features of the tumour cells which resembled those of pneumocyte type II adenocarcinoma. These findings suggest that the present case has some malignant characteristics and originates from immature bronchiolar or alveolar cells, with a potential to develop into both type II pneumocyte and Clara cell type adenocarcinomas.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental pollutant causing public concern. Its toxic effects include disruption of the immune, endocrine, and reproductive systems, impairment of fetal development, carcinogenicity, and lethality in rodents. Here, we report that TCDD induces apoptosis in two cultured human leukemic lymphoblastic T cell lines. This cell death was found not to be dependent on an aryl hydrocarbon receptor and to be inhibited by the inhibitor of tyrosine kinases and caspases. Apoptosis-linked c-Jun N-terminal kinase is rapidly activated in these cells by the treatment with TCDD. A dominant-negative mutant of c-Jun N-terminal kinase prevented cell death in the treatment with TCDD. Furthermore, TCDD decreases the Bcl-2 protein level in these cell lines. These findings will help in the understanding of the molecular mechanism underlying TCDD-mediated immunotoxicity.

To understand genetic events which play a role in the development and/or progression of human endometrial cancer, we studied allelotypes on all autosomal chromosomes, as well as chromosome X, with 42 microsatellite markers and 56 endometrial cancers. The most frequent loss of heterozygosity (LOH) was observed on the long arm of chromosome 10 (14 of 30, 47%), which was commonly detected in grade 1 cancer. We constructed a detailed deletion map and defined two commonly deleted regions in 10q25-q26; one was the 8 cM region between D10S209 and D10S216, the other was the 12 cM region between D10S217 and D10S590. Replication errors at two or more loci were observed in 24 of 56 tumours (43%), suggesting that disruption of the DNA mismatch repair system also plays an important role in the course of endometrial carcinogenesis.

The B-cell leukemia/lymphoma-2 (bcl-2) proto-oncogene is peculiar, as its product appears to provide survival advantage to B cells by blocking apoptosis. Expression of bcl-2 protein was analyzed in 54 cases of primary non-Hodgkin's malignant lymphomas of the oral cavity by immunohistologic staining of paraffin-embedded tissue. The immunophenotype of each tumor was established with the use of a panel of monoclonal and polyclonal antibodies to lymphoid cell differentiation antigens. The cases in the present study were 42 B-cell lymphomas, 7 T-cell lymphomas and 5 lymphomas revealing histiocytic markers. Sixteen of the 42 B-cell lymphomas were positive for bcl-2 protein, and were composed of 7 low-grade B-cell lymphomas and 9 highgrade B-cell lymphomas. Seven low-grade B-cell lymphomas were composed of one mucosa-associated lymphoid tissue type, three centrocytic types and three centroblastic-centrocytic types. Nine high-grade B-cell lymphomas comprised four centroblastic types, one immunoblastic type and four lymphoblastic types. Enhanced expression of the bcl-2 oncogenic protein was detectable in lymphoma cells in 2 cases for the T-cell lymphoma, and one case for the true histiocytic lymphoma. In contrast to the previous reports of American node-based lymphomas, Japanese primary oral lymphomas in our series expressed a lower frequency of bcl-2 protein. Furthermore, the present study indicated that bcl-2 protein was expressed on a wide variety of Bcell lymphomas, T-cell lymphomas and true histiocytic lymphoma, and that differences in bcl-2 protein expression may be useful in the diagnostic separation of lymphoblastic lymphoma with B-cell marker from Burkitt's lymphoma.