Cytogenetic studies were performed on endometrial specimens from four patients with hyperplasia, six with adenocarcinoma and one with mixed mesodermal tumor. Except for one cell, all 65 cells from the hyperplastic specimens had a normal female karyotype. However, a total of 92 cells from the 5 adenocarcinoma specimens had chromosomal abnormalities, though all 20 cells from a specimen of a well differentiated adenocarcinoma showed a normal karyotype. The chromosome number and morphology of the aneuploid cells had minimal changes. The modal number of chromosomes was pseudodiploid in one case and hyperdiploid in four. Three kinds of structural abnormalities involving chromosomes 1q were identified as of clonal origin: del. 1 (p21) in 2 cases, t. dic (1;16) (p21;q24) in one case and i (1q) markers in 2 cases. Since the carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to a partial trisomy or tetrasomy of the long arm of a chromosome 1. This involvement of the long arm of chromosome 1, therefore, may be assumed to represent a karyotypic change in the characteristics of adenocarcinoma of the endometrium. Complex karyotypes with many rearranged chromosomes were observed in cells from the mixed mesodermal tumor. The karyotypic differences between endometrial carcinoma and the mixed mesodermal tumor suggest that the genesis (and its mechanism) of the former may differ from that of the latter.

A family diagnosed as cancer family syndrome because endometrial cancer was found in a member of this colorectal cancer-prone family was reported. The fact that uterine (endometrial) cancer was found in a family member during the serial follow-up of this family shows that there is no more than a difference of time between familial colorectal cancer and cancer family syndrome. The clinical significance of the familial cancer aggregation would be an important clue in the early detection of another new cancer in the family.

The direct and indirect anti-cell proliferation effects of IFN-alpha produced by BALL-1 cells were examined. Of 23 cell lines, 7 including 2 normal diploids were resistant to a dose 1000 IU/ml of IFN-alpha. On the other hand, 16 cell lines were sensitive and showed IC50 values of less than 1000 IU/ml. This anti-cell proliferation spectrum showed no specificity to tumor origin and its activity was reversible. Cellular oncogene expression was markedly suppressed by IFN-alpha treatment. This finding showed that there might be some correlation between anti-cell proliferation activity and anti-oncogene expression activity. Furthermore, by activating natural killer cell activity and antibody dependent cell-mediated cytotoxicity, IFN-alpha potentiated indirect anti-cell activity.

Adult T-cell leukemia/lymphoma (ATL) is an endemic disease in the Southwestern districts of Japan. Intrafamilial cluster of ATL and other T-malignancy frequently reported in these area. We reported cases of ATL and non-Hodgkin's lymphoma in brothers, they were born in Hokkaido where is non-endemic area of ATL. The first case (ATL) is 53 y. male and the second case (non-HD), younger brother of the first case, is 55 y male. Anti-ATLA (ATL-virus associated antigen) antibody were positive in both of them, their elder sister, wife and child of the first cases. Examination of anti-ATLA antibody and follow up study is necessary in the family members of ATL, because they may be in a high risk group of ATL outbreak.