Co-amplification of c-myc and c-erbB-2 oncogenes in a poorly differentiated human gastric cancer

c-erbB-2 oncogene has been reported to be frequently amplified in differentiated, tubular type of gastric cancer. Here we report a human gastric cancer which bore co-amplified c-myc and c-erbB-2 oncogenes: a portion of the amplified c-erbB-2 oncogene was found to be rearranged. Furthermore, c-myc and c-erbB-2 oncogenes were over-expressed in the tumor cells. In contrast to the previous reports, this gastric adenocarcinoma was classified as a poorly differentiated type, and was highly tumorigenic in nude mice. These results might suggest that activated c-myc and c-erbB-2 oncogenes co-operate and influence the malignant state of some gastric carcinomas.     

Surgical resection of pulmonary metastases from colorectal cancer. 10-year follow-up

Pulmonary resection of metastatic lesions from colorectal cancer was performed in 62 patients, and their cumulative 5-year and 10-year survival rates were 42% and 22%, respectively. The overall median survival was 24 months. The survival curve decrease even after 5 years after pulmonary resection; four of 13 patients who survived more than 5 years subsequently died of metastatic disease and only two patients survived more than 10 years. The number and size of the pulmonary metastases were significantly correlated with postthoracotomy survival. Solitary metastases less than 3.0 cm in diameter were good indicators of favorable postthoracotomy survival. There were no significant differences in survival based on Dukes' classification or location of the primary lesion. Sex, age, disease-free interval between the primary tumor and appearance of metastasis, and extent of pulmonary resection had no influence on survival. It is impossible to say from our experience that surgical resection of pulmonary metastases increased the cure rate. Presumably a good 5-year survival rate after thoracotomy would be a reflection of a length bias caused by the biologic behavior of the metastatic pulmonary lesions.     

Comparative, immunological studies on lymphangiectasia of the small intestine revealed in protein losing gastroenteropathy and Beh?et's disease.

Lymphangiectasia of the small intestine was demonstrated in 9 to 18 cases with protein losing gastroenteropathy and in 10 of 26 cases with Beh?het's disease. Protein losing gastroenteropathy was compared to Beh?et's disease in view of immunological aspects. Immunoglobulin containing cells in the jejunal mucosa of protein losing gastroenteropathy were decreased, whereas Beh?et's disease had normal or increased distribution. This suggested that suggested that immunoglobulin may be lost into the intestinal lumen or that production of those cells may be inhibited in protein losing gastroenteropathy. Decreased DNCB skin reaction and impaired blastoid transformation of peripheral lymphocytes in both of two diseases suggested that there should be immunological defect in those diseases. However, in Beh?et's disease, investigation of the thymus disclosed hyperplasia and the presence of lymphoid follicle which does not appear in normal state. In conclusion, protein losing gastroenteropathy is in immunological deficiency state due to the congenital or acquired disorders of lymphatics which implies abnormal protein loss, decreased immunoglobulin containing cells in the jejunal mucosa and decreased sensitivity. On the contrary, in Beh?et's disease hyperimmune state is present based on thymic hyperplasia.