Alterations in copy number of c-erbB-2 and c-myc proto-oncogenes in advanced stage of human breast cancer.

In our previous study, amplification of c-erb B-2 and c-myc proto-oncogenes in DNA of human breast cancer occurred in 16% and 4% of cases, respectively, and increased copy number of these genes is suggested to be associated with aggressive primary tumors. We examined change in the copy number of c-erb B-2 and c-myc proto-oncogenes between primary and multiple metastatic tumors in 10 patients with breast cancer, who underwent breast surgery and were later autopsied, by using DNAs isolated from formalin-fixed paraffin-embedded tissues and the dot blot-hybridization method. In primary tumors, amplification of c-erb B-2 and c-myc was detected in three and two cases, whereas at the stage with systemic metastasis, it was detected in four and three cases, respectively.

Multicentric independent development of hepatocellular carcinoma revealed by analysis of hepatitis B virus integration pattern.

Two separate nodular lesions of hepatocellular carcinoma (HCC) were surgically removed from a patient with positive serum hepatitis B surface antigen. Southern blot analysis of DNA from the two separate HCC lesions showed different restriction patterns of integrated hepatitis B virus DNA, indicating their independent origins. The two lesions were composed mainly of poorly differentiated HCC; however, well-differentiated HCC was also observed in the periphery of the lesions.

Clonal origin of atypical adenomatous hyperplasia of the liver and clonal identity with hepatocellular carcinoma.

We present details of two separate nodular lesions of atypical adenomatous hyperplasia, within one of which a small area of overt hepatocellular carcinoma was detected. The patient was positive for serum hepatitis B surface antigen, and Southern blot analysis revealed that deoxyribonucleic acid from the lesions of hepatocellular carcinoma and surrounding atypical adenomatous hyperplasia showed the same restriction pattern of integrated hepatitis B virus deoxyribonucleic acid, indicating that the two lesions were derived from an identical clone. It was also indicated that the two separate lesions of atypical adenomatous hyperplasia were independently derived through clonal expansion of different cells.

Recombinant human tumor necrosis factor depresses serum iron in mice.

Recently many findings about the physiological and biochemical functions of recombinant human tumor necrosis factor (rHu-TNF) have been reported. In the present study, the effect of rHu-TNF on serum iron in C3H/HeN and C57BL/6 mice was determined. Blood samples were obtained before intravenous injection of rHu-TNF, and also at various times after the injection.