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K Nishida

Publications and source records attributed to K Nishida.

596 records · Page 34Linked to original sources

Introduction of the c-kit gene leads to growth suppression of a breast cancer cell line, MCF-7.

Normal ductal cells of the breast are exceptional on that their epithelial cells abundantly express the c-kit receptor. Loss of c-kit expression has been reported in 80-90% of breast cancer specimens, suggesting a possible role in the development of tumors. In the present study, we introduced a c-kit expression vector into a breast cancer cell line. MCF-7, which does not express c-kit but does express its ligand, stem cell factor (SCF). Anchorage dependent and independent growth was found to be inhibited in bulk cultures of the c-kit transfectants, although this suppression appeared to be incomplete, allowing a considerable fraction to tolerate c-kit expression. Heterogeneous sensitivity to the suppressive effects mediated by the c-kit receptor was also observed among individual clones isolated from the bulk cultures. These results suggest that c-kit can mediate inhibitory signals for the growth of breast cancer cells, but that cellular heterogeneity exists regarding the response. Further studies are warranted to elucidate the molecular basis for the inhibitory effects of c-kit.

Animals↗

In vivo tumouricidal effect of T lymphocytes activated by liposomes containing adriamycin on chemically-induced rat malignant fibrous histiocytoma.

The augmentative effect of liposomes containing adriamycin (LADM) in the host-tumour immune mechanism was assessed using 9,10-dimethyl-1,2-benzanthracene induced rat malignant fibrous histiocytoma (MFH). The antitumour effect of LADM was analyzed using a double grafted tumour system in which F344 rats first received simultaneous s.c. inoculations of MFH cells in both right and left flanks and were then injected with 0.2 mg of LADM into the right tumour on Day 10, 12, and 14. The growth of a remote, non-treated tumour was strongly inhibited, and the infiltration of CD8+ or CD4+ cells at the tumour periphery was histologically revealed. This inhibition was not observed in F344 nu/nu athymic rats. Winn neutralizing assay with T cell-rich splenic lymphocytes from each drug-treated MFH-bearing rat showed that complete regression of the tumour at a low effector/target ratio occurred only in the LADM-treated group. Furthermore, the tumouricidal effects were demonstrated in coexistence with CD8+ cells and CD4+ cells by assay with FACS sorting splenic lymphocytes. These results strongly suggest that intratumoural administration of LADM caused the systemic augmentation of the MFH-bearing host immune mechanism, and that the augmented response after LADM treatment was induced by the cytotoxic CD8+ lymphocytes dependent on the CD4+ lymphocytes.

9,10-Dimethyl-1,2-benzanthracene↗