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Biomedical subjects

K Nishitani

Publications and source records attributed to K Nishitani.

64 records · Page 4Linked to original sources
PubMed1978

Tumor cell phagocytosis and cytotoxicity of lymphoblastoid cells following concanavalin A treatment.

Cell-to-cell interaction was investigated in various malignant tumor cells (human ovarial tumor, lung cancer, carcinoma of larynx and hamster melanoma cell) and in human lymphoblastoid cells (T-cell (MOLT-4 cell), thymoma cells and B-cells (Burkitt lymphoma cell)). Live lymphoblastoid cells did not adhere to the cell surfaces of tumor cells nor the lymphoblastoid cells were ingested by tumor cells without immunologic and specific treatment. Tumor cells as well as T-cells and B-cells had receptors to concanavalin A on their surfaces, and they showed marked cell binding of tumor cells and lymphoblastoid cells. Moreover, tumor cells that phagocytized lymphoblasts underwent marked cell destruction within 4 hours of cell binding. The cytolytic mechanism of the target tumor cell was probably related to contact with the lymphoblastoid cells and was increased by ingestive activity, and metabolic disturbance by lymphotoxin in tumor cells.

Animals↗
PubMed1978

Carcinogenesis in tissue culture. 29: Neoplastic transformation of a normal human diploid cell strain, WI-38, with Co-60 gamma rays.

WI-38 normal human diploid fibroblasts were exposed to Co-60 gamma rays 4 times at a total dose of 1400 rads and transformed into neoplastic cells in culture. The transformed WI-38 cells which are growing steadily without showing aging phenomena at the present time showed epithelial-like morphology, abnormal karyology, B-type isoenzyme pattern of glucose-6-phosphate dehydrogenase (G6PD), and produced sarcomas when transplanted into cheek pouches of hamsters treated with anti-hamster thymocyte serum.

Animals↗
PubMed1977

Carcinogenesis in tissue culture. 28. Comparison of various effects of a chemical carcinogen, 4-nitroquinoline I-oxide, on normal human cells and on normal mouse cells in culture.

A comparison of the effects on cultured cells of a chemical carcinogen, 4-nitroquinoline 1-oxide (4NQO), between normal human cells which were resistant to malignant transformation with 4NQO and normal mouse cells rather easily transformable was carried out. We studied the following effects of 4NQO on normal human and normal rodent cells; 1) cytotoxicity, 2) DNA, RNA and protein synthesis, 3) incorporation of 4NQO into cells and time course changes of the drug bound with macromolecular substances in cells, 4) DNA repair synthesis, and 5) chromosomal changes. Our results demonstrated that there were no differences in cytotoxicity and inhibition of cellular macromolecular syntheses between human and mouse cells. On the other hand, significant differences were noted in DNA repair synthesis and chromosomal aberrations between human and rodent cells. These differences suggest that mouse cells are easily transformed into neoplastic cells with chemical carcinogens as compared with human cells.

4-Nitroquinoline-1-oxide↗
PubMed1975

A human malignant cell line established from ascites of patient with embryonal carcinoma of ovarium.

In our attempts at establishing a cancer cell line from various ascites of cancer bearing patients, a cell line was successfully established from the ascites of a 63-year-old female with primary ovarian tumor (embryonal carcinoma). Histological findings of the peritoneum, due to metastasis, appeared to be cystadenocarcinoma, revealing the differentiation to non-epithelial cells which formed coarse networks and fibers, and morphologic changes of tissue cultures also reflected such histologic findings. At present the subculture has reached the 95th population doubling level, and cultured cells have assumed the morphology of mesothelial cells or fibroblasts with about 50 chromosomes. As a human malignant cell line, it is useful for the study of human malignant tumor cell.

Acid Phosphatase↗
PubMed1975

Phagocytosis of lymphoblastoid cells and cell destruction of human malignant tumor cells.

On the basis of the previous study, on the cell interaction between malignant tumor cells and other cells, especially with lymphocytes, the present study was carried out by investigating cell to cell interaction of human malignant tumor cells and human lymphoblastoid cells such as T-cell (MOLT-4 cell) and B-cell (Burkitt lymphoma cell). As a result it has been revealed that live lymphoblastoid cells were not adhered on the cell surface of the tumor cells, nor is it ingested by tumor cells, but in thepresence of HVJ (Sendai virus: 2,000 H.A. units) it adheres slightly on the cell surface of tumor cell but no cell fusion of tumor cells and lymphoblastoid cells is observable. On the other hand, the tumor cell as well as T-cell and B-cell all have receptors to concanavalin A (Con. A) on their cell surfaces, and they show a marked cell binding such as tumor cell and T-cell, tumor cell and B-cell, and there can be observed a marked phagocytosis of lymphoblastoid cells by tumor cells. Moreover, the tumor cells that have phagocytized lymphoblastoid cells undergo a marked cell destruction within 4 hours of cell-binding and phagocytosis, which is especially prominent in the case of phagocytosis of E.B cell by tumor cell.

Animals↗
PubMedDate not supplied

Multistep carcinogenesis of normal human fibroblasts. Human fibroblasts immortalized by repeated treatment with Co-60 gamma rays were transformed into tumorigenic cells with Ha-ras oncogenes.

Two normal mortal human fibroblast cell strains were transformed into immortal cell lines, SUSM-1 and KMST-6, by treatment with 4-nitroquinoline 1-oxide (4NQO) and Co-60 gamma rays, respectively. These immortalized cell lines showed morphological changes of cells and remarkable chromosome aberrations, but neither of them grew in soft agar or formed tumors in nude mice. The immortal cell line, KMST-6, was then converted into neoplastic cells by treatment with Harvey murine sarcoma virus (Ha-MSV) or the c-Ha-ras oncogene derived from a human lung carcinoma. These neoplastically transformed cells acquired anchorage-independent growth potential and developed tumors when transplanted into nude mice. All the tumors grew progressively without regression until the animals died of tumors. In addition, the tumors were transplantable into other nude mice. Normal human fibroblasts, on the other hand, were not transformed into either immortal or tumorigenic cells by treatment with Ha-MSV or c-Ha-ras alone. Our present data indicate that (1) the chemical carcinogen, 4NQO, or gamma rays worked as an initiator of carcinogenesis in normal human cells, giving rise to immortality, and (2) the ras gene played a role in the progression of the immortally transformed cells to more malignant cells showing anchorage-independent growth and tumorigenicity. In other words, the immortalization process of human cells seems to be a pivotal or rate-limiting step in the carcinogenesis of human cells.

4-Nitroquinoline-1-oxide↗