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Biomedical subjects

Y Hashimoto

Publications and source records attributed to Y Hashimoto.

At least 1,369 records · Page 76Linked to original sources
PubMed1986

[Phase II study of bronchial artery infusion of mitomycin C in non-small cell lung cancer].

A phase II study of bronchial artery infusion of mitomycin C (MMC) was performed in 14 patients with non-small cell lung cancer (6 patients with adenocarcinoma, 6 patients with squamous cell carcinoma and 2 patients with large cell carcinoma). MMC at a dose of 20 mg was infused into the bronchial artery (total dose 20-60 mg, mean 27 mg). Among the 14 patients, one with adenocarcinoma of the lung showed partial response. The response rate for bronchial artery infusion of MMC was thus 7.1%. The toxic effects included anemia (35.7%), leukopenia (28.6%), thrombopenia (14.3%), elevation of GPT (14.3%), anorexia (14.3%), nausea (7.1%) and eruption (7.1%).

Adult↗
PubMed1986

Malignant transformation of rat liver cells by N-benzoyloxy-3'-methyl-4-methylaminoazobenzene and its related compound.

N-Benzoyloxy-3'-methyl-4-methylaminoazobenzene-(N-benzoyloxy-3'-Me-MAB) was highly toxic to rat liver epithelial cells (Ac2F) and induced many more chromosome aberrations and unscheduled DNA synthesis than did 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB). N-Benzoyloxy-3'-Me-MAB and its related compound, N-acetoxy-4-methylaminoazobenzene, efficiently induced malignant transformation of the cells, but 3'-Me-DAB was not so effective. The cells transformed by N-acyloxy-4-methylaminoazobenzene (N-acyloxy-MAB) derivatives showed significant increases in plating efficiency in liquid medium and in the size of aggregates in rotation culture. Such increases were not seen in the 3'-Me-DAB-transformed cells. The results indicate that the N-acyloxy form of the 4-dimethylaminobenzene derivatives seems very likely to be the ultimate metabolite.

Animals↗
PubMed1986

[A case of colon cancer associated with schistosomiasis japonica].

A case of colon cancer associated with schistosomiasis japonica is reported. A 60-year-old man was admitted with the complaint of melena. Barium enema study revealed a colon tumor (type 1') 11 cm from the anal ring. Sigmoidectomy was performed, and no lymph node metastasis was observed. Histologically, the tumor was diagnosed as well-differentiated adenocarcinoma, and also many schistosoma ova were found not only in the lesion of the carcinoma, but also in the tissue surrounding the carcinoma. In the latter lesion, ova were observed beneath muscularis mucosae. The distributions of the ova in the anal side of the tumor were more dominant than those in oral side. We review the direct correlation between gastrointestinal tract cancer and the schistosomiasis japonica in other reports.

Adenocarcinoma↗
PubMed1986

Radioimmunoimaging of human bladder tumor xenografts in nude mice by using monoclonal antibodies.

Monoclonal antibodies HBJ127 and HBJ8, raised against T24 human bladder cancer cells, predominantly react with the cells in proliferating stages and with a portion of epithelial tumor cells, respectively. To investigate the in vivo localization of these monoclonal antibodies, the antibodies were labeled with radioiodine and indium-111 (111In) and injected into nude mice transplanted with human bladder tumors. The BT-11 bladder tumor had the highest concentration of radioiodinated HBJ127 and HBJ8 monoclonal antibodies, with 11.6 and 14.3% of the injected dose per gram and with a tumor-to-blood ratio of 2.6 and 1.6, respectively, at 4 days after the administration. An irrelevant monoclonal antibody did not show any specific accumulation in the BT-11 tumor. The 111In-labeled HBJ127 antibody was also localized in the tumor with a higher tumor-to-blood ratio than the radioiodinated antibody. The xenografted BT-11 tumor was successfully visualized with the radiolabeled HBJ127 and HBJ8 antibodies by scintigraphy. These monoclonal antibodies and the human bladder tumor xenografts may provide a good model for radioimmunoimaging and possibly therapy.

Animals↗
PubMed1986

[Activation of oncogenes by chemical modification with carcinogens].

This article reviews the chemical modification of DNA (mainly proto-Ha-ras sequence) which causes mutation and induction of transforming activity. An initial chemical event caused by chemical carcinogens is modification of DNA with metabolically activated carcinogens. The chemical modification of DNA is thought to result in activation of oncogenes by mutation or reconstruction. The activated transforming oncogenes (mainly of the ras family, by point mutation) have been found in tumors induced by diverse carcinogens in vivo (reviewed briefly). Recently, results establishing that chemical modification of proto-oncogenes with carcinogens, such as benz (a) pyrene, acetylaminofluorene, Glu-P-1, 4NQO, and aflatoxin B1, induces transforming activity of the gene when transfected into NIH3T3 cells have been reported. The mechanism of activation of proto-Ha-ras by chemical modification has been investigated by RFLP (restriction fragment length polymorphism) assay and/or Southern blot analysis using synthetic oligonucleotides. Point mutations at codon 12 or 61 have been found. The correlation between the established chemistry of chemical modification of DNA with diverse carcinogens and activation of proto-oncogenes is discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Activation of c-Ha-ras proto-oncogene by in vitro chemical modification with 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) and 4-nitroquinoline N-oxide (4NQO).

Chemical modification of a plasmid containing the human c-Ha-ras proto-oncogene (pSVMBras-gpt) in vitro with the ultimate carcinogens N-acetoxy-2-amino-6-methyldipyrido[1,2-a: 3',2'-d]imidazole (N-OAc-Glu-P-1) and N-acetoxy-4-aminoquinoline N-oxide (N-OAc-4AQO) generated an activated oncogene that transformed NIH3T3 cells. As DNA is only cellular macromolecule present in the reactions, the results clearly show that the chemical modification of DNA with carcinogens alone can cause the induction of transformation of mammalian cells.

4-Nitroquinoline-1-oxide↗
PubMed1986

Relationship of macrophages to defective delayed-type hypersensitivity in B6/lpr mice.

These experiments were undertaken to clarify whether or not suppressor macrophages contribute to deficiency of delayed-type hypersensitivity induced by BCG CW immunization in B6/lpr mice. Addition of indomethacin in vitro did not increase MIF production by immunized lpr lymph node cells. Adherent cells in lymph node cell suspensions from lpr mice did not interfere with MIF production by nonadherent lymph node cells from immunized B6 mice. On the other hand, MIF production by nonadherent lymph node cells from immunized B6/lpr mice was not restored even if they were cultured with adherent lymph node cells from immunized B6 mice. In addition, macrophages from nonimmunized B6/lpr mice showed normal reactivity to MIF when lymphocytes coexisting with the macrophages in large proportions were depleted from PEC. These results suggest that macrophages make no contribution to the deficiency of DTH expression of B6/lpr mice.

Animals↗