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Biomedical subjects

M Watatani

Publications and source records attributed to M Watatani.

43 records · Page 3Linked to original sources
PubMed1989

Primary small intestinal adenocarcinoma diagnosed by endoscopic examination prior to operation.

Progress in diagnostic procedures has made it possible to diagnose neoplasms of the gastrointestinal tract preoperatively. However, preoperative diagnosis of tumors of the small intestine remains difficult. We report here detection of an adenocarcinoma of the jejunum by endoscopic examination prior to operation. A 73-year-old woman was admitted with complaints of intermittent periumbilical pain, nausea, and vomiting. An upper gastrointestinal series showed an abnormal segmet 10 cm distal to the duodenojejunal flexure. Small intestinal endoscopic examination revealed a tumor with a crater and an irregular surface of mucosa near the duodenojejunal flexure, and annular constriction due to tumor extension, and endoscopic biopsy specimens contained tissue from a poorly differentiated adenocarcinoma. Wide resection, including the duodenum, proximal jejunum, and adjacent mesentery was performed. The resected tumor was confirmed histologically to be a poorly differentiated adenocarcinoma of the jejunum.

Adenocarcinoma↗
PubMed1987

Activated neu oncogene sequences in primary tumors of the peripheral nervous system induced in rats by transplacental exposure to ethylnitrosourea.

Neurogenic tumors were selectively induced in high incidence in F344 rats by a single transplacental exposure to the direct-acting alkylating agent N-ethyl-N-nitrosourea (EtNU). We prepared DNA for transfection of NIH 3T3 cells from primary glial tumors of the brain and from schwannomas of the cranial and spinal nerves that developed in the transplacentally exposed offspring between 20 and 40 weeks after birth. DNA preparations from 6 of 13 schwannomas, but not from normal liver, kidney, or intestine of tumor-bearing rats, transformed NIH 3T3 cells. NIH 3T3 clones transformed by schwannoma DNA contained rat repetitive DNA sequences, and all isolates contained rat neu oncogene sequences. One schwannoma yielded a transformant with rat-specific sequences for both neu and N-ras. A point mutation in the transmembrane region of the putative protein product of neu was identified in all six transformants and in the primary tumors from which they were derived as well as in 5 of 6 schwannomas tested that did not transform NIH 3T3 cells. Of 59 gliomas, only one yielded transforming DNA, and an activated N-ras oncogene was identified. The normal cellular neu sequence for the transmembrane region, but not the mutated sequence, was identified in DNA from all 11 gliomas surveyed by oligonucleotide hybridization. Activation of the neu oncogene, originally identified [Schechter, A.L., Stern, D.F., Vaidyanathan, L., Decker, S.J., Drebin, J.A., Greene, M.I. & Weinberg, R.A. (1984) Nature (London) 312, 513-516] in cultured cell lines derived from EtNU-induced neurogenic tumors that by biochemical but not histologic criteria were thought to originate in the central nervous system in BD-IX rats, appears specifically associated with tumors of the peripheral nervous system in the F344 inbred strain.

Animals↗
PubMed1987

Sensitivity to UV radiation of fibroblasts from a Japanese group A xeroderma pigmentosum patient with mild neurological abnormalities.

A 12-year-old girl, suffering from xeroderma pigmentosum (XP), had mild cutaneous and neurological abnormalities. She showed no neurological abnormalities at the age of seven, but areflexia of the patellar tendons at II. She had no malignant tumours. The skin fibroblasts from the patient were about twice as sensitive to the lethal effects of 254 nm ultraviolet (UV) radiation as those of Group C XP patients, and about twice as resistant as those of typical Group A XP patients. The ability of these fibroblasts to reactivate UV-damage adenovirus 5 was intermediate between those of Group C and typical Group A patients. The patient's cells were assigned to genetic complementation Group A by use of the cell-fusion technique. This is the first case in Japan of a Group A XP patient with mild neurological abnormalities. The mild cutaneous manifestations of this patient may be explained by the residual ability of the cells to repair UV-damaged DNA.

Adenoviruses, Human↗
PubMed1987

O6-methylguanine methyltransferase activity and sensitivity of Japanese tumor cell strains to 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)- 3-nitrosourea hydrochloride.

Using 40 tumor cell strains derived from various organs of Japanese tumor patients and also 12 normal cell strains, we have measured the activity of O6-methylguanine-DNA methyltransferase (MT), which can repair O6-methylguanine produced in DNA by alkylating agents. Then, the lethal sensitivities of the strains to the anti-tumor drug 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-)2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) were measured. The MT activity was assayed by measuring the 3H radioactivity transferred from the substrate DNA containing [methyl-3H]-O6-methylguanine to acceptor molecules in the cell extracts. Extracts from the majority of tumor strains and all normal cell strains contained substantial MT activity of varying degree, while the extracts of 6 tumor strains showed virtually undetectable MT activity. Hence these 6 strains were assigned as Mer-, the phenotype which is characterized by the inability to repair O6-methylguanine in DNA due to the lack of MT. The Mer- tumor strains were much more sensitive to ACNU than the rest of Mer+ strains, as measured by colony-forming ability. Furthermore, with all the tumor and normal strains tested, a good correlation was observed between MT activity and cellular resistance to ACNU. These results indicate that the frequency of Mer- strain is about 15% among Japanese tumor cell strains so far analyzed, and further suggest that MT may be the only system able to repair lethal DNA damage induced by ACNU.

Cell Survival↗
PubMed1985

Analysis of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced DNA damage in tumor cell strains from Japanese patients and demonstration of MNNG hypersensitivity of Mer xenografts in athymic nude mice.

Among 15 human tumor cell strains from Japanese patients, one strain derived from a patient with thyroid cancer showed inability to support the growth of adenovirus 5 treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). When plated on this Mer- strain, adenovirus 5 showed 3-4 times higher sensitivity to MNNG-induced killing than when plated on any of the other 14 Mer+ tumor cell strains. Biochemical analysis showed that the Mer- strain was defective in demethylation repair of O6-methylguanine produced by MNNG treatment. The sensitivities of 12 of the 15 human tumor strains, including the Mer- strain, to MNNG were compared by measuring their colony-forming abilities. All the strains tested showed the Rem- phenotype (having higher sensitivity to MNNG-produced cell killing than normal fibroblasts). The differential killing effects of MNNG on Mer- and Mer+ tumor cells under in vivo conditions were tested using the Mer+ HeLa S3 strain and its Mer- variant. Mer+ cells and Mer- cells were implanted subcutaneously into the left and right flanks, respectively, of 10 nude mice and the next day, MNNG solution (0.25 ml at 1 mg/ml) was injected into the implantation sites of eight mice. Mer- tumor cells in six of eight treated mice showed no growth and those in the other two mice did grow, but regressed after approximately 3 weeks. In contrast, Mer+ tumor cells continued to grow in all the eight mice treated, indicating that Mer- tumor cells may be selectively inactivated by suitable therapeutic regimens with appropriate methylating drugs.

Adenoviruses, Human↗
PubMed1984

Cell-stage dependence of the formation of SCEs and chromosomal aberrations.

Sister chromatid exchanges (SCEs) and homologous chromatid exchanges (chromatid exchanges between homologous chromosomes at homologous sites) are similar, not only in the type of chromosomal alteration but also in their high yields in Bloom syndrome cells or in cells treated with mitomycin C (MMC). However, the similarity between SCEs and homologous exchanges seems superficial as evidenced by the present experiments. In human lymphocytes, when caffeine was added during the S phase under conditions of concurrent exposure to MMC, both SCEs and homologous exchanges increased. However, when caffeine was added during the G2 phase, the frequency of SCEs remained unaffected whereas the frequency of homologous and nonhomologous chromatid exchanges decreased and that of other types of chromatid aberrations increased. We conclude that the process of formation of SCEs is, at least partly, different from that of chromatid exchanges or other types of chromatid aberrations, the former presumably occurring during the S phase and the latter during the G2 phase.

Caffeine↗