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Biomedical subjects

H Ochi

Publications and source records attributed to H Ochi.

At least 271 records · Page 15Linked to original sources
PubMed1987

[Heredity in clinical cancer].

Familial clustering of cancer causes a problem whether significant differences exist from one person to the next in cancer susceptibility. Such clustering could occur simply by the chance occurrence of common environmental exposure, but in rare families, clustering is caused by discrete genetic factors, some being recessive and some being dominant inheritance with mendelian segregation. In this review article, heritable cancers are listed and discussed. Recent laboratory developments, such as the study on chromosome fragile sites and restriction enzyme-fragment length-polymorphism, to find the predisposition for cancer was introduced. Other analysis for individual difference by the genetic epidemiology was also summarized.

Ataxia Telangiectasia↗
PubMed1987

Frequency of multiple primary cancers and risk factors for lung and breast cancer patients.

Among nearly 50,000 cancer patients at the National Cancer Center, about 2,000 have multiple primary cancer (MPC), and its frequency has been increasing in recent years. MPC is considered to be a reflection of severe exposure to carcinogens or of a predisposition to cancer, or sometimes it is thought to be an individual expression within familial aggregation. To clarify the roles of these proposed mechanisms, case-control studies and chromosome analyses, including fragile sites on chromosomes, were performed focusing in particular on breast and lung cancer patients. A histology-matched case-control study of multicentric lung cancer revealed a risk of cigarette smoking, which was also recognized in MPC in different sites among breast cancer patients, in addition to the radiotherapy. The frequency of heritable (rare) fragile sites among 87 lung cancer patients was more than double that of the general population, and the rare fragile site, 17q12, was clustered in the adenocarcinoma. The frequencies of heritable fragile sites among breast cancer patients were the same as the general population. MPC occurred in 10 of 87 lung cancer cases, and in 9 of 90 breast cancer patients; these individuals did not have heritable fragile sites. Heavy smoking and hazardous occupations were recognized in MPC cases with lung cancer, and a family history of rather rare cancers was also more common in MPC cases with breast cancer. One of three triple cancer cases had breast cancer as a feature in chromosomal aberrations of the peripheral blood lymphocytes, which may signify predisposition to cancer in these patients.

Breast Neoplasms↗
PubMed1986

Effects of Y-20811, a long-lasting thromboxane synthetase inhibitor, on thromboxane production and platelet function.

Effects of a new imidazole derivative, sodium 4-[alpha-hydroxy-5-(imidazolyl)-2-methylbenzyl]-3,5-dimethyl benzoate dihydrate (Y-20811), on thromboxane (TX) production and platelet aggregation were investigated. Y-20811 inhibited TX synthetase (IC50 = 2.2 X 10(-8) M) and platelet aggregation induced by arachidonic acid (AA) in human, guinea pig and rabbit platelets in vitro. Administered orally to rabbits, Y-20811 at a dose of 1 mg/kg decreased serum TXB2 concomitant with increasing 6-keto PGF1 alpha and at a dose of 3 mg/kg inhibited AA-induced platelet aggregation, in both cases for at least 48 hours. Y-20811 (0.3 mg/kg/day) administered to rabbits for 7 days decreased serum TXB2 levels by 50-90% during the medication, and these levels were restored to initial values 3 days after withdrawal of the drug. At a dose of 1 mg/kg Y-20811 protected rabbits against death induced by AA (2 mg/kg). These results indicate that Y-20811 is a selective and long-lasting TX synthetase inhibitor and an anti-aggregating agent useful in preventing thrombotic disorders.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Rearrangement of chromosome 3 in renal cell carcinoma.

Rearrangements involving chromosome #3 were detected in 8 of 12 nonfamilial renal cell carcinomas. These results suggest that rearrangement of chromosome #3 is associated with the genesis and progression of a subclass of human renal cell carcinoma.

Adult↗
PubMed1986

Cytogenetic studies in primary gastric cancer.

We have analyzed five primary gastric cancers with a G-banding technique. All tumors had clonal chromosome abnormalities; a total of 67 numerical and 83 structural karyotypic anomalies were identified as clonal. The most prominent and recurring numerical abnormality was a missing Y chromosome (three of four tumors in the male patients). No recurrent structural abnormalities were found. However, the breakpoints at bands 1p22, 3p21, and 19p13 were frequently involved. These chromosome abnormalities and their role in oncogenesis are discussed.

Adult↗
PubMed1986

Characterization of a new primary human pancreatic tumor line.

A primary human pancreatic tumor line (BxPC-3) has been established from a biopsy specimen of a histologically confirmed adenocarcinoma of the body of the pancreas. Tumorigenicity was proven by xenograft in athymic nude mice. Upon re-establishment of tumor xenografts in tissue culture, the epithelial tumor cells retained their original morphology. Histopathologically, the tumors grown in nude mice exhibited the original characteristics of the primary adenocarcinoma in the patient, producing traceable mucin and displaying moderately well to poorly differentiated adenocarcinomas with occasional lymphocytic infiltrations at the tumor peripheries. Furthermore, the tumor xenografts differentially expressed carcinoembryonic antigen, human pancreas cancer-associated antigen, and human pancreas-specific antigen. Karyotyping and glucose-6-phosphate dehydrogenase isoenzyme characterization revealed that this tumor line was of human origin and devoid of HeLa cell contamination. The BxPC-3 tumor line has been maintained for more than four years in our laboratory and represents a valuable model for primary human pancreatic cancer.

Adenocarcinoma↗
PubMed1986

Cytogenetic effects of multiagent chemotherapy on the peripheral lymphocytes of patients with small cell lung cancer.

Peripheral lymphocytes of 8 patients with small cell lung cancer (SCLC), who received combination chemotherapy consisting of cisplatin and VP-16 (PVP), were examined for frequency of sister chromatid exchange (SCE) and chromosomal aberrations. Three of the 8 patients were treated with the PVP regimen only; however, the others had previously been treated with multiagent chemotherapy consisting of a cyclophosphamide, adriamycin, and vincristine (CAV) regimen or a cyclophosphamide, ACNU and vincristine (CAV') regimen with or without radiotherapy. Significantly increased SCE frequency was observed in previously untreated patients 3 or 4 days after PVP treatment, compared with the pretreatment values. The earlier analysis in the previously treated patients also showed increased SCE frequency, which seemed to return to the normal value as time elapsed after PVP. In addition, abnormal chromosome count distribution and/or increased incidence of structural changes were observed in cultures from all the patients. In general, striking changes in chromosomes were observed in previously treated patients. The aberrations observed in pretreated patients consisted of chromatid gaps and breaks, exchanges, fragments and dicentric chromosomes. In addition to these abnormalities, double minutes like microchromosomes were seen irrespective of radiotherapy. Further studies are needed to elucidate whether any of the chromosomal aberrations observed in this study could participate in the induction of secondary neoplasms.

Aged↗
PubMed1986

Cytogenetic effects of etoposide (VP-16) on human lymphocytes; with special reference to the relation between sister chromatid exchange and chromatid breakage.

The effects of etoposide (VP-16) on sister chromatid exchange (SCE) and chromosome abnormalities were studied by using human peripheral lymphocytes. This drug produced a significant increase in the SCE frequency and chromosomal aberrations such as breaks, exchanges, and tetraploidy with or without endoreduplication. Analysis of the breakpoints of chromatid deletion with respect to their association with SCE in the metaphases from the second division demonstrated that VP-16-induced deletions arose with little dependence on the site of SCE. It is suggested that chromatid deletions induced by this drug derive from unrepaired chromatid breaks rather than from incomplete exchanges.

Cells, Cultured↗
PubMed1986

[Left ventricular wall motion abnormalities evaluated by factor analysis as compared with Fourier analysis].

Factor analysis was applied to multigated cardiac pool scintigraphy to evaluate its ability to detect left ventricular wall motion abnormalities in 35 patients with old myocardial infarction (MI), and in 12 control cases with normal left ventriculography. All cases were also evaluated by conventional Fourier analysis. In most cases with normal left ventriculography, the ventricular and atrial factors were extracted by factor analysis. In cases with MI, the third factor was obtained in the left ventricle corresponding to wall motion abnormality. Each case was scored according to the coincidence of findings of ventriculography and those of factor analysis or Fourier analysis. Scores were recorded for three items; the existence, location, and degree of asynergy. In cases of MI, the detection rate of asynergy was 94% by factor analysis, 83% by Fourier analysis, and the agreement in respect to location was 71% and 66%, respectively. Factor analysis had higher scores than Fourier analysis, but this was not significant. The interobserver error of factor analysis was less than that of Fourier analysis. Factor analysis can display locations and dynamic motion curves of asynergy, and it is regarded as a useful method for detecting and evaluating left ventricular wall motion abnormalities.

Adult↗