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Biomedical subjects

Y Shimosato

Publications and source records attributed to Y Shimosato.

At least 163 records · Page 9Linked to original sources
PubMed1988

Detection of amplified N-myc gene in neuroblastoma by in situ hybridization using the single-step silver enhancement method.

Amplification of the N-myc oncogene in 27 cases of neuroblastoma group tumor was examined by in situ hybridization using the single-step silver enhancement technique. The N-myc gene copy numbers of these neuroblastoma group tumors were previously examined by dot-blot hybridization using DNA extracted from formalin-fixed, paraffin-embedded tissues (H Tsuda et al., Lab Invest, 59:321, 1988). Silver grains were deposited just over the nuclei of tumor cells, but no or only faint deposition was observed over those of infiltrating lymphocytes, stromal fibroblasts, and endothelial cells. We judged a case to be positive for gene amplification when silver grains precipitated over the nuclei of the tumor cells to a greater extent than over nuclei of lymphocytes or endothelial cells in the same section. According to this criterion, 14 cases (12 cases of neuroblastoma and 2 cases of ganglioneuroblastoma) were positive for N-myc gene amplification of 27 cases (18 cases of neuroblastoma, 5 cases of ganglioneuroblastoma, and 4 cases of composite ganglioneuroblastoma). These results corresponded well to those of the dot-blot hybridization analysis using the same materials. Thirteen of 15 cases that carried 4 copies or more of N-myc gene were judged positive, and 11 of 12 cases that carried less than 4 copies of the N-myc gene were judged negative by in situ hybridization. In neuroblastoma group tumors with amplification of the N-myc gene, tumor cells were stained almost homogenously, except for two cases of ganglioneuroblastoma, in which less differentiated small round tumor cells were stained more intensely than differentiated ganglion-like cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1988

The incidence of secondary tumors of the heart and pericardium: a 10-year study.

Secondary tumors of the heart and pericardium are much more common than primary tumors. During a 10-year period (1976-1985), only one instance of a primary tumor (malignant mesothelioma) was identified among 2,649 autopsies of malignant tumors at the National Cancer Center Hospital. In contrast, there were 407 cases in which heart and/or pericardium were secondarily involved with a malignant tumor from other organs. In 78 cases, the secondary tumors were present only in the pericardium, while in 329 cases, the tumors involved the heart itself with or without pericardial involvement. Among the primary tumors, three-quarters were carcinomas of various organs. In addition there were 53 hematologic malignancies, 19 melanomas and 17 sarcomas. In 31 cases, cardiac failure was the direct cause of death. The secondary tumors of the heart were often overlooked clinically because the cardiac dysfunction appeared to be part of the deteriorating general condition. Electrocardiography and echocardiography were often helpful in suggesting the presence of cardiac metastases. Appropriate diagnostic procedures and therapeutic intervention should be considered for the care of patients with advanced malignancy and sudden onset of cardiac failure.

Electrocardiography↗
PubMed1988

Retrospective study on amplification of N-myc and c-myc genes in pediatric solid tumors and its association with prognosis and tumor differentiation.

DNA was extracted from formalin-fixed and paraffin-embedded tissues of 85 patients with pediatric malignant solid tumors which had been resected at surgery or obtained at autopsy during a 24-year period. The tumors examined included 25 rhabdomyosarcomas, 12 Wilms' tumors, 10 hepatoblastomas and 37 neuroblastoma group tumors. Neuroblastoma group tumors were subclassified into 25 neuroblastomas and 12 ganglioneuroblastomas among which 6 composite ganglioneuroblastomas were included. Sample blocks were selected from both tumors and normal tissues in the majority of cases. We were able to reliably detect N- and c-myc gene amplification in tumor DNA by dot blot-hybridization. The N-myc gene showed approximately from 3- to 500-fold amplification in 19 of 33 cases of stage IV neuroblastoma group tumor. All of these 33 patients had been intensively treated with chemotherapy and/or radiotherapy. The c-myc was amplified 8-fold in 1 case of rhabdomyosarcoma, but neither N-myc nor c-myc was amplified in any cases of Wilms' tumor or hepatoblastoma. We retrospectively examined the association among N-myc gene amplification, prognosis, and histologic subtype in 33 patients with stage IV neuroblastoma group tumors. The survival of the patients with N-myc gene amplification was shorter than that of the patients without amplification of N-myc (p less than 0.05). There was no significant difference in prognosis between the 2 histologic subtypes; neuroblastoma and ganglioneuroblastoma, and the cases of tumors with amplified N-myc showed shorter survivals for each subtype (p less than 0.05). In every case of neuroblastoma group tumor, the copy number of the N-myc gene was the same among primary site and multiple metastatic tumors, even when the lesions showed differences in histologic subtype like neuroblastoma and ganglioneuroblastoma.

Child↗
PubMed1987

Reversible squamous cell characteristics induced by vitamin A deficiency in a small cell lung cancer cell line.

A cultured small cell lung cancer cell line (Lu-134-B-S) established from a xenotransplanted tumor in a nude mouse, which had originated from a primary focus of small cell lung cancer, showed morphological changes when the medium was changed from RPMI 1640 supplemented with 10% fetal calf serum to RPMI 1640 supplemented with 10% delipidized fetal calf serum. That is, it consisted of "classic" small cells in the former medium, but after eight passages in the latter medium many cells became squamous cells, possessing abundant eosinophilic cytoplasm and intercellular bridges. Immunohistochemically, they reacted to antikeratin and antiinvolucrin antibodies. Electron microscopically, well developed desmosomes and associated tonofibrils were noted, and electrophoretically, the amount of medium (Mr 57,000 and 59,000) and large-sized (Mr 67,000) keratins were found to increase with the change of the medium. These changes reversed to the original small cell morphology within 4 weeks after addition of vitamin A (retinoic acid) to the medium. These findings suggested that deficiency of vitamin A caused the change of the cell from small to squamous cell and vice versa.

Aromatic-L-Amino-Acid Decarboxylases↗
PubMed1987

Molecular evidence for the lack of epidermal growth factor receptor gene expression in small cell lung carcinoma cells.

It has been shown that none of the small cell lung carcinoma (SCLC) cell lines possess epidermal growth factor (EGF) binding activity on their surface. We have examined several SCLC cell lines for the possibility that they may have EGF receptors but that the receptors are masked by an EGF-like protein factor(s), which may be produced by an autocrine mechanism. No evidence, however, was found for the production of such factors. We then used an EGF receptor complementary DNA to determine the state of the EGF receptor gene by Southern blot analysis. The receptor gene appears to be present in these cells in an intact, unrearranged form. These cells, however, were found to lack detectable levels of EGF receptor mRNA, suggesting a possible reason for the absence of EGF receptors on the cell surface. Furthermore, karyotype analysis revealed that SCLC cell lines Lu134 and H69 contained a morphologically normal chromosome 7, which carries the EGF receptor gene. Also, these SCLC cells contained the apparently normal chromosome 3 and exhibited the presence of c-raf-1 gene in an unrearranged form. Thus, the previously noted partial deletion of chromosome 3 is not necessarily common to the SCLC cells. Instead, the lack of EGF receptor is frequently found in SCLC cell lines and is distinct from the other types of lung cancer. We postulate that SCLC cells have some active regulatory mechanism which prevents the expression of EGF receptor gene.

Carcinoma, Small Cell↗
PubMed1987

Monoclonal antibody that distinguishes small-cell lung cancer from non-small-cell lung cancer.

To examine whether a monoclonal antibody, TFS-4, can distinguish small-cell lung cancer from non-small-cell lung cancers, an extensive survey of fresh lung tumors, cancers from other organs, and normal tissue specimens has been carried out. The antibody has been shown to react specifically with small-cell lung cancer (15 of 15) but not with squamous cell carcinoma (0 of 20), adenocarcinoma (0 of 20) of the lung, or large-cell lung cancer (0 of 2). It reacted neither with other malignancies, including colorectal cancer, gastric cancer, and malignant lymphoma, nor with such normal tissues as trachea, lung, liver, pancreas, colon, kidney, spleen, skin, striated muscle, bone marrow, or peripheral blood cells. Interestingly, the antibody cross-reacted with central nervous tissues. The antigenic determinant on small-cell lung cancer and that on human brain were both heat labile and trypsin sensitive, but resisted treatment with neuraminidase, suggesting that they represent similar peptides. TFS-4 may be of clinical use in the diagnosis of small-cell lung cancer, while the antigen may help investigate the nature and origin of small-cell lung cancer.

Antibodies, Monoclonal↗
PubMed1987

Hamartoma of the parotid gland: a case report with immunohistochemical and electron microscopic study.

A case of a solid parotid tumour in a 16-year-old boy is presented. Histologically, the tumour demonstrated some peculiar findings. An acinar pattern was predominant although every component seen in the normal salivary gland was present, namely, serous and mucous gland acini, ducts, myoepithelial cells, adipose and lymphoid tissue. Large eosinophilic granules were abundant in the large acinar cell cytoplasm. Immunohistochemically, the tumour demonstrated the proteins which are present in the normal parotid gland, for example, amylase, lactoferrin and lysozyme. Electron microscopic features were quite similar to those of normal parotid tissue except for accumulation of a large number of cytoplasmic granules in the acinar cells. There has been no previous report of a tumour with the same features as seen in this case. Our pathological diagnosis is hamartoma, although the possibility of hyperplasia or neoplasia can not be excluded.

Adolescent↗
PubMed1987

Normal and neoplastic myoepithelial cells in salivary glands: an immunohistochemical study.

To determine the difference between normal and neoplastic myoepithelial cells, we performed immunoperoxidase staining for contractile proteins (actin and myosin) and intermediate filament proteins (vimentin and 55- to 57-kilodalton keratin) on paraffin sections from salivary gland tumors. Normal myoepithelial cells were positive for actin and myosin but negative for vimentin and keratin. Outer tubular cells of organoid double-layered tubular structures seen in pleomorphic and monomorphic adenoma and adenoid cystic carcinoma, and "cyst"-lining cells and outermost cells of adenoid cystic carcinoma were occasionally positive for actin and myosin. These outer tubular cells, "cyst"-lining cells, and outermost cells were considered to be neoplastic myoepithelial cells. However, their stainability was much lower than that of normal myoepithelial cells. On the other hand, these neoplastic myoepithelial cell were always positive for vimentin. "Mesenchymal" cells and hyaline cells of pleomorphic adenoma and indifferent cells of adenoid cystic carcinoma were negative for both actin and myosin but positive for vimentin and occasionally also positive for keratin. The significance of vimentin staining in neoplastic myoepithelial cells and the coexpression of vimentin and keratin in some tumor cells is discussed.

Adenoma, Pleomorphic↗
PubMed1987

Loss of heterozygosity on chromosomes 3, 13, and 17 in small-cell carcinoma and on chromosome 3 in adenocarcinoma of the lung.

By a molecular genetic approach using polymorphic DNA markers that detect allelic deletion of specific chromosomal regions, we analyzed for possible loss of chromosomal heterozygosity in five different histological types of lung cancers obtained from 47 patients. In small-cell carcinomas, the incidence of allelic deletions at three different chromosomal loci was extremely high; loss of heterozygosity was detected on chromosomes 3p in 7 of 7 patients (100%), 13q in 10 of 11 patients (91%), and 17p in 5 of 5 patients (100%). The deletions at these loci in small-cell carcinomas were observed even in the tumors without any clinical evidence of metastasis. Furthermore, loss of heterozygosity on chromosomes 3p and 13q occurred prior to NMYC amplification and chromosome 11p deletion. Loss of heterozygosity on chromosome 3p was also detected with high frequency in adenocarcinomas [5 of 6 patients (83%)]. Heterozygosity of chromosomes 13q and 17p was lost in 10 of 31 patients (32%) and in 3 of 12 patients (25%), respectively, of lung cancers other than small-cell carcinomas. These results indicate that recessive genetic changes involving sequences on chromosomes 3p, 13q, and 17p may play important roles in the genesis of small-cell carcinoma, and those on chromosome 3p may play an important role in the genesis of adenocarcinoma.

Adenocarcinoma↗
PubMed1987

Multiple thymic squamous cell carcinomas associated with mixed type thymoma.

A 49-year-old woman was admitted to the hospital because of abnormal shadows on a chest roentgenogram that suggested enlargement of bilateral hilar and mediastinal lymph nodes. Chest surgery was performed after a diagnosis of malignant thymoma that was following a left supraclavicular lymph node biopsy. The tumor consisted of several nodules, the largest of which was 6.5 cm. One nodule had invaded the pericardium and left upper lobe of the lung. Metastases to the peribronchial and mediastinal lymph nodes were present along with implantation on multiple pleural sites. Histological examination revealed that the tumor was of a mixed type with features of thymoma and squamous cell carcinoma, and that these two histological types were present in the same nodule with gradual transition between the two. Immunohistochemical surface marker studies revealed that lymphocytes in the squamous cell carcinoma were of the peripheral blood type. We conclude that squamous cell carcinoma may originate in the epithelial cells of a thymoma.

Carcinoma, Squamous Cell↗
PubMed1987

Plasmacytoma of the lung associated with nodular deposits of immunoglobulin.

A case of extramedullary plasmacytoma of the lung associated with nodular immunoglobulin deposits is presented. The main tumor was located in the posterior basal segment of the lower lobe of the left lung and showed intrabronchial polypoid growth. Multiple metastatic tumors were observed in regional lymph nodes and the visceral and parietal pleura. Histologically, the tumor was composed of sheets of plasma cells with mild atypia. A large amount of amorphous material resembling amyloid was observed in the tumors, and was more marked in the metastatic lesions. Immunohistochemically, the tumor cells were shown to contain monoclonal IgG-kappa immunoglobulin. The amorphous deposits were not identical to amyloid since congo red stain was negative and amyloid fibrils were not observed ultrastructurally. By Western blotting, immunoglobulin (IgG, kappa) was identified as the major component in an extract from the nodular deposits. In the preoperative serum from the patient, M-protein (IgG-kappa) was detected by immunoelectrophoresis. Bone marrow examination revealed no abnormality.

Female↗
PubMed1987

Resistance of human bronchial epithelial cells to teleocidin in a two-stage carcinogenesis experiment.

The tumor-promoting activity of teleocidin in two-stage carcinogenesis was tested using human bronchi grafted into athymic nude mice. On treatment with 7,12-dimethylbenz(a) anthracene (DMBA) plus teleocidin, no bronchial carcinomas were produced in 44 grafted human bronchi, but 8 spindle cell sarcomas developed in mouse tissues. Application of DMBA to grafted human bronchi produced only 3 spindle cell sarcomas in the tissues of 30 mice. Application of teleocidin did not produce any tumors in 24 grafts of bronchi obtained from heavy smokers. Thus, teleocidin had an effect on mouse tissues, but seemed to have no effect on human bronchial cells, although it is uncertain whether the grafted human bronchi were initiated by DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1987

Monoclonal antibody raised by sera of athymic mice bearing human lung cancer xenografts.

A monoclonal antibody, NCC-LU-165 (IgM, k), was obtained by somatic cell hybridization between mouse myeloma cells (P3-X63-Ag8-U1) and spleen cells of an immunocompetent mouse (BALB/c, nu/+) immunized with sera of immunodeficient athymic mice (BALB/c, nu/nu) bearing human giant cell lung cancer xenografts (Lu65). Immunohistochemically, the antibody was reactive with most nonsmall cell carcinoma of the lung. It also reacted with adenocarcinoma of the stomach, colon, pancreas and breast. Antigens were detected in sera of athymic mice bearing human lung cancer xenografts and in cell-free conditioned media of Lu65 cells by a sandwich enzyme immunoassay. This immunization method may be useful to raise monoclonal antibodies that detect circulating tumor-associated antigen.

Animals↗
PubMed1987

Expression of Lewis blood group antigens in cancerous and non-cancerous liver.

The expression of Lewis blood group antigens, Lewisa, Lewisb, Lewisx and Lewisy, in 40 non-cancerous livers and in 20 hepatocellular carcinomas (HCC), 5 cholangiocarcinomas (CC), and 6 combined hepatocellular and cholangiocarcinomas (Comb) was studied by immunohistochemistry using monoclonal antibodies. Although normal hepatocytes did not express any of the four Lewis antigens, Lewisy expression was detected in some hepatocytes at the periphery of pseudolobules in cirrhotic liver. While Lewisx in bile duct epithelial cells was undetectable in normal livers, it was detected in some cases with non-cancerous liver diseases. Lewisx and Lewisy were detected in 30% of HCC and 100% of CC and Comb. Non-cancerous bile duct epithelial cells in almost all instances were stained strongly by anti-Lewisa and/or anti-Lewisb antibody. Proliferating bile ductules within Glisson's sheath and pseudolobules could be clearly detected by Lewisa and Lewisb staining. Lewisa and Lewisb were never detected in non-cancerous hepatocytes, and were only rarely detected in HCC, but were expressed in most cases of CC and Comb. These results suggested that Lewisa and Lewisb are useful markers for differentiation towards biliary epithelial cells in the liver, and that Lewisx and Lewisy expression might be associated with states of increased or altered cell proliferation.

Adenoma, Bile Duct↗
PubMed1987

Smoking, occupation and family history in lung cancer patients under fifty years of age.

A hospital based case-control study was conducted to investigate the factors affecting the development of lung cancer among young adults. A total of 185 inpatients (males: 128, females: 57) aged from 30 to 49 have been histologically classified in the National Cancer Center Hospital during the last 10 years. Most frequent was adenocarcinoma in both males (57.0%) and females (73.7%). Basic factors were obtained from clinical charts including smoking history, occupation and family history of cancers. Elevated risks were found for squamous cell carcinoma in patients with a history of smoking (all had smoked v. 15/20 for controls) and an occupation possibly related to respiratory irritations (15/20 v. 3/20 for controls). Heavy smokers were distributed more in the cancer patients. Moreover, the average Smoking Index among those without "at risk" occupation was 1,002 with the least being 700, while that with such an occupation was 723. Heavy smoking alone and a smoking/occupation combination could contribute to an early onset of squamous cell carcinoma. On the other hand, there were no significant risk factors for adenocarcinoma, the relative risk from a history of smoking being less than 1.00 and from a family history of cancer, approximately 1.00.

Adenocarcinoma↗
PubMed1987

Loss of genes on the short arm of chromosome 11 in human lung carcinomas.

Since loss of genes on the short arm of chromosome 11 (11p) is known to be closely associated with several human tumors, we analyzed DNA of lung carcinomas from 45 patients with respect to loss of heterozygosity at loci on 11p. We observed that loss of heterozygosity at 11p loci was quite frequent (17 of 41 informative cases, 41%) and it appeared that the loss might be associated with more advanced carcinomas than those of stage Ia. In many cases, sequences at the CAT and/or the D11S12-IGF2 loci were commonly deleted. These observations suggest that loss of genes at particular regions on 11p might be involved in progression of human lung carcinomas.

Carcinoma↗
PubMed1987

Trend of lung cancers in the National Cancer Center of Japan and comparison with that of Japanese pathological autopsy records.

Trends in the histologic types of lung cancers during 1966-1985 by 5-year intervals were analyzed by using 4,419 cases in the National Cancer Center Hospital, Japan. Histologically confirmed cases increased to 76.6% in the last 5-year interval. The proportions of histological types in males have remained relatively unchanged; about 40% squamous cell carcinoma, one-third adenocarcinoma, and about 10% each of large cell carcinoma, small cell carcinoma and other types. In females, an increase of adenocarcinoma from 52% to 69.1% and a decrease of squamous cell carcinoma from 21% to 11.4% were noteworthy, and the other three types amounted to less than 10% each. These trends were compared with those obtained from the Annals of Pathological Autopsy Records in Japan during 1974-1983, which contained 26,844 lung cancer cases; the results were similar except for an increase of small cell carcinoma. The recent increase of small cell carcinoma was considered to be due to a change in diagnostic categorization, associated with a decreased rate of undifferentiated carcinoma. However, the increase of small cell carcinoma as well as adenocarcinoma in younger patients requires further study from both demographic and etiological viewpoints.

Adenocarcinoma↗