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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 397 records · Page 22Linked to original sources
PubMed1991

[Detection of point mutation of Kirsten ras oncogene in pancreatic carcinoma by polymerase chain reaction].

Regarding to the pancreatic cancer, outcomes of the patients surgically treated have been poor. By using polymerase chain reaction (PCR), paraffin-embedded specimens of the pancreatic carcinoma were confined point mutation in Kirsten (K)-ras codon 12. Then, incidence and type of point mutation of this oncogene and correlative studies with stage, T or N factor of pancreatic cancer were analysed. Extremely high incidence of K-ras gene mutation was shown in present report. The highest mode of point mutation of K-ras oncogene was GGT to GAT coded aspartic acid. Cases without point mutation in K-ras codon 12 were significantly frequent in papillary adenocarcinoma than in tubular type. There were not correlative result among mutation types, stage and T factor of pancreatic cancer. Most patients with pancreatic cancer who survived more than 2 years have not shown mutation to aspartic acid. Four cases including two cases of mucin producing pancreatic cancer did not have point mutation in K-ras codon 12. Pathogenesis of mucin producing cancer can be distinguished from typical pancreatic cancer by detection of point mutation in K-ras codon 12 using PCR.

Codon↗
PubMed1991

[A case of infantile Sertoli cell tumor].

A case of infantile Sertoli cell tumor of the testis is presented. A 2-year-old child visited our hospital with the complaint of painless swelling of the left scrotal content. A solid tumor was demonstrated in the left testis by scrotal echography. Physical and laboratory examinations were within normal limits and alpha-fetoprotein and beta-HCG were not elevated. The left testis was removed. The tumor sized 3.0 x 3.0 x 2.2 cm and weighted 14.5 g. Pathohistological diagnosis was benign Sertoli cell tumor. Tumor cells were vimentin positive and TM-1 reactive antigen positive and revealed electronmicroscopically some features of Sertoli cells such as intermediated microfilament, rich lysosomes and interdigitation between adjacent cells. The patient was well with no evidence of diseases one and a half years after the operation.

Age Factors↗
PubMed1990

Point mutation of the p53 gene resulting in splicing inhibition in small cell lung carcinoma.

The p53 gene is functionally inactivated mostly by point mutations resulting in amino acid substitutions in a wide variety of human cancers. We found a novel mutation of the p53 gene in a small cell lung carcinoma cell line, Lu-143. One of the allelic p53 genes was lost accompanied by loss of heterozygosity for chromosome 17. In the remaining allelic p53 gene, there was a single-base substitution of G to T at position 1 within the splice donor site of intron 7, and the mutated intron was not spliced out during the mRNA maturation process. As a result of this mutation, larger sized p53 mRNA was expressed and no p53 specific protein was detected in this cell line. These results suggest that mutations causing splicing abnormalities are one of the molecular mechanisms for the p53 gene inactivation in human cancer.

Alleles↗
PubMed1990

[The movement of antineoplastic solutions in transcatheter hepatic arterial embolization].

Transcatheter hepatic arterial embolization (TAE) with gelatin sponge particles soaked in anticancer agents has been widely employed in the treatment of Hepatocellular carcinoma (HCC). The mechanism of TAE has been explained by blocking of blood flow to the tumor, however the role of anticancer agents used with embolic materials has remained unclear. The purpose of this study is to prove the role of anticancer agents used in TAE. 1) In eighteen cases of HCC and 4 cases of metastatic liver cancer, TAE was performed with gelatin sponge, anticancer agents and contrast media. The livers were examined by CT 4, 24 and 48 hours after TAE. A selective retention of contrast media containing anticancer agent in the tumor area was observed in 14 of 14 cases examined 4 hr. in 15 of 17 cases examined 24 hr and in 6 of 6 cases examined 48 hr after TAE. In the cases of metastatic liver cancer, retention of contrast media, was also observed in 4 of 4 cases examined at 24 hr and 3 of 3 cases examined 48 hr after TAE. 2) TAE was done in 12 cases of HCC by using gelatin sponge soaked in anticancer agent mixed with 99M-Tc-pertechnetate. Livers were observed by a scintillation camera 4 hr and 24 hr after TAE. A selective retention of 99M-Tc-pertechnetate in the tumor was observed in 12 of 12 cases examined 4 hr and in 3 of 3 cases examined 24 hr after TAE. 3) In one cases of HCC, hepatectomy was performed 2 days after TAE.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Correlation between histologic grade of malignancy and copy number of c-erbB-2 gene in breast carcinoma. A retrospective analysis of 176 cases.

A system of histologic grade of malignancy in human breast carcinoma was devised by significantly modifying the way of evaluating number of mitoses and architectural atypia in the histologic grading of Bloom and Richardson. The modified grading system was applicable to all histologic subtypes of adenocarcinoma and showed a good association with prognosis of breast carcinoma patients in retrospective analysis of 176 consecutive surgical cases (P less than 0.0001). Of the three components of histologic grade, architectural atypia and number of mitotic figures independently had a significant effect on the prognosis. The copy number of c-erbB-2, a prognostic factor independent of tumor size and nodal status, was strongly correlated with the histologic grade, number of mitotic figures, and degree of nuclear atypia (P less than 0.001, each). Cox's regression model analysis showed that nodal status and histologic grade were two determinants of prognosis, and the independent effect of c-erbB-2 amplification was absorbed within that of the histologic grade. Although the importance of c-erbB-2 gene copy number seemed to be inferior to that of the histologic grade, both were shown to be strongly associated with the aggressiveness of the tumor itself rather than the extent of tumor spread.

Breast Neoplasms↗
PubMed1990

Glutathione-S-transferase pi as a determinant of drug resistance in transfectant cell lines.

A series of glutathione S-transferase pi (GST-pi) transfectant cell lines have been constructed in activated c-H-ras-transformed NIH-3T3 cells (pT22-3) by using a pKOneo plasmid and an expression vector containing cDNA for GST-pi with a beta-actin gene promoter. From the wild type pT22-3 cells, two clones were selected and designated RGN1 and RGN2. The degree of overexpression of GST-pi was estimated by Northern and Southern blot analysis to be incrementally higher in RGN2 compared with RGN1. Translation of mRNA was estimated by Western blot analysis using isozyme-specific polyclonal antibodies and confirmed the relative GST-pi levels. Each cell line, including the wild type, expressed alpha and mu class isozymes to the same degree and had similar but negligible expression of the mdr 1 gene. Sensitivity to various anticancer drugs and radiation was estimated by a series of cytotoxicity assays. The data confirmed that GST-pi provided a degree of protection against the toxicity of ethacrynic acid and adriamycin, but sensitivity to alkylating agents such as chlorambucil, melphalan, and cis-platinum was not influenced by GST-pi. Similarly, the response to ionizing radiation was similar for each line. Since the levels of intracellular GSH were also not significantly different, the availability of co-substrate was not a factor in determining response. In creating the GST-pi transfectants, these data establish that while increased isozyme levels can play a role in determining sensitivity to some agents, the protective effect is selective.

Actins↗
PubMed1990

[Effects of experimental hepatic artery embolization with lipiodol and gelatin sponge on liver tissue].

The effect of hepatic artery embolization with Lipiodol (Lp) and Gelatin sponge particles (GSP) on liver tissue was evaluated in 17 dogs embolized with GSP, 12 dogs with Lp and 19 dogs with Lp + GSP. Survival rate and extent of liver damage were used as evaluation criteria. None of the dogs with GSP died during the 4 week period, two exhibited small liver infarctions. Of the dogs with 0.2 to 5 ml/kg Lp, two dogs with 4 ml/kg or 5 ml/kg Lp died of cardiac failure. Gross liver examination did not show any liver infarction. Eight of the 19 dogs with Lp + GSP died of liver failure. Gross examination of the surviving dogs demonstrated infarction in 9 of the 11 livers with 100% incidence in those with 0.2 ml/kg or 0.5 ml/kg Lp. Liver infarction increased in size with the increase of Lp volume. In combination with Lp + GSP, the Lp volume should be less than 0.1 ml/kg.

Animals↗
PubMed1990

Human papillomavirus DNA in squamous cell carcinoma of the upper aerodigestive tract.

Nineteen samples of DNA from squamous cell carcinoma of the upper aerodigestive tract were analyzed by Southern blot hybridization for the presence of human papillomavirus (HPV) DNA. Two samples of DNA contained HPV 16 DNA or its homologous sequence. In one maxillary carcinoma, the sequences homologous to HPV 16 were detected. In one tonsillar carcinoma, HPV 16 sequence was also shown to be present. The patients positive for HPV DNA were female and had neither smoking nor drinking habits. These results indicate that HPV infections may play a role in the development of some types of squamous cell carcinomas of the upper aerodigestive tract.

Adult↗
PubMed1990

Molecular biology of the hst-1 gene.

The hst-1 gene (or HSTF1 by human gene nomenclature) was originally identified in our laboratory by an NIH/3T3 focus formation assay using DNA from a human gastric cancer. Sequence analysis predicted the hst-1 product to be a novel growth factor with 30-50% homology with six other heparin-binding growth factors: basic and acidic fibroblast growth factors (FGFs), the int-2 protein, FGF5, the hst-2/FGF6 protein and keratinocyte growth factor (KGF). A recombinant hst-1 protein was synthesized in silkworm cells and found to be a potent heparin-binding mitogen for murine fibroblasts and human vascular endothelial cells. Although hst-1 expression cannot be detected in most cancer cells, including gastric cancers, it is expressed in mouse embryos and in some germ cell tumours. Both hst-1 and int-2 are located on band q13.3 of human chromosome 11 within a distance of 35 kbp; in the mouse genome these two genes are separated by less than 20 kbp. They are differentially transcribed in the F9 mouse teratocarcinoma cell line; hst-1 is expressed in undifferentiated stem cells and int-2 in differentiated endodermal cells. The hst-1 and int-2 genes were coamplified in a variety of cancer cells, most notably in more than 50% of oesophageal cancers.

Amino Acid Sequence↗
PubMed1990

Frequent expression of receptors for granulocyte-macrophage colony-stimulating factor on human nonhematopoietic tumor cell lines.

Receptors for granulocyte-macrophage colony-stimulating factor (GM-CSF) were identified on 9 of 35 (26%) human nonhematopoietic tumor cell lines including non-small cell lung cancer, stomach cancer, colon cancer, and osteosarcoma cells. GM-CSF receptors distributed on these human tumor cells were low affinity types with an equilibrium dissociation constant of 1.5-10.0 nM. Cross-linking studies revealed that the molecular weights of the low affinity GM-CSF receptors were 65-85 kilodaltons. The high affinity receptors identified on hematopoietic cells were not detected on human nonhematopoietic tumor cells which we studied, and we could detect no effects of GM-CSF on cell growth of these tumor cells.

Carcinoma, Non-Small-Cell Lung↗
PubMed1990

Small cell carcinoma of the pancreas and biliary tract.

Four cases of anaplastic carcinoma of the pancreas or biliary tract were studied clinicopathologically and immunohistochemically. All four cases were intermediate cell type and contained a minimum amount of microscopic foci of differentiated glandular adenocarcinoma. Argyrophilic tumor cells were not seen in any of the four tumors. Immunohistochemically, no tumor was positive for hormonal products, but all tumors were positive for epithelial markers. These findings suggest that the anaplastic carcinoma are not derived from argyrophilic cells, but rather from adenocarcinomas which have the potential for anaplastic metaplasia. The long-term survival of one patient emphasized the importance of chemotherapy in the treatment of small cell carcinoma of the pancreas and biliary tract.

Aged↗
PubMed1990

Presence of human papillomavirus type-6-related sequences in inverted nasal papillomas.

Twenty DNA samples obtained from seven cases of inverted papillomas, eight cases of nasal polyps and five cases of chronic sinusitis were investigated by Southern blot hybridization for the possible presence of sequences homologous to human papillomavirus (HPV) types 6, 11, 16 and 18. HPV type-6-related DNA was identified in one of the seven inverted papillomas. The restriction endonuclease cleavage patterns showed that this latter DNA is a new subtype of HPV type 6 DNA. In the other six papillomas and in all cases of nasal polyps and chronic sinusitis, no HPV sequence could be demonstrated, even under low stringent conditions (Tm-40 degrees C). These results indicate that HPV infection might be one of the possible causative factors in the pathogenesis of inverted papillomas but is not essential for the induction of the tumor.

Aged↗
PubMed1990

Morphometric study of the superior cervical and stellate ganglia of spontaneously hypertensive rats during the prehypertensive stage.

To compare the functional state of the superior cervical (SCG) and stellate sympathetic ganglia (SG) of spontaneously hypertensive rats (SHR) with those of age-matched normotensive Wistar Kyoto rats (WKY), ganglion cell volume and area occupied by ganglion cells relative to each whole ganglionic area were morphometrically examined using the Texture Analyse System (TAS) in rats at 0, 10 and 30 days of age. The weight of each ganglion relative to animal weight was also measured. The ganglion cell volume and the relative area of ganglionic cells in both ganglia of SHR were significantly larger (P less than 0.05) than those of age-matched WKY at ages 0 and 10 days after birth. The relative ganglionic weights of SHR were significantly larger (P less than 0.01) compared with those of WKY at all ages examined, except for SG at 0 days after birth. These results show that the relative volume of sympathetic ganglion cells is greater in both SCG and SG of SHR than that of WKY, suggesting that hyperfunction of sympathetic ganglia occurs at the prehypertensive stage as a primary factor in the development of hypertension in SHR.

Animals↗
PubMed1990

K-sam, an amplified gene in stomach cancer, is a member of the heparin-binding growth factor receptor genes.

DNA fragments amplified in a stomach cancer-derived cell line, KATO-III, were previously identified by the in-gel DNA renaturation method, and a 0.2-kilobase-pair fragment of the amplified sequence was subsequently cloned. By genomic walking, a portion of the exon of the gene flanking this 0.2-kilobase-pair fragment was cloned, and the gene was designated as K-sam (KATO-III cell-derived stomach cancer amplified gene). The K-sam cDNAs, corresponding to the 3.5-kilobase K-sam mRNA, were cloned from the KATO-III cells. Sequence analysis revealed that this gene coded for 682 amino acid residues that satisfied the characteristics of the receptor tyrosine kinase. The K-sam gene had significant homologies with bek, FLG, and chicken basic fibroblast growth factor receptor gene. The K-sam gene was amplified in KATO-III cells with the major transcript of 3.5-kilobases in size. This gene was also expressed in some other stomach cancer cells, a small cell lung cancer, and germ cell tumors.

Amino Acid Sequence↗
PubMed1990

Allele loss on chromosome 16 associated with progression of human hepatocellular carcinoma.

Loss of heterozygosity on chromosome 16 is a common genetic alteration in human hepatocellular carcinoma (HCC). To clarify the pathogenetic significance of allele loss on chromosome 16, we performed restriction fragment length polymorphism analysis of 70 surgically resected tumors by using 15 polymorphic DNA markers for chromosome 16. Loss of heterozygosity on chromosome 16 was detected in 36 (52%) of 69 informative cases, and the common region of allele loss in these 36 tumors was located between the HP locus (16q22.1) and the CTRB locus (16q22.3-q23.2). These losses occurred more frequently in HCCs of poor differentiation, of larger size, and with metastasis, whereas they were not detected in HCC at the earliest stage. In addition, these losses were not associated with presence or absence of hepatitis B virus DNA integration or hepatitis C virus infection. These results show that loss of heterozygosity on chromosome 16 is a late event occurring after hepatocarcinogenesis and strongly suggest that this phenomenon is involved in enhancement of tumor aggressiveness during progression of HCC.

Alleles↗