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Biomedical subjects

S Hama

Publications and source records attributed to S Hama.

69 records · Page 4Linked to original sources
PubMed1983

Presence of antibodies against herpes simplex virus-specific antigens in human serum.

Sera from 110 healthy pregnant women in the third trimester and from 47 controls matched for age, sex and socio-economic status were tested for the presence of antibodies to three antigenic preparations believed to contain mainly alpha, beta, and gamma polypeptides of herpes simplex virus (HSV) type I. Sixty-five of the 110 pregnant women and 22 of the 47 controls possessed antibodies against HSV immediate early antigen, or alpha polypeptides. Among them, three women possessed antibodies against immediate early antigen only. The pregnant group had significantly more women with antibody against all of the three antigenic preparations (60/110) than did the control group (18/47). We conclude that in some women only early genetically determined viral products were produced and that the pregnant state affected the genetic expression of latently infecting HSV.

Antibodies, Viral↗
PubMed1980

Phenotypic characterization of adenovirus type 12 temperature-sensitive mutants in productive infection and transformation.

Eleven temperature-sensitive mutants of adenovirus type 12, capable of forming plaques in human cells at 33 C but not at 39.5 C, were isolated from a stock of a wild-type strain after treatment with either nitrous acid or hydroxylamine. Complementation tests in doubly infected human cells permitted a tentative assignment of eight of these mutants to six complementation groups. Temperature-shift experiments revealed that one mutant is affected early and most of the other mutants are affected late. Only the early mutant, H12ts505, was temperature sensitive in viral DNA replication. Infectious virions of all the mutants except H12ts505 and two of the late mutants produced at 33 C, appeared to be more heat labile than those of the wild type. Only H12ts505 was temperature sensitive for the establishment of transformation of rat 3Y1 cells. One of the late mutants (H12ts504) had an increased transforming ability at the permissive temperature. Results of temperature-shift transformation experiments suggest that a viral function affected in H12ts505 is required for "initiation" of transformation. Some of the growth properties of H12ts505-transformed cells were also temperature dependent, suggesting that a functional expression of a gene mutation in H12ts505 is required to maintain at least some aspects of the transformed state.

Adenoviridae↗
PubMed1976

Decreased transforming ability of a temperature-sensitive mutant of human adenovirus type 12.

A mutant of human adenovirus type 12, temperature-sensitive for virus replication an for the enhancement of thymidine incorporation in resting human embryonic kidney cells, is described. The mutant was also temperature-sensitive for transformation of rat cells. The results indicate that a viral gene required for the virus growth cycle is also required for transformation.

Adenoviruses, Human↗
PubMed1972

Virus-specific ribonucleic acid in the nucleus and cytoplasm of rat embryo cells transformed by adenovirus type 2.

Nuclei were isolated from rat embryo cells transformed by adenovirus type 2. Nuclear and cytoplasmic virus-specific ribonucleic acids (RNA) were characterized and quantitated by deoxyribonucleic acid (DNA)-RNA hybrid formation with adenovirus DNA. The results indicate that most, if not all, virus-specific RNA molecules are synthesized in the cell nucleus and subsequently transported into cytoplasm where they degrade with a half-life of 1 to 2 hr. No difference in base sequences between nuclear and cytoplasmic virus-specific RNA species can be detected by hybridization competition experiment with viral DNA.

Adenoviridae↗
PubMedDate not supplied

Absence of mutations in the NBS1 gene in B-cell malignant lymphoma patients.

BACKGROUND: Nijmegen breakage syndrome (NBS), also known as ataxia-telangiectasia (AT) variant, is an autosomal recessive disorder characterized by microcephaly, growth retardation, severe combined immunodeficiency and a high incidence of lymphoid carcinoma, the majority of which are B-cell lymphomas. To determine whether the NBS1 gene is a tumor suppressor gene in B-cell lymphoma, we screened B-cell malignant lymphoma (ML) for any evidence of NBS1 mutation. MATERIALS AND METHODS: Sequence analysis of the NBS1 gene was performed from PCR products amplified from the DNA of 12 extracranial ML or RT-PCR products amplified from cDNA of 8 primary central nervous system lymphoma. RESULTS: Direct sequence analysis revealed that no NBS1 mutations were present in any of these patients. CONCLUSION: The present results suggested that the contribution of NBS1 mutations to B-cell ML was minimal, despite the fact that the NBS1 gene was causative factor in these cases.

Adolescent↗
PubMedDate not supplied

Adenovirus-mediated p16 gene transfer changes the sensitivity to taxanes and Vinca alkaloids of human ovarian cancer cells.

BACKGROUND: Deletions and point mutations of the p16 gene are detectable in more than 50% of ovarian cancer cells. In this study, we examined the effect of p16 gene transduction on the growth of ovarian cancer cells and on the effect of anti-cancer agents. MATERIALS AND METHODS: p16-null human ovarian cancer cell lines, SKOV-3 and OVCAR-5, were used in this study. We transduced the full-length human p16 gene using recombinant adenovirus (AxCA-hp16). RESULTS: The spontaneous growth of these cells was significantly inhibited by hp16 transduction. MTT assay revealed that AxCA-hp16 infection induced chemoresistance in both cell lines. Flow cytometric analysis revealed that only hp16 -transduced SKOV-3, were arrested at the G1-phase for 3 days whereas those infected with AxCA-mock and OVCAR-5 infected with both recombinant viruses did not. Western blot analysis showed increased microtubule-associated proteins 4 (MAP4) in both cell lines. CONCLUSION: These results suggest that in SKOV-3 cells, G1-arrest induced by p16-transduction prevents paclitaxel- and vindesine-induced cell death, and in OVCAR-5 cells, the other unknown mechanisms play a role of chemoresistance.

Adenoviridae↗
PubMedDate not supplied

Transformation of human glioma cell lines with the p16 gene inhibits cell proliferation.

We examined the genomic status of the p16 gene in 5 human glioma cell lines by Southern blot analysis. The p16 gene was located in the 9p21 chromosomal region and homozygous deletion was detected in 4 of 5 (80%) human glioma cell lines and 5 of 15 (33%) clinical samples. We transfected the full-length human p16 gene into p16-null human glioma cell line, U251MG cells, using the plasmid vector pRc/CMV-p16 and evaluated the effect of p16 gene transfer on the growth suppression of malignant glioma cells. The transfection of p16 cDNA caused growth suppression through G1 cell cycle arrest in U251MG cells. We also examined the effect of p16 gene transfer on the chemosensitivity to cis-diamminedichloroplatinum II (CDDP), 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl) -3-nitrosourea hydrochloride (ACNU), and 5'-azacytidine (AZC). We did not detect any change in them after p16 gene transfer. These results might suggest that deletion of p16 genes promoted unrestrained growth in human glioma but has no relationship to the chemosensitivity to CDDP, ACNU and AZC.

Antineoplastic Agents↗
PubMedDate not supplied

High concentrations of recombinant adenovirus expressing p16 gene induces apoptosis in lung cancer cell lines.

In this study, we discussed the effects of treatment with recombinant adenovirus expressing p16 (AX-p16) on cell growth and cell death. Ax-p16 at 10 m.o.i. groups showed growth inhibition 3 days after gene transfection, but the cells regrew and did not undergo cell death. On the other hand, Ax-p16 at 300 m.o.i. groups showed complete cell growth inhibition leading to cell death which was apparent 7 days after p16 gene transfection. In the high m.o.i. Ax-mock groups, cell death was marked just after infection, but had diminished by 7 days after infection. Downregulation of pRB was detected only in Ax-p16 at 300 m.o.i. groups. These data suggest that a) high m.o.i. condition of Ax-p16 gives therapeutic benefits due to the combined effects of adenovirus and high expression of p16; and b) the cell killing mechanism of the p16 transgene is different from that of high m.o.i. adenoviral infection.

Adenoviruses, Human↗