Biomedical subjects

Masamune Higashigawa

Publications and source records attributed to Masamune Higashigawa.

3 recordsLinked to original sources

PubMed2002

Marginal decrease in mortality and marked increase in incidence as a result of neuroblastoma screening at 6 months of age: cohort study in seven prefectures in Japan.

PURPOSE: To determine the usefulness of 6-month screening for neuroblastoma. PATIENTS AND METHODS: The cumulative incidence rates (IRs) and cumulative mortality rates (MRs) of neuroblastoma in children younger than 60 months of age were analyzed for control (n = 713,025), qualitative screening (Qual Screen, n = 1,142,519), and quantitative screening (Quan Screen, n = 550,331) cohorts, and for Screened and Unscreened subgroups within screening cohorts. RESULTS: IRs (per 100,000) for infants aged 6 to 11 months were 1.12 in Control, 5.69 in Qual Screen (P <.0001), and 17.81 in Quan Screen (P <.0001); IRs for children aged 12 to 59 months were 7.29 in Control, 5.86 in Qual Screen (P =.28), and 6.36 in Quan Screen (P =.60). IRs for children aged 12 to 59 months in Unscreened or Screened subgroups remained at the same level. When patients diagnosed at younger than 6 months of age were excluded, the MR (per 100,000) under 60 months for Control was 4.21; those in Unscreened and Screened subgroups were 3.84 and 2.53 in Qual Screen (P =.30), and 3.20 and 1.97 in Quan Screen (P =.73), respectively; MRs between Control and Unscreened subgroups revealed no significant differences (P =.89 in Qual Screen, P =.85 in Quan Screen). CONCLUSION: Six-month screening resulted in a marked increase in incidence for infants with no significant decrease in incidence for children older than 1 year of age. A decrease in mortality was observed, but it was not significant. The usefulness of screening is questionable, because the decrease of mortality should be balanced against the adverse effect of overdiagnosis and the psychological burden on parents and children.

Age Factors↗

PubMed2002

Role of Ca2+ in the intracellular signaling pathway of anti-IgM-induced apoptosis in the human B-cell line, MBC-1, established from Burkitt lymphoma.

The role of Ca2+ in the intracellular signal transduction process that causes antibody-induced apoptotic cell death in B-cells is not completely understood. We previously established a B-cell line (MBC-1) from a patient with Burkitt lymphoma at the leukemic stage that demonstrated the typical morphology and internucleosomal DNA fragmentation of apoptosis when treated with anti-immunoglobulin (Ig)M antibody. This antibody-induced cell death was partially inhibited by pretreatment with ethyleneglycol-bis-tetraacetic acid (EGTA) and actinomycin-D. FK506, an immunosupressive agent and calcineurin inhibitor, also partially rescued the anti-IgM antibody-induced death of MBC-1 cells. These results show that the calcium signaling pathway, which leads to a change in gene expression, plays an important role in anti-IgM-induced apoptosis in MBC-1 cells. Flow cytometric measurement of the cytosolic free Ca2+ concentration ([Ca2+]i) showed that nontoxic concentrations of 4-bromo-calcium ionophore A23187 (Ca2+ IP) increased [Ca2+]i more than did the anti-IgM antibody. A brief Ca2+ spike was observed on anti-IgM antibody treatment, but a gradual increase and decrease were observed when the cells were treated with Ca2+ IP at a nontoxic concentration of 1 microg/mL. These findings suggest that interpretations differ for the 2 patterns of calcium signaling and that the brief spiked elevation of Ca2+ produces distinct biological and cellular responses compared to the gradual increase and decrease of [Ca2+]i. Our results support the hypothesis that Ca2+ plays a significant role as a multifunctional second messenger providing specific information to the nucleus in anti-IgM antibody-induced apoptosis in MBC-1 cells.

Antibodies, Anti-Idiotypic↗

PubMed1996

Increased Deoxycytidine Kinase mRNA Level After Treatment with Interleukin-3.

Pretreatment of IL-3 to Kasumi-1 human acute myeloid leukemia cells enhanced 1-B-D-arabinofuranosyl cytosine (ara-C) cytotoxicity 1.2. to 1.4-fold (median 1.3). To clarify the mechanism of interleukin-3 (IL-3) on ara-C cytotoxicity, we investigated the level of deoxycytidine kinase mRNA with the competitive polymerase chain reaction method and enzyme activities, the incorporation of [(3)H] ara-C into DNA and intracellular ara-cytidine triphosphate (CTP) levels with high-performance liquid chromatography and analyzed cell cycles. The level of deoxycytidine kinase mRNA showed a fourfold increase (88.3 plus minus 4.33 amol &mgr;g of total RNA) at 3 days after treatment with IL-3 compared to control (20.3 plus minus 4.33 amol &mgr;g). After IL-3 treatment, ara-C incorporation into the DNA was increased to 1.33 to 1.83-fold (median, 1.73-fold). The G0/G1 late-phase and S-phase percentages of cells were increased from 28.99 to 78.73% in the IL-3 treatment group as compared to control. These results indicate that IL-3 pretreatment increases the level of deoxycytidine kinase mRNA and ara-C incorporation into the DNA and also increases ratios of G0/G1 late-phase and S-phase subsequent to an enhancement of ara-C cytotoxicity against leukemia cells.

Journal Article↗