Biomedical subjects

A Iwazaki

Publications and source records attributed to A Iwazaki.

17 recordsLinked to original sources

PubMed2001

[Result of surgical treatment to early stage peripheral non-small cell lung cancer].

In the lung cancer, the announcement of the definition, the clinical behavior and the treatment result of the central early stage lung cancer, especially in situ lung cancer, have been seen. However, the definition and a clinicopathological concept of the peripheral lung cancer are still uncertain. The so-called small lung cancer of the tumor diameter 20 mm or less are peripheral lung adenocarcinoma. These patients' prognosis is excellent better, in contradiction to the prognosis of the patients with positive for pleural involvement or vessels invasion is worse. We studied the clinicopathological features, the Noguchi's classification, and prognosis of the 101 patients with small lung adenocarcinoma which were performed the operation, and refere about the selection of the operation method including the VATS and the limited operation.

Adult↗

PubMed1999

Enhanced expression of glucose transporter GLUT3 in tumorigenic HeLa cell hybrids associated with tumor suppressor dysfunction.

Previous studies on human cell hybrids between HeLa and normal human fibroblasts have indicated that the tumorigenicy may be controlled by a putative tumor suppressor gene on chromosome 11. We previously demonstrated a twofold increase in glucose uptake with a reduced Km by tumorigenic HeLa cell hybrids which expressed a highly glycosylated GLUT1. In this study, we reported that a tumorigenic cell hybrid, CGL4, also expressed a glucose transporter isoform, GLUT3, that was undetectable in nontumorigenic CGL1 cells. The expression of GLUT3 together with GLUT1 of 70 kDa was also evident in three gamma-ray-induced tumorigenic clones isolated from CGL1 cells, while control nontumorigenic irradiated cells expressed 50 kDa GLUT1 alone. In accordance with this, GLUT3 mRNA was specifically expressed in tumorigenic cell hybrids. To examine the role of GLUT3, clones which stably overexpress GLUT3 were developed from both CGL1 and CGL4 cells. In these transfectants, the affinity for 2-deoxyglucose markedly increased, in parallel with the amount of expressed GLUT3 irrespective of its N-glycosylation state. These results suggest that the enhanced GLUT3 expression in HeLa cell hybrids associated with the tumorigenic phenotypes may account for the increased affinity for 2-deoxyglucose. Possible roles of the putative tumor suppressor in control of gene expression and glucose uptake is discussed.

Biological Transport↗

PubMed1998

1-Methyl-3-propyl-7-butylxanthine, a novel biochemical modulator, enhances therapeutic efficacy of adriamycin.

We have screened xanthine derivatives for activity as novel biochemical modulators by assay of their inhibitory effect on adriamycin efflux from tumor cells. Strong inhibition of adriamycin efflux was shown by some xanthine derivatives with various alkyl or oxoalkyl substituents at the 1-, 3- and 7-positions. 1-Methyl-3-propyl-7-butylxanthine (XT-77), which had the greatest inhibitory effect on adriamycin efflux in vitro among the compounds tested, potentiated adriamycin-induced antitumor activity by causing an increase of adriamycin concentration in the tumor in vitro. Furthermore, XT-77 reduced the adverse drug reactions of adriamycin by decreasing the adriamycin concentrations in the heart and the liver. Thus, the combination of XT-77 with adriamycin not only increased the antitumor activity of adriamycin, but also decreased the adverse drug reactions.

Animals↗

PubMed1998

[Effects of methylxanthine derivatives on antitumor activity and toxic side effect of adriamycin induced by inhibition of DNA biosynthesis].

The antitumor activity of adriamycin (ADR) was enhanced by combination with theobromine or pentoxifylline. Theobromine increased the concentration of ADR in the tumor without any effects on that in the heart and the liver. The influence of the combination of theobromine or pentoxifylline with ADR on the lipid peroxide level (indicating the ADR-induced side effect) and on DNA biosynthesis (indicating the side effect and antitumor activity) were examined. When ADR was administered into mice, the lipid peroxide level in the liver and the heart increased. However, the combination of theobromine or pentoxifylline did not enhance the ADR-induced increment of the lipid peroxide level in the liver, and moreover, it inhibited that in the heart. The decrease of DNA biosynthesis in the liver and the heart, induced by ADR, were not enhanced by combination with theobromine or pentoxifylline. On the other hand, the combination of theobromine with ADR significantly increased the inhibition of DNA biosynthesis in the tumor. These findings indicate that the combination of theobromine or pentoxifylline with ADR have no effect on the side effects of ADR in the liver and the heart, with the increase of antitumor activity of ADR in the tumor, and it is suggested that these drugs will be of value as a biochemical modulator of ADR.

Animals↗

PubMed1997

Altered N-glycosylation of glucose transporter-1 associated with radiation-induced tumorigenesis of human cell hybrids.

Studies on human cell hybrids between a cervical carcinoma cell line, HeLa, and normal fibroblasts have indicated that their tumorigenicity is under the control of a putative tumor suppressor on chromosome 11. We have previously demonstrated that a tumorigenic cell hybrid CGL4 expresses a larger glucose transporter, GLUT1, due to altered glycosylation when compared to the nontumorigenic counterpart CGL1. In this study, we demonstrated this glycosylation change in GLUT1 in gamma-ray-induced tumorigenic mutants (GIMs) isolated from CGL1 cells as expressing a tumor-associated surface antigen, intestinal alkaline phosphatase. In contrast, GLUT1 in the gamma-irradiated nontumorigenic control cells (CONs) did not show this alteration. In accordance with this glycosylation change, affinity to 2-deoxyglucose in these GIM clones was increased by about twofold when compared to the nontumorigenic CONs. These results suggest a close correlation between the glycosylation change in GLUT1 with increased affinity to D-glucose and tumorigenicity of these human cell hybrids.

Alkaline Phosphatase↗

PubMed1995

Effects of methylxanthine derivatives on adriamycin concentration and antitumor activity.

We studied the mechanism whereby caffeine acts as a biochemical modulator of adriamycin, and examined various methylxanthine derivitives to determine whether they would be of value as biochemical modulators. In an in vitro study of adriamycin efflux in Ehrlich ascites carcinoma cells, theophylline, pentoxifylline, and theobromine inhibited this efflux, while caffeine metabolites did not. The effects of several methylxanthine derivatives on the antitumor activity of adriamycin and on adriamycin concentration in tissue were also examined in CDF1 tumor-bearing mice. Theobromine, which inhibited adriamycin efflux in vitro, increased the antitumor activity of adriamycin and the concentration of adriamycin in tumors. The caffeine metabolites, which had no effect on the adriamycin efflux, did not increase antitumor activity. These results suggest that the metabolism of caffeine may weaken its effect as a biochemical modulator, and that pentoxifylline and theobromine would be of value as biochemical modulators of adriamycin.

Animals↗

PubMed1995

Caffeine enhances adriamycin antitumor activity in Ehrlich ascites carcinoma-bearing mice.

We examined whether caffeine enhances the antitumor activity of adriamycin (ADR), in terms of prolonging survival in Ehrlich ascites carcinoma(ascites-type)-bearing mice. After administration of ADR at a dose of 0.5 mg/kg/d for 5d together with caffeine (100 mg/kg/d x 5 d), the survival period was increased by 39%. However, caffeine had little effect on this ADR induced-prolongation of survival following administration of ADR at 2.0 mg/kg/d for 4 d. Although a significant increase in ADR concentration in the ascites tumor was seen after administration of ADR at a dose of 0.5 mg/kg, caffeine failed to increase ADR concentration in the ascites tumor after administration of ADR at a dose of 2.0 mg/kg. The effect of caffeine thus appears to be due to its effect on the tumor distribution of ADR.

Animals↗

PubMed1993