Yasuyo Suga
Ajinomoto
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Publication
Featured researches published by Yasuyo Suga.
Bioorganic & Medicinal Chemistry Letters | 1998
Koji Ohsumi; Toshihiro Hatanaka; Koichi Fujita; Ryusuke Nakagawa; Yumiko Fukuda; Yukio Nihei; Yasuyo Suga; Yoshihiro Morinaga; Yukio Akiyama; Takashi Tsuji
A series of cis-restricted combretastatin analogues with 5-membered heterocycles were synthesized and their inhibitory activity against microtubule assembly and cytotoxic activity against the colon 26 adenocarcinoma cancer cell line were evaluated. Some of the heterocyclic analogues showed potent antitubulin activity and cytotoxicity. Compounds 16 and 35 showed marked tumor growth suppression in the colon 26 murine tumor model.
Bioorganic & Medicinal Chemistry Letters | 1998
Toshihiro Hatanaka; Koichi Fujita; Koji Ohsumi; Ryusuke Nakagawa; Yumiko Fukuda; Yukio Nihei; Yasuyo Suga; Yukio Akiyama; Takashi Tsuji
A series of B-ring modified combretastatin analogues were synthesized and their inhibitory activity against microtubule assembly, cytotoxic activity against Colon 26 adenocarcinoma cancer cell line were evaluated. Among these, pyridone derivative (19) showed strong antimitotic activity and cytotoxicity, along with excellent water-solubility.
Japanese Journal of Cancer Research | 1999
Yukio Nihei; Yasuyo Suga; Yoshihiro Morinaga; Kazuo Ohishi; Akira Okano; Koji Ohsumi; Toshihiro Hatanaka; Ryusuke Nakagawa; Takashi Tsuji; Yukio Akiyama; Sachiko Saito; Katsuyoshi Hori; Yasufumi Sato; Takashi Tsuruo
AC‐7700, a novel combretastatin A‐4 derivative, suppresses the growth of solid tumors by inhibiting tumor perfusion. We evaluated the antitumor activity of AC‐7700 on solid tumors in two experimental models, an advanced tumor model (murine colon 26 (c26) adenocarcinoma, colon 38 (c38) adenocarcinoma, MethA fibrosarcoma, Sarcoma 180 (S180), Lewis lung carcinoma (3LL), human LS180 adenocarcinoma) and an orthotopically transplanted tumor model (c26), compared with that of cisplatin (CDDP). The maximum tolerable dose (MTD) of CDDP suppressed early‐stage c26 and c38 tumor growth when treatment was started after the tumor volume (TV) reached 0.2–0.5 cm3, but it showed reduced activity against the same tumors at an advanced growth stage when TV exceeded 2 cm3. At its MTD, AC‐7700 was active against all tumors tested except 3LL in both early and advanced growth stages, reducing the tumor mass and having a curative effect in advanced c38 tumors. AC‐7700 was also effective on orthotopically transplanted c26 tumors, showing a comparable activity to that on subcutaneous tumors. Unlike flavon acetic acid, which damages tumor vasculature by inducing endogenous tumor necrosis factor‐α production, AC‐7700 potently suppressed the growth of advanced c26 tumors in athymic as well as euthymic mice. These results suggest that AC‐7700 is a novel antivascular agent that may have potent activity against advanced‐stage cancer in the clinical setting.
Cancer Science | 2003
Yoshihiro Morinaga; Yasuyo Suga; Sumiko Ehara; Katsuhiro Harada; Yukio Nihei; Manabu Suzuki
The in vivo combination effect of AC‐7700, a novel combretastatin A‐4 derivative, and cisplatin (CDDP) was examined. The combination of AC‐7700 and CDDP increased antitumor activity against murine colon 26 tumor in mice and cured the mice. This combination effect was found over wide dosage ranges of AC‐7700 (20–80 mg/kg) and CDDP (2.5–5 mg/kg). Moreover, this combination augmented antitumor activity against murine S180 and M109 tumors, and human LX‐1 and LS180 tumor xenografts in mice. The effect was the strongest when AC‐7700 and CDDP were administered simultaneously. To study this combination effect we measured the concentrations of CDDP in tumors, plasma and kidneys of the mice with colon 26 tumor. In the combination with AC‐7700, the concentration of CDDP in the tumors increased from 0.5 to 96 h after administration, but did not change or decrease in plasma or kidneys. Against human LS180 xenografts in mice, the combination similarly increased the concentration of CDDP in the tumors. These results suggest that AC‐7700 may specifically augment the accumulation of CDDP in tumors, and thus has the potential to be useful in combination chemotherapy with CDDP. (Cancer Sci 2003; 94: 200–204)
Bioorganic & Medicinal Chemistry Letters | 1999
Seiichi Sato; Yasuyo Suga; Toshihiko Yoshimura; Ryusuke Nakagawa; Takashi Tsuji; Ken Umemura; Toshiwo Andoh
A series of methoxycarbonyl group modified nidulalin A analogs were synthesized to improve stability against esterases. The amide derivatives showed cytotoxic activity along with inhibitory activity against DNA topoisomerase II. Among the analogs, amide 9a exhibited antitumor activity in Colon 26 murine tumor model.
Cancer Chemotherapy and Pharmacology | 1996
Kazuo Ohishi; Yoshihiro Morinaga; Koji Ohsumi; Ryusuke Nakagawa; Yasuyo Suga; Takashi Tsuji; Yukio Akiyama; Takashi Tsuruo
Abstract Purpose: We have previously shown that a series of N-alkylated 1,4-dihydropyridines potentiate the therapeutic efficacy of vincristine in vincristine-resistant P388 leukemia. The purpose of this study was to investigate the ability of one of the compounds, AC394, and its enantiomers to potentiate the antitumor activity of adriamycin against colon cancer cells in vitro and in vivo. Methods: The effects of AC394 on potentiation of adriamycin cytotoxicity and enhancement of its accumulation were evaluated using colon 26, HCT-15 and MCF-7 cells. Furthermore, the activities of AC394 and its enantiomers were compared. We also studied the combined effects of (+)-AC394 and adriamycin on subcutaneously (s.c.)-implanted and liver metastasis tumor models. Results: AC394 potentiated the cytotoxicity of adriamycin and enhanced its accumulation in colon cancer cells (colon 26 and HCT-15), which are known to express P-GP (P-glycoprotein) intrinsically. Enhancement of adriamycin accumulation by AC394 was found in s.c.-implanted colon 26 cells in vivo. Although both enantiomers of AC394 showed equal activity in vitro, (+)-AC394 was more effective than (−)-AC394 given orally. (−)-AC394 was found to be cleared more rapidly from the plasma than (+)-AC394. Thus, (+)-AC394 was evaluated for further study. Administration of (+)-AC394 significantly potentiated the antitumor activities of adriamycin in human colon cancer HCT-15 cells implanted s.c. Furthermore, in the liver metastasis model using colon 26 cells, a model completely resistant to adriamycin, the combination therapy of adriamycin with (+)-AC394 produced superior antitumor effects over adriamycin alone. Conclusions: A newly synthesized N-alkylated 1,4-dihydropyridine derivative, (+)-AC394, showed superior effects on the potentiation of adriamycin antitumor and antimetastatic activities in vivo. These results suggest that this combination may have therapeutic efficacy not only against primary colon cancers but also against metastatic liver cancer.
International Immunopharmacology | 2017
Yasuyo Suga; Kenji Takehana
Abstract S‐1 is an oral agent containing tegafur (a prodrug of 5‐fluorouracil) that is used to treat various cancers, but adverse effects are frequent. Two pilot clinical studies have suggested that lentinan (LNT; &bgr;‐1,3‐glucan) may reduce the incidence of adverse effects caused by S‐1 therapy. In this study, we established a murine model for assessment of gastrointestinal toxicity associated with S‐1 and studied the effect of LNT. S‐1 was administered orally to BALB/c mice at the effective dose (8.3 mg/kg, as tegafur equivalent) once daily (5 days per week) for 3 weeks. Stool consistency and intestinal specimens were examined. We investigated the effect of combined intravenous administration of LNT at 0.1 mg, which is an effective dose in murine tumor models. We also investigated the effect of a single administration of S‐1. During long‐term administration of S‐1, some mice had loose stools and an increase in apoptotic bodies was observed in the ileal crypts. An increase in apoptotic bodies was also noted after a single administration of S‐1 (15 mg/kg). Prior or concomitant administration of LNT inhibited the increase in apoptotic bodies in both settings. Administration of LNT also increased the accumulation of CD11b+TIM‐4+ cells in the ileum, while depletion of these cells by liposomal clodronate diminished the inhibitory effect of LNT on S‐1 toxicity. Combined administration of LNT with S‐1 led to a decrease in apoptotic bodies in the ileal crypts, possibly because LNT promoted phagocytosis of damaged cells by CD11b+TIM‐4+ cells. HighlightsLentinan inhibited the increase of apoptotic bodies in the ileal crypts associated with S‐1.Lentinan administration increased CD11b+TIM‐4+ cells in the ileal crypts.The inhibitory effect of lentinan was blocked after depletion of CD11b+TIM‐4+ cells.
Gastroenterology | 2009
Takaaki Kawaguchi; Keiko Saito; Yasuyo Suga; Masaki Hashimoto; Akira Mitsui; Mayuki Nakajima; Minako Sako; Naoki Yoshimura; Manabu Suzuki; Masakazu Takazoe
IFN-γ plays an important role in the generation and perpetuation of mucosal inflammation in IBD. TL1A, a TNF superfamily member, synergizes with IL-12 and IL-18 to augment IFN-γ production in human T cells. Enhanced TL1A expression is detected in IBD with a strong TL1A SNP association reported in Crohns disease. We have previously shown TL1A expression is induced in peripheral monocytes and in-vitro derived dendritic cells (DC). The molecular mechanisms regulating TL1A expression during DC differentiation however, remain poorly defined. The human monocytic cell line, KG-1, provides a valuable model for dendritic cell differentiation. The round non-adherent KG1 cells develop a DC-like phenotype following activation by PMA/ionomycin. These cells become loosely adherent with long cytoplasmic projections. A concomitant induction of membrane TL1A and mRNA is observed with mRNA expression being detectable within 2 hours and peaking at 8 hours following stimulation. A strikingly similar kinetics of TL1A expression was likewise noted following PMA/ionomycin stimulation of peripheral monocytes. Further DC maturation of KG-1 cells following treatment with LPS results in additional enhancement of TL1A expression. Transient transfection of KG-1 with TL1A promoter-constructs up to 1.5 kb in length reveals up to 90-fold enhanced expression compared to cells transfected with the promoterless vector. EMSA analysis demonstrates PMA/ionomycin mediated upregulation of nucleo-protein binding to a putative TL1A NFκB binding site. Binding is competed by excess unlabeled wt TL1A NFκB, but not mutant oligonucleotide and is likewise attenuated following proteasomal inhibition by MG132. Our data suggests in the human monocytic KG-1 cell line, differentiation of immature cells towards a mature DC phenotype is associated with functional upregulation of surface TL1A expression and binding of NFκB to the TL1A promoter. These studies provide a molecular basis for future studies which may help elucidate the mechanism modulating TL1A expression during DC maturation.
Journal of Medicinal Chemistry | 1998
Koji Ohsumi; Ryusuke Nakagawa; Yumiko Fukuda; Toshihiro Hatanaka; Yoshihiro Morinaga; Yukio Nihei; Kazuo Ohishi; Yasuyo Suga; Yukio Akiyama; Takashi Tsuji
Archive | 2006
Yukio Nihei; Yoshihiro Morinaga; Manabu Suzuki; Yasuyo Suga