10 results on '"Miyazaki, Y."'
Search Results
2. The prognostic significance of vasohibin-1 expression in patients with prostate cancer
- Author
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Kosaka, T, primary, Miyazaki, Y, additional, Miyajima, A, additional, Mikami, S, additional, Hayashi, Y, additional, Tanaka, N, additional, Nagata, H, additional, Kikuchi, E, additional, Nakagawa, K, additional, Okada, Y, additional, Sato, Y, additional, and Oya, M, additional
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- 2013
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3. Acquired platinum resistance enhances tumour angiogenesis through angiotensin II type 1 receptor in bladder cancer
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Tanaka, N, primary, Miyajima, A, additional, Kosaka, T, additional, Miyazaki, Y, additional, Shirotake, S, additional, Shirakawa, H, additional, Kikuchi, E, additional, and Oya, M, additional
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- 2011
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4. Monitoring gastric cancer progression with circulating tumour DNA.
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Hamakawa, T, Kukita, Y, Kurokawa, Y, Miyazaki, Y, Takahashi, T, Yamasaki, M, Miyata, H, Nakajima, K, Taniguchi, K, Takiguchi, S, Mori, M, Doki, Y, and Kato, K
- Subjects
STOMACH cancer ,DISEASE progression ,CIRCULATING tumor DNA ,BIOMARKERS ,GENETIC mutation - Abstract
Background:Circulating tumour DNA (ctDNA) is an emerging candidate biomarker for malignancies and may be useful for monitoring the disease status of gastric cancer.Methods:We performed targeted deep sequencing of plasma cell-free DNA (cfDNA) by massively parallel sequencing in patients with tumours harbouring TP53 mutations. The quantitative values of TP53-ctDNA during the clinical course were compared with the tumour status.Results:Three out of ten patients with TP53 mutations in primary tumours showed detectable TP53 mutation levels in preoperative cfDNA. Although the cfDNA concentrations were not always reflective of the disease course, the ctDNA fraction correlated with the disease status.Conclusions:ctDNA may serve as a useful biomarker to monitor gastric cancer progression and residual disease. [ABSTRACT FROM AUTHOR]
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- 2015
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5. Met/HGF receptor modulates bcl-w expression and inhibits apoptosis in human colorectal cancers
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Kitamura, S, primary, Kondo, S, additional, Shinomura, Y, additional, Kanayama, S, additional, Miyazaki, Y, additional, Kiyohara, T, additional, Hiraoka, S, additional, and Matsuzawa, Y, additional
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- 2000
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6. Anti-glypican-1 antibody-drug conjugate is a potential therapy against pancreatic cancer.
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Nishigaki T, Takahashi T, Serada S, Fujimoto M, Ohkawara T, Hara H, Sugase T, Otsuru T, Saito Y, Tsujii S, Nomura T, Tanaka K, Miyazaki Y, Makino T, Kurokawa Y, Nakajima K, Eguchi H, Yamasaki M, Mori M, Doki Y, and Naka T
- Subjects
- Animals, Antibodies, Monoclonal pharmacology, Cell Line, Tumor, Cell Proliferation drug effects, Humans, Mice, Oligopeptides pharmacology, Pancreatic Neoplasms genetics, Pancreatic Neoplasms pathology, Xenograft Model Antitumor Assays, Antibodies, Anti-Idiotypic pharmacology, Glypicans genetics, Immunoconjugates pharmacology, Pancreatic Neoplasms drug therapy
- Abstract
Background: Pancreatic cancer (PDAC) is the most lethal malignancy. New treatment options for it are urgently required. The aim was to develop an antibody-drug conjugate (ADC) targeting glypican-1 (GPC-1) as a new therapy for PDAC., Methods: We evaluated GPC-1 expression in resected PDAC specimens and PDAC cell lines. We then measured the antitumour effect of anti-GPC-1 monoclonal antibody conjugated with the cytotoxic agent monomethyl auristatin F (MMAF) in vitro and in vivo., Results: GPC-1 was overexpressed in most primary PDAC cells and tissues. The PDAC cell lines BxPC-3 and T3M-4 strongly expressed GPC-1 relative to SUIT-2 cells. Compared with control ADC, GPC-1-ADC showed a potent antitumour effect against BxPC-3 and T3M-4, but little activity against SUIT-2 cells. In the xenograft and patient-derived tumour models, GPC-1-ADC significantly and potently inhibited tumour growth in a dose-dependent manner. GPC-1-ADC-mediated G2/M-phase cell cycle arrest was detected in the tumour tissues of GPC-1-ADC-treated mice relative to those of control-ADC-treated mice., Conclusions: GPC-1-ADC showed significant tumour growth inhibition against GPC-1-positive pancreatic cell lines and patient-derived, GPC-1-positive pancreatic cancer tissues. Our preclinical data demonstrated that targeting GPC-1 with ADC is a promising therapy for patients with GPC-1-positive pancreatic cancer.
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- 2020
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7. TAS-116 inhibits oncogenic KIT signalling on the Golgi in both imatinib-naïve and imatinib-resistant gastrointestinal stromal tumours.
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Saito Y, Takahashi T, Obata Y, Nishida T, Ohkubo S, Nakagawa F, Serada S, Fujimoto M, Ohkawara T, Nishigaki T, Sugase T, Koh M, Ishida T, Tanaka K, Miyazaki Y, Makino T, Kurokawa Y, Nakajima K, Yamasaki M, Hirota S, Naka T, Mori M, and Doki Y
- Subjects
- Animals, Cell Line, Tumor, Cell Proliferation drug effects, Drug Resistance, Neoplasm, ErbB Receptors genetics, ErbB Receptors metabolism, Gastrointestinal Neoplasms genetics, Gastrointestinal Neoplasms metabolism, Gastrointestinal Stromal Tumors genetics, Gastrointestinal Stromal Tumors metabolism, Golgi Apparatus metabolism, HSP90 Heat-Shock Proteins antagonists & inhibitors, HSP90 Heat-Shock Proteins metabolism, Humans, Lung Neoplasms drug therapy, Lung Neoplasms genetics, Lung Neoplasms metabolism, Lung Neoplasms pathology, Mice, Mice, Inbred BALB C, Mice, Nude, Mice, SCID, Proto-Oncogene Proteins c-kit metabolism, Signal Transduction drug effects, Xenograft Model Antitumor Assays, Benzamides pharmacology, Gastrointestinal Neoplasms drug therapy, Gastrointestinal Stromal Tumors drug therapy, Golgi Apparatus drug effects, Imatinib Mesylate pharmacology, Proto-Oncogene Proteins c-kit antagonists & inhibitors, Pyrazoles pharmacology
- Abstract
Background: Despite the effectiveness of imatinib mesylate (IM), most gastrointestinal stromal tumours (GISTs) develop IM resistance, mainly due to the additional kinase-domain mutations accompanied by concomitant reactivation of KIT tyrosine kinase. Heat-shock protein 90 (HSP90) is one of the chaperone molecules required for appropriate folding of proteins such as KIT., Methods: We used a novel HSP90 inhibitor, TAS-116, which showed specific binding to HSP90α/β with low toxicity in animal models. The efficacy and mechanism of TAS-116 against IM-resistant GIST were evaluated by using IM-naïve and IM-resistant GIST cell lines. We also evaluated the effects of TAS-116 on the other HSP90 client protein, EGFR, by using lung cell lines., Results: TAS-116 inhibited growth and induced apoptosis in both IM-naïve and IM-resistant GIST cell lines with KIT activation. We found KIT was activated mainly in intracellular compartments, such as trans-Golgi cisternae, and TAS-116 reduced autophosphorylated KIT in the Golgi apparatus. In IM-resistant GISTs in xenograft mouse models, TAS-116 caused tumour growth inhibition. We found that TAS-116 decreased phosphorylated EGFR levels and inhibited the growth of EGFR-mutated lung cancer cell lines., Conclusion: TAS-116 may be a novel promising drug to overcome tyrosine kinase inhibitor-resistance in both GIST and EGFR-mutated lung cancer.
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- 2020
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8. Overexpression of glypican-1 implicates poor prognosis and their chemoresistance in oesophageal squamous cell carcinoma.
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Hara H, Takahashi T, Serada S, Fujimoto M, Ohkawara T, Nakatsuka R, Harada E, Nishigaki T, Takahashi Y, Nojima S, Miyazaki Y, Makino T, Kurokawa Y, Yamasaki M, Miyata H, Nakajima K, Takiguchi S, Morii E, Mori M, Doki Y, and Naka T
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- Biomarkers, Tumor genetics, Cell Line, Tumor, Esophageal Squamous Cell Carcinoma, Humans, Immunohistochemistry methods, Kaplan-Meier Estimate, Prognosis, Carcinoma, Squamous Cell genetics, Carcinoma, Squamous Cell pathology, Drug Resistance, Neoplasm genetics, Esophageal Neoplasms genetics, Esophageal Neoplasms pathology, Glypicans genetics
- Abstract
Background: Despite the recent improvements in multimodal therapies for oesophageal squamous cell carcinoma (ESCC), the prognosis remains poor. The identification of suitable biomarkers for predicting the prognosis and chemo-sensitivity is required to develop targeted treatments and improve treatment results., Methods: Proteins highly expressed in ESCC cell lines compared with normal oesophageal cell lines were screened by isobaric tag for relative and absolute quantitation (iTRAQ). We identified glypican-1 (GPC1) as a novel molecule. The clinicopathological characteristics of GPC1 were evaluated by immunohistochemistry using ESCC specimens, and clinical parameters were assessed. The correlation between GPC1 expression levels and chemo-sensitivity were analysed in vitro., Results: In the immunohistochemical assessment of 175 ESCC patients, 98.8% expressed GPC1. These patients demonstrated significantly poorer prognosis compared with patients with low-GPC1 expression by survival assay (P<0.001). Higher chemoresistance was observed in the GPC1 high-expression group. GPC1 expression levels positively correlated with chemo-sensitivity against cis-Diammineplatinum (II) dichloride (CDDP), and are potentially associated with anti-apoptotic function based on alterations in the MAPK downstream signalling pathway and Bcl-2 family member proteins., Conclusions: GPC1 is an independent prognostic factor in ESCC and is a critical molecule for altering the threshold of chemoresistance to CDDP.
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- 2016
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9. Improvement of cisplatin-related renal dysfunction by synthetic ghrelin: a prospective randomised phase II trial.
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Yanagimoto Y, Takiguchi S, Miyazaki Y, Makino T, Takahashi T, Kurokawa Y, Yamasaki M, Miyata H, Nakajima K, Hosoda H, Kangawa K, Mori M, and Doki Y
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- Aged, Antineoplastic Combined Chemotherapy Protocols adverse effects, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Carcinoma, Squamous Cell drug therapy, Carcinoma, Squamous Cell metabolism, Cisplatin administration & dosage, Creatinine blood, Drug Interactions, Esophageal Neoplasms drug therapy, Esophageal Neoplasms metabolism, Esophageal Squamous Cell Carcinoma, Female, Humans, Insulin-Like Growth Factor I metabolism, Kidney drug effects, Kidney metabolism, Kidney Diseases blood, Male, Prospective Studies, Cisplatin adverse effects, Ghrelin therapeutic use, Kidney Diseases chemically induced, Kidney Diseases prevention & control
- Abstract
Background: Ghrelin, a 28-amino acid peptide predominantly produced by the stomach, exerts powerful renal protective effects by increasing levels of insulin-like growth factor-1 (IGF-1). The aim of this study was to evaluate the effects of ghrelin on the incidence of renal dysfunction in patients receiving cisplatin-based chemotherapy., Methods: Forty patients with oesophageal cancer receiving cisplatin-based chemotherapy were assigned to either the ghrelin group (n=20), which received ghrelin (0.5 μg kg(-1) h(-1)) for 5 days, or a placebo group (n=20). The primary endpoint was serum creatinine. Secondary endpoints were serum cystatin C, chemotherapy-related adverse events, changes in serum ghrelin-related hormone levels, correlation between markers of renal injury and hormone concentrations, and effects on the second cycle of chemotherapy., Results: Blood acyl ghrelin, total ghrelin, and IGF-1 concentrations on day 4 were significantly higher in the ghrelin group. The renal dysfunction, serum creatinine and cystatin C levels, dose reduction, and delay in the initiation of the second cycle of chemotherapy were lower in the ghrelin group than in the control group. Serum creatinine levels were significantly correlated with serum IGF-1 levels., Conclusion: Continuous synthetic ghrelin administration during cisplatin-based chemotherapy attenuated renal dysfunction and harmful effects on subsequent chemotherapy, possibly by increasing IGF-1 levels.
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- 2016
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10. Gene therapy with SOCS1 for gastric cancer induces G2/M arrest and has an antitumour effect on peritoneal carcinomatosis.
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Natatsuka R, Takahashi T, Serada S, Fujimoto M, Ookawara T, Nishida T, Hara H, Nishigaki T, Harada E, Murakami T, Miyazaki Y, Makino T, Kurokawa Y, Yamasaki M, Miyata H, Nakajima K, Takiguchi S, Kishimoto T, Mori M, Doki Y, and Naka T
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- Animals, Carcinoma genetics, Carcinoma pathology, Cell Line, Tumor, Cell Proliferation genetics, Female, Humans, Mice, Mice, Inbred ICR, Mice, Nude, Mice, Transgenic, Peritoneal Neoplasms genetics, Peritoneal Neoplasms pathology, Stomach Neoplasms genetics, Stomach Neoplasms pathology, Suppressor of Cytokine Signaling 1 Protein, Xenograft Model Antitumor Assays, Carcinoma therapy, G2 Phase Cell Cycle Checkpoints genetics, Genetic Therapy methods, Peritoneal Neoplasms therapy, Stomach Neoplasms therapy, Suppressor of Cytokine Signaling Proteins genetics
- Abstract
Background: Suppressor of cytokine signaling1 (SOCS1) is a negative regulator of various cytokines. Recently, it was investigated as a therapeutic target in various cancers. However, the observed antitumour effects of SOCS1 cannot not be fully explained without taking inhibition of proliferation signalling into account. Our aim was to discover a new mechanism of antitumour effects of SOCS1 for gastric cancer (GC)., Methods: We analysed the mechanism of antitumour effect of SOCS1 in vitro. In addition, we evaluated antitumour effect for GC using a xenograft peritoneal carcinomatosis mouse model in preclinical setting., Results: We confirmed that SOCS1 suppressed proliferation in four out of five GC cell lines. SOCS1 appeared to block proliferation by a new mechanism that involves cell cycle regulation at the G2/M checkpoint. We showed that SOCS1 influenced cell cycle-associated molecules through its interaction with ataxia telangiectasia and Rad3-related protein. The significant difference in therapeutic effects was noted in terms of the post-treatment weight and total photon count of the intra-abdominal tumours., Conclusion: Forced expression of SOCS1 revealed a heretofore-unknown mechanism for regulating the cell cycle and may represent a novel therapeutic approach for the treatment of peritoneal carcinomatosis of GC.
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- 2015
- Full Text
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