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Article ; Online: Rapid and dramatic glucose-lowering effect of bromocriptine in an inadequately controlled type 2 diabetes patient with prolactinoma.

Igata, Motoyuki / Yagi, Yoshitaka / Hanatani, Satoko / Sakaguchi, Masaji / Ishii, Norio / Yoshinaga, Kayo / Kawashima, Junji / Motoshima, Hiroyuki / Araki, Eiichi

Journal of diabetes investigation

2020 Volume 12, Issue 4, Page(s) 668–671

Abstract: Dopamine receptor agonists are typically used to treat Parkinson's disease and certain pituitary tumors, such as prolactinoma or a growth hormone-producing tumor. A 53-year-old woman with a history of prolactinoma was referred to Kumamoto University ... ...

Abstract	Dopamine receptor agonists are typically used to treat Parkinson's disease and certain pituitary tumors, such as prolactinoma or a growth hormone-producing tumor. A 53-year-old woman with a history of prolactinoma was referred to Kumamoto University Hospital (Kumamoto, Japan) with poorly controlled type 2 diabetes. Her glycated hemoglobin and serum prolactin levels were increased (8.8% and 160.3 ng/mL, respectively). Bromocriptine, a dopamine D
MeSH term(s)	Blood Glucose/drug effects ; Bromocriptine/pharmacology ; Bromocriptine/therapeutic use ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Dopamine Agonists/pharmacology ; Dopamine Agonists/therapeutic use ; Female ; Humans ; Middle Aged ; Prolactinoma/complications ; Prolactinoma/drug therapy
Chemical Substances	Blood Glucose ; Dopamine Agonists ; Bromocriptine (3A64E3G5ZO)
Language	English
Publishing date	2020-08-25
Publishing country	Japan
Document type	Case Reports
ZDB-ID	2625840-7
ISSN	2040-1124 ; 2040-1116
ISSN (online)	2040-1124
ISSN	2040-1116
DOI	10.1111/jdi.13369
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Article: Inhibition of inflammation-mediated DPP-4 expression by linagliptin increases M2 macrophages in atherosclerotic lesions

Nishida, Shuhei / Matsumura, Takeshi / Senokuchi, Takafumi / Murakami-Nishida, Saiko / Ishii, Norio / Morita, Yutaro / Yagi, Yoshitaka / Motoshima, Hiroyuki / Kondo, Tatsuya / Araki, Eiichi

Biochemical and biophysical research communications. 2020 Mar. 26, v. 524, no. 1

2020

Abstract: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage ... ...

Abstract	Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage polarization in vitro and in vivo.Mouse bone marrow macrophages (BMMs) were used in in vitro assays. High fat diet (HFD)-fed Apoe⁻/⁻ mice were treated orally with linagliptin (10 mg/kg⁻¹•day⁻¹) or a vehicle (water) control.In in vitro assays using BMMs, treatment with LPS and IFNγ decreased the mRNA-expression levels of alternatively activated macrophage (M2) markers, and linagliptin treatment prevented these reductions. The mRNA levels of M2 markers and the number of M2 macrophages in the aorta were higher in linagliptin groups than in control groups. Linagliptin decreased the size of atherosclerotic lesions in HFD-fed Apoe⁻/⁻ mice. Interestingly, inflammatory stimulation increased DPP-4 expression, and linagliptin suppressed these effects in BMMs. Treatment with DPP-4 small-interfering RNA (siRNA) reproduced linagliptin-mediated alteration of M2 polarization.Linagliptin increased M2 macrophage polarization by inhibiting DPP-4 expression and activity. These findings may indicate the beneficial effects of DPP-4 inhibitors on the progression of diabetic macrovascular complications.
Keywords	aorta ; atherosclerosis ; bone marrow ; high fat diet ; macrophages ; mice ; research
Language	English
Dates of publication	2020-0326
Size	p. 8-15.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.01.027
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Article ; Online: Inhibition of inflammation-mediated DPP-4 expression by linagliptin increases M2 macrophages in atherosclerotic lesions.

Nishida, Shuhei / Matsumura, Takeshi / Senokuchi, Takafumi / Murakami-Nishida, Saiko / Ishii, Norio / Morita, Yutaro / Yagi, Yoshitaka / Motoshima, Hiroyuki / Kondo, Tatsuya / Araki, Eiichi

Biochemical and biophysical research communications

2020 Volume 524, Issue 1, Page(s) 8–15

Abstract: Background and aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, ... ...

Abstract	Background and aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage polarization in vitro and in vivo. Methods: Mouse bone marrow macrophages (BMMs) were used in in vitro assays. High fat diet (HFD)-fed Apoe Results: In in vitro assays using BMMs, treatment with LPS and IFNγ decreased the mRNA-expression levels of alternatively activated macrophage (M2) markers, and linagliptin treatment prevented these reductions. The mRNA levels of M2 markers and the number of M2 macrophages in the aorta were higher in linagliptin groups than in control groups. Linagliptin decreased the size of atherosclerotic lesions in HFD-fed Apoe Conclusions: Linagliptin increased M2 macrophage polarization by inhibiting DPP-4 expression and activity. These findings may indicate the beneficial effects of DPP-4 inhibitors on the progression of diabetic macrovascular complications.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/pharmacology ; Aorta/metabolism ; Atherosclerosis/drug therapy ; Bone Marrow Cells/drug effects ; Diet, High-Fat ; Dipeptidyl Peptidase 4/genetics ; Dipeptidyl Peptidase 4/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/chemistry ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/drug therapy ; Linagliptin/chemistry ; Linagliptin/pharmacology ; Macrophages/cytology ; Macrophages/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; RNA, Messenger/metabolism ; RNA, Small Interfering/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Dipeptidyl-Peptidase IV Inhibitors ; RNA, Messenger ; RNA, Small Interfering ; Linagliptin (3X29ZEJ4R2) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2020-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.01.027
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Article: Effect of liver toxicity on clinical outcome of patients with non-small-cell lung cancer treated with pemetrexed.

Sakamori, Yuichi / Kim, Young Hak / Yoshida, Hironori / Nakaoku, Takashi / Nagai, Hiroki / Yagi, Yoshitaka / Ozasa, Hiroaki / Mishima, Michiaki

Molecular and clinical oncology

2014 Volume 3, Issue 2, Page(s) 334–340

Abstract: Liver toxicity (LT) is a common side effect of pemetrexed (PEM); however, the effect of LT on clinical outcome has not been investigated in patients with non-small-cell lung cancer (NSCLC) treated with PEM. Between June, 2009 and June, 2012, a total of ... ...

Abstract	Liver toxicity (LT) is a common side effect of pemetrexed (PEM); however, the effect of LT on clinical outcome has not been investigated in patients with non-small-cell lung cancer (NSCLC) treated with PEM. Between June, 2009 and June, 2012, a total of 95 chemo-naive NSCLC patients received a PEM-containing regimen in our hospital. We reviewed the medical records of those 95 patients and evaluated the incidence of LT. Furthermore, we investigated the association between LT and clinical outcome. In this analysis, LT was defined as any grade of aspartate aminotransferase or alanine aminotransferase elevation. A total of 67 patients (70.5%) developed LT, which occurred mostly during the first treatment cycle. Among these, 10 patients (10.5%) required a delay in treatment or a dose reduction from the subsequent cycle and PEM discontinuation was required in 1 patient. The response rate (RR) was 43.3 and 21.4% in patients with and in those without LT, respectively (P=0.0387). The median progression-free survival (PFS) and overall survival (OS) were 6.3 and 24.2 months in patients with LT and 2.9 and 18.3 months in patients without LT, respectively (P<0.0001 for PFS and P=0.2426 for OS). The multivariate analysis demonstrated that LT exerted a significant positive effect on PFS (hazard ratio = 0.341; P<0.0001). In conclusion, LT was frequently observed in NSCLC patients treated with PEM; however, it was generally easily manageable. The improvement in RR and PFS observed in patients with LT suggested that LT may be a useful predictor of a favorable outcome in this patient population.
Language	English
Publishing date	2014-11-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2796865-0
ISSN	2049-9469 ; 2049-9450
ISSN (online)	2049-9469
ISSN	2049-9450
DOI	10.3892/mco.2014.452
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Article ; Online: Significance of c-MET overexpression in cytotoxic anticancer drug-resistant small-cell lung cancer cells.

Ozasa, Hiroaki / Oguri, Tetsuya / Maeno, Ken / Takakuwa, Osamu / Kunii, Eiji / Yagi, Yoshitaka / Uemura, Takehiro / Kasai, Daishi / Miyazaki, Mikinori / Niimi, Akio

Cancer science

2014 Volume 105, Issue 8, Page(s) 1032–1039

Abstract: The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor. Recently, activation of the c-MET/hepatocyte growth factor signaling pathway was associated with poor prognosis in various solid tumors and was one of the mechanisms of ... ...

Abstract	The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor. Recently, activation of the c-MET/hepatocyte growth factor signaling pathway was associated with poor prognosis in various solid tumors and was one of the mechanisms of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib. But the link between c-MET activation and the cytotoxic anticancer drug has not been fully examined. Here, we found that the enhanced expression and activation of c-MET in cytotoxic anticancer agent-resistant small-cell lung cancer cells. Downregulation of c-MET expression by siRNA against the c-MET gene or inhibition of c-MET activation by SU11274, a c-MET inhibitor, in the resistant cells altered resistance to the cytotoxic anticancer agent. These results indicated that c-MET overexpression might play an important role in acquired resistance to cytotoxic anticancer drugs. Furthermore, the number of c-MET gene loci was increased in the resistant cells compared to the parental cells. In conclusion, increased c-Met expression through an increase in the number of c-MET gene loci is one of the mechanisms of acquired resistance to cytotoxic anticancer drugs. Our results add a new strategy, the targeting of c-MET, for overcoming resistance to cytotoxic agents in small-cell lung cancer.
MeSH term(s)	Apoptosis ; Blotting, Western ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; In Situ Hybridization, Fluorescence ; Proto-Oncogene Proteins c-met/biosynthesis ; Proto-Oncogene Proteins c-met/genetics ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/metabolism ; Transfection
Chemical Substances	RNA, Small Interfering ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2014-07-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.12447
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Article ; Online: Clinical Impact of Single Nucleotide Polymorphism in PD-L1 on Response to Nivolumab for Advanced Non-Small-Cell Lung Cancer Patients.

Nomizo, Takashi / Ozasa, Hiroaki / Tsuji, Takahiro / Funazo, Tomoko / Yasuda, Yuto / Yoshida, Hironori / Yagi, Yoshitaka / Sakamori, Yuichi / Nagai, Hiroki / Hirai, Toyohiro / Kim, Young Hak

Scientific reports

2017 Volume 7, Page(s) 45124

Abstract: This study was intended to determine the efficacy of nivolumab, we evaluated treatment response with respect to PD-1/PD-L1 SNPs among patients with NSCLC. A total of 50 patients with NSCLC were treated with nivolumab and were also evaluated for PD-1/PD- ... ...

Abstract	This study was intended to determine the efficacy of nivolumab, we evaluated treatment response with respect to PD-1/PD-L1 SNPs among patients with NSCLC. A total of 50 patients with NSCLC were treated with nivolumab and were also evaluated for PD-1/PD-L1 single nucleotide polymorphisms (SNPs) from plasma DNA. We investigated the association among PD-1/PD-L1 SNPs, objective response rate (ORR) and progression-free survival (PFS). Two of seven SNPs studied showed association with ORR and PFS, with maximum evidence at the marker rs2282055. The ORR was 25%, 15%, and 0% for the G/G, G/T and T/T genotypes of PD-L1 rs2282055, respectively. The G allele of PD-L1 rs2282055 was significantly associated with better clinical response compared with the T allele (P = 0.0339 [Cochran-Armitage trend test]). The median PFS time was 2.6 months (95% confidence interval [CI], 1.8 months to 4.3 months) for the G/G and G/T genotypes and 1.8 months (95% confidence interval [CI], 0.4 months to 2.2 months) for the T/T genotype (P = 0.0163). Moreover, the C/C and C/G genotypes of PD-L1 rs4143815 were significantly associated with better ORR and PFS in NSCLC patients treated with nivolumab. These results suggest that rs2282055 and rs4143815 may be a biomarker for the efficacy of nivolumab.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Alleles ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Agents/therapeutic use ; B7-H1 Antigen/genetics ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/mortality ; Carcinoma, Non-Small-Cell Lung/pathology ; Female ; Genotype ; Humans ; Kaplan-Meier Estimate ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/mortality ; Lung Neoplasms/pathology ; Male ; Middle Aged ; Neoplasm Staging ; Polymorphism, Single Nucleotide ; Programmed Cell Death 1 Receptor/genetics ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents ; B7-H1 Antigen ; CD274 protein, human ; Programmed Cell Death 1 Receptor ; nivolumab (31YO63LBSN)
Language	English
Publishing date	2017-03-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep45124
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Article ; Online: Clinical impact of high serum hepatocyte growth factor in advanced non-small cell lung cancer.

Tsuji, Takahiro / Sakamori, Yuichi / Ozasa, Hiroaki / Yagi, Yoshitaka / Ajimizu, Hitomi / Yasuda, Yuto / Funazo, Tomoko / Nomizo, Takashi / Yoshida, Hironori / Nagai, Hiroki / Maeno, Ken / Oguri, Tetsuya / Hirai, Toyohiro / Kim, Young Hak

Oncotarget

2017 Volume 8, Issue 42, Page(s) 71805–71816

Abstract: Activation of c-MET through hepatocyte growth factor (HGF) increases tumorigenesis, induces resistance, and is associated with poor prognosis in various solid tumors. However, the clinical value of serum HGF (sHGF) in patients with advanced non-small ... ...

Abstract	Activation of c-MET through hepatocyte growth factor (HGF) increases tumorigenesis, induces resistance, and is associated with poor prognosis in various solid tumors. However, the clinical value of serum HGF (sHGF) in patients with advanced non-small cell lung cancer (NSCLC), especially those receiving cytotoxic chemotherapy, remains unknown. Here, we show that sHGF may be useful to predict tumor response and progression-free survival (PFS) in patients with advanced NSCLC. A total of 81 patients with NSCLC were investigated. sHGF levels were evaluated using ELISA at 4 time-points: at pre-treatment, at response-evaluation (1-2 months after treatment initiation), at the best tumor response, and at disease progression. As a control biomarker, CEA was also evaluated in lung adenocarcinoma. Positive-sHGF at response-evaluation predicted poor PFS compared with Negative-sHGF in both first-line (median, 153.5 vs. 288.0;
Language	English
Publishing date	2017-05-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.17895
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Article ; Online: Alectinib Resistance in ALK-Rearranged Lung Cancer by Dual Salvage Signaling in a Clinically Paired Resistance Model.

Molecular cancer research : MCR

2018 Volume 17, Issue 1, Page(s) 212–224

Abstract: The mechanisms responsible for the development of resistance to alectinib, a second-generation anaplastic lymphoma kinase (ALK) inhibitor, are still unclear, and few cell lines are currently available for investigating ALK-rearranged lung cancer. To ... ...

Abstract	The mechanisms responsible for the development of resistance to alectinib, a second-generation anaplastic lymphoma kinase (ALK) inhibitor, are still unclear, and few cell lines are currently available for investigating ALK-rearranged lung cancer. To identify the mechanisms underlying acquired resistance to alectinib, two patient-derived cell lines were established from an alectinib-naïve ALK-rearranged lung cancer and then after development of alectinib resistance. The properties acquired during treatments were detected by comparisons of the two cell lines, and then functional analyses were performed. Coactivation of c-Src and MET was identified after the development of alectinib resistance. Combinatorial therapy against Src and MET significantly restored alectinib sensitivity
MeSH term(s)	Animals ; Carbazoles/pharmacology ; Carbazoles/therapeutic use ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Male ; Mice ; Mice, SCID ; Piperidines/pharmacology ; Piperidines/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction ; Xenograft Model Antitumor Assays
Chemical Substances	Carbazoles ; Piperidines ; Protein Kinase Inhibitors ; alectinib (LIJ4CT1Z3Y)
Language	English
Publishing date	2018-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-18-0325
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Article: Long survival of a small-cell lung cancer patient who received maintenance chemotherapy with irinotecan.

Yagi, Yoshitaka / Kim, Young Hak / Tajima, Noriyuki / Baba, Kiichiro / Aihara, Kensaku / Soo, Hong Hyun / Yamaoka, Shinpachi / Mishima, Michiaki

Case reports in oncology

2013 Volume 6, Issue 3, Page(s) 569–573

Abstract: Lung cancer is the leading cause of cancer-related death worldwide. Small-cell lung cancer (SCLC) accounts for approximately 15% of all lung cancers. It is characterized by rapid tumor growth and early metastasis to multiple organs. Response to initial ... ...

Abstract	Lung cancer is the leading cause of cancer-related death worldwide. Small-cell lung cancer (SCLC) accounts for approximately 15% of all lung cancers. It is characterized by rapid tumor growth and early metastasis to multiple organs. Response to initial chemotherapy is generally good; however, the majority of patients develop recurrence and the prognosis of such patients is reportedly 2-4 months. Evolution of the treatment for SCLC has stagnated, and cisplatin + etoposide has been the standard chemotherapy for decades. Meanwhile, the combination of cisplatin + irinotecan has demonstrated equivalent efficacy to cisplatin + etoposide. Recently, maintenance chemotherapy has been extensively investigated in non-small-cell lung cancer (NSCLC), and is currently recommended as a standard treatment in clinical guidelines. On the contrary, a maintenance strategy has not been established for SCLC. Here, we describe an SCLC patient who received maintenance chemotherapy with irinotecan for more than 2 years after induction chemotherapy with cisplatin + irinotecan, and survived long term with no recurrence.
Language	English
Publishing date	2013-11-14
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2458961-5
ISSN	1662-6575
ISSN	1662-6575
DOI	10.1159/000356826
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Article ; Online: High-dose crizotinib for brain metastases refractory to standard-dose crizotinib.

Kim, Young Hak / Ozasa, Hiroaki / Nagai, Hiroki / Sakamori, Yuichi / Yoshida, Hironori / Yagi, Yoshitaka / Nakaoku, Takashi / Mishima, Michiaki

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

2013 Volume 8, Issue 9, Page(s) e85–6

MeSH term(s)	Adenocarcinoma/drug therapy ; Adenocarcinoma/pathology ; Adult ; Bone Neoplasms/drug therapy ; Bone Neoplasms/secondary ; Brain Neoplasms/drug therapy ; Brain Neoplasms/secondary ; Drug Resistance, Neoplasm ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/secondary ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Male ; Protein Kinase Inhibitors/therapeutic use ; Pyrazoles/therapeutic use ; Pyridines/therapeutic use
Chemical Substances	Protein Kinase Inhibitors ; Pyrazoles ; Pyridines ; crizotinib (53AH36668S)
Language	English
Publishing date	2013-09
Publishing country	United States
Document type	Case Reports ; Comparative Study ; Journal Article
ZDB-ID	2432037-7
ISSN	1556-1380 ; 1556-0864
ISSN (online)	1556-1380
ISSN	1556-0864
DOI	10.1097/JTO.0b013e31829cebbb
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