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Pancreatic Neoplasms: HELP
Articles by Ryota Takahashi
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Ryota Takahashi wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Cholinergic Signaling via Muscarinic Receptors Directly and Indirectly Suppresses Pancreatic Tumorigenesis and Cancer Stemness. 2018

Renz, Bernhard W / Tanaka, Takayuki / Sunagawa, Masaki / Takahashi, Ryota / Jiang, Zhengyu / Macchini, Marina / Dantes, Zahra / Valenti, Giovanni / White, Ruth A / Middelhoff, Moritz A / Ilmer, Matthias / Oberstein, Paul E / Angele, Martin K / Deng, Huan / Hayakawa, Yoku / Westphalen, C Benedikt / Werner, Jens / Remotti, Helen / Reichert, Maximilian / Tailor, Yagnesh H / Nagar, Karan / Friedman, Richard A / Iuga, Alina C / Olive, Kenneth P / Wang, Timothy C. ·Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, Munich, Germany; German Cancer Consortium (DKTK), Partner Site Munich; and German Cancer Research Center (DKFZ), Heidelberg, Germany. · Division of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Department of Surgery, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan. · Department of Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany. · Division of Oncology, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Perlmutter Cancer Center, New York University Langone Medical Center, New York, New York. · Department of Pathology, and Molecular Medicine and Genetics Center, The Fourth Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. · Department of Gastroenterology, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan. · Department of Internal Medicine III, Hospital of the University of Munich, Munich, Germany; German Cancer Consortium (DKTK), Partner Site Munich; and German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York. · Biomedical Informatics Shared Resource of the Herbert Irving Comprehensive Cancer Center and Department of Biomedical Informatics, Columbia University Medical Center, New York, New York. · Department of Pathology and Cell Biology and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. · Division of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York. tcw21@columbia.edu. ·Cancer Discov · Pubmed #30185628.

ABSTRACT: In many solid tumors, parasympathetic input is provided by the vagus nerve, which has been shown to modulate tumor growth. However, whether cholinergic signaling directly regulates progression of pancreatic ductal adenocarcinoma (PDAC) has not been defined. Here, we found that subdiaphragmatic vagotomy in LSL-

2 Article β2 Adrenergic-Neurotrophin Feedforward Loop Promotes Pancreatic Cancer. 2018

Renz, Bernhard W / Takahashi, Ryota / Tanaka, Takayuki / Macchini, Marina / Hayakawa, Yoku / Dantes, Zahra / Maurer, H Carlo / Chen, Xiaowei / Jiang, Zhengyu / Westphalen, C Benedikt / Ilmer, Matthias / Valenti, Giovanni / Mohanta, Sarajo K / Habenicht, Andreas J R / Middelhoff, Moritz / Chu, Timothy / Nagar, Karan / Tailor, Yagnesh / Casadei, Riccardo / Di Marco, Mariacristina / Kleespies, Axel / Friedman, Richard A / Remotti, Helen / Reichert, Maximilian / Worthley, Daniel L / Neumann, Jens / Werner, Jens / Iuga, Alina C / Olive, Kenneth P / Wang, Timothy C. ·Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, 81377 Munich, Germany; Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Oncology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. · Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, 81675 Munich, Germany. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Internal Medicine III, Hospital of the University of Munich, 81377 Munich, Germany. · Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, 81377 Munich, Germany. · Institute for Cardiovascular Prevention, University of Munich, 80336 Munich, Germany. · Department of Internal Medicine and Surgery (DIMEC), Alma Mater Studiorum, University of Bologna, Sant'Orsola-Malpighi Hospital, 40138 Bologna, Italy. · Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Sant'Orsola-Malpighi Hospital, 40138 Bologna, Italy. · Biomedical Informatics Shared Resource, Herbert Irving Comprehensive Cancer Center, Department of Biomedical Informatics, Columbia University Medical Center, New York, NY 10032, USA. · Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Medicine, University of Adelaide, Adelaide, SA 5005, Australia. · Department of Pathology, Hospital of the University of Munich, 81377 Munich, Germany. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. · Department of Digestive and Liver Diseases and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, 1130 St. Nicholas Avenue, New York, NY 10032, USA. Electronic address: tcw21@columbia.edu. ·Cancer Cell · Pubmed #29249692.

ABSTRACT: Catecholamines stimulate epithelial proliferation, but the role of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Catecholamines promoted ADRB2-dependent PDAC development, nerve growth factor (NGF) secretion, and pancreatic nerve density. Pancreatic Ngf overexpression accelerated tumor development in LSL-Kras

3 Article Stromal remodeling by the BET bromodomain inhibitor JQ1 suppresses the progression of human pancreatic cancer. 2016

Yamamoto, Keisuke / Tateishi, Keisuke / Kudo, Yotaro / Hoshikawa, Mayumi / Tanaka, Mariko / Nakatsuka, Takuma / Fujiwara, Hiroaki / Miyabayashi, Koji / Takahashi, Ryota / Tanaka, Yasuo / Ijichi, Hideaki / Nakai, Yousuke / Isayama, Hiroyuki / Morishita, Yasuyuki / Aoki, Taku / Sakamoto, Yoshihiro / Hasegawa, Kiyoshi / Kokudo, Norihiro / Fukayama, Masashi / Koike, Kazuhiko. ·Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan. · Hepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan. · Department of Pathology and Diagnostic Pathology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan. · Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan. · Second Department of Surgery, Dokkyo Medical University, Mibu, Tochigi 321-0293, Japan. ·Oncotarget · Pubmed #27528027.

ABSTRACT: Inhibitors of bromodomain and extraterminal domain (BET) proteins, a family of chromatin reader proteins, have therapeutic efficacy against various malignancies. However, the detailed mechanisms underlying the anti-tumor effects in distinct tumor types remain elusive. Here, we show a novel antitumor mechanism of BET inhibition in pancreatic ductal adenocarcinoma (PDAC). We found that JQ1, a BET inhibitor, decreased desmoplastic stroma, a hallmark of PDAC, and suppressed the growth of patient-derived tumor xenografts (PDX) of PDACs. In vivo antitumor effects of JQ1 were not always associated with the JQ1 sensitivity of respective PDAC cells, and were rather dependent on the suppression of tumor-promoting activity in cancer-associated fibroblasts (CAFs). JQ1 inhibited Hedgehog and TGF-β pathways as potent regulators of CAF activation and suppressed the expression of α-SMA, extracellular matrix, cytokines, and growth factors in human primary CAFs. Consistently, conditioned media (CM) from CAFs promoted the proliferation of PDAC cells along with the activation of ERK, AKT, and STAT3 pathways, though these effects were suppressed when CM from JQ1-treated CAFs was used. Mechanistically, chromatin immunoprecipitation experiments revealed that JQ1 reduced TGF-β-dependent gene expression by disrupting the recruitment of the transcriptional machinery containing BET proteins. Finally, combination therapy with gemcitabine plus JQ1 showed greater efficacy than gemcitabine monotherapy against PDAC in vivo. Thus, our results reveal BET proteins as the critical regulators of CAF-activation and also provide evidence that stromal remodeling by epigenetic modulators can be a novel therapeutic option for PDAC.

4 Article [IPMN and pancreatic cyst as high risk of pancreatic cancer]. 2015

Tada, Minoru / Takagi, Kaori / Kawakubo, Kazumichi / Hakuta, Ryunosuke / Ishigaki, Kazunaga / Takeda, Tsuyoshi / Fujiwara, Hiroaki / Umefune, Gyotane / Saito, Kei / Saito, Tomotaka / Watanabe, Takeo / Akiyama, Dai / Uchino, Rie / Kishikawa, Takahiro / Takahara, Naminatsu / Takahashi, Ryota / Yamamoto, Keisuke / Hamada, Tsuyoshi / Mizuno, Suguru / Miyabayashi, Koji / Mohri, Dai / Matsubara, Saburo / Kogure, Hirofumi / Nakai, Yousuke / Yamamoto, Natsuyo / Sasaki, Takashi / Sasahira, Naoki / Hirano, Kenji / Ijichi, Hideaki / Tateishi, Keisuke / Isayama, Hiroyuki / Koike, Kazuhiko. ·Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo. ·Nihon Shokakibyo Gakkai Zasshi · Pubmed #26250126.

ABSTRACT: -- No abstract --

5 Article Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer. 2013

Takahashi, Ryota / Hirata, Yoshihiro / Sakitani, Kosuke / Nakata, Wachiko / Kinoshita, Hiroto / Hayakawa, Yoku / Nakagawa, Hayato / Sakamoto, Kei / Hikiba, Yohko / Ijichi, Hideaki / Moses, Harold L / Maeda, Shin / Koike, Kazuhiko. ·Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo. ·Cancer Sci · Pubmed #23237571.

ABSTRACT: c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase (MAPK) family, and it is reportedly involved in the development of several cancers. However, the role of JNK in pancreatic cancer has not been elucidated. We assessed t he involvement of JNK in the development of pancreatic cancer and investigated the therapeutic effect of JNK inhibitors on this deadly cancer. Small interfering RNAs against JNK or the JNK inhibitor SP600125 were used to examine the role of JNK in cellular proliferation and the cell cycles of pancreatic cancer cell lines. Ptf1a(cre/+) ;LSL-Kras(G12D/+) ;Tgfbr2(flox/flox) mice were treated with the JNK inhibitor to examine pancreatic histology and survival. The effect of JNK inhibition on tumor angiogenesis was also assessed using cell lines and murine pancreatic cancer specimens. JNK was frequently activated in human and murine pancreatic cancer in vitro and in vivo. Growth of human pancreatic cancer cell lines was suppressed by JNK inhibition through G1 arrest in the cell cycle with decreased cyclin D1 expression. In addition, oncogenic K-ras expression led to activation of JNK in pancreatic cancer cell lines. Treatment of Ptf1a(cre/+) ;LSL-Kras(G12D/+) ;Tgfbr2(flox/flox) mice with the JNK inhibitor decreased growth of murine pancreatic cancer and prolonged survival of the mice significantly. Angiogenesis was also decreased by JNK inhibition in vitro and in vivo. In conclusion, activation of JNK promotes development of pancreatic cancer, and JNK may be a potential therapeutic target for pancreatic cancer.