Researcher Profile and Settings

Master

Affiliation (Master)

• Institute for Genetic Medicine　Disease Control

Affiliation (Master)

• Institute for Genetic Medicine　Disease Control

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Profile and Settings

Degree

• (BLANK)（The University of Tokyo）
• Ph.D（Kyoto University）

Profile and Settings

• Name (Japanese)

  Sonoshita

• Name (Kana)

  Masahiro

• Name

  200901081557099385

Alternate Names

https://bmoncology.wixsite.com/mysite

Achievement

Research Interests

• 個体表現型スクリーニング   化学遺伝学   膵臓がん   大腸がん   培養細胞   ショウジョウバエ   臨床検体   マウス   認知症   実験腫瘍学   計算機科学   キナーゼ阻害薬   生化学   細胞生物学   分子生物学   遺伝学   キナーゼ   予後マーカー   がん治療薬リード開発   甲状腺髄様がん   転移   Prostaglandin（プロスタグランジン）   Cyclooxygenase（シクロオキシゲナーゼ）   消化管腫瘍   Metastasis   Prostaglandin   cyclooxygenase   Gastrointestinal Tumorigenesis   

Research Areas

• Life sciences / Pathobiochemistry
• Life sciences / Medical biochemistry
• Life sciences / Pharmaceuticals - chemistry and drug development
• Life sciences / Pharmaceuticals - health and biochemistry
• Life sciences / Genetics
• Life sciences / Cell biology
• Life sciences / Functional biochemistry
• Life sciences / Molecular biology
• Life sciences / Tumor diagnostics and therapeutics
• Life sciences / Tumor biology
• Life sciences / Laboratory animal science
• Nanotechnology/Materials / Biochemistry
• Nanotechnology/Materials / Chemical biology
• Nanotechnology/Materials / Molecular biochemistry
• Life sciences / Experimental pathology
• Life sciences / Pharmacology

Research Experience

• 2023/09 - Today FlyWorks Co., Ltd. CSO
• 2022/04 - Today 北海道大学 遺伝子病制御研究所 感染癌研究センター センター長（兼任）
• 2018/09 - Today Hokkaido University Institute for Genetic Medicine
• 2019/04 - 2022/03 Hokkaido University Institute for Genetic Medicine
• 2019/08 - 2021/07 Ministry of Education,Culture,Sports,Science and Technology
• 2017/04 - 2018/08 Icahn School of Medicine at Mount Sinai Dept. Cell, Developmental & Regenerative Biology Postdoctoral Fellow
• 2013/09 - 2017/03 Icahn School of Medicine at Mount Sinai Dept. Cell, Developmental & Regenerative Biology Visiting Researcher
• 2012/04 - 2017/03 Kyoto University Graduate School of Medicine
• 2011/01 - 2012/03 Kyoto University Graduate School of Medicine
• 2008/04 - 2010/12 Kyoto University Graduate School of Medicine
• 2004/04 - 2008/03 日本学術振興会特別研究員PD
• 2002/04 - 2004/03 日本学術振興会特別研究員DC1

Education

• 2001/04 - 2004/03  Kyoto University  Graduate School of Medicine  Physiology
•        - 2003  Kyoto University  Graduate School, Division of Medicine  Physiology
• 1999/04 - 2001/03  The University of Tokyo  Graduate School of Pharmaceutical Sciences  Department of Pharmaceutical Technology
•        - 2001  The University of Tokyo  Graduate School, Department of Pharmaceutical Sciences
• 1997/04 - 1999/03  The University of Tokyo  Faculty of Pharmaceutical Sciences
• 1995/04 - 1997/03  The University of Tokyo  College of Arts and Sciences
•        - 1995/03  鹿児島ラ・サール高校

Awards

• 2022/02 光産業創成大学院大学 Photonics Challenge 最優秀ビジネス賞
  
• 2022/02 NEDO Technology Commercialization Program 優秀賞・VC賞
  
• 2022/02 北海道 令和３年度 北海道科学技術奨励賞
   個体レベルの効率的な新規膵がん研究基盤の確立
• 2021/10 経済産業省北海道経済産業局 NoMaps Dream Pitch 2021 優秀賞・NEDO賞
   「創薬支援スタートアップ FlyMe」
• 2018/08 The New York Hideyo Noguchi Memorial Society, Inc. Hideyo Noguchi Memorial Scholarship
   「Exploring therapeutic network in pancreatic cancer」 

  受賞者: 園下 将大
• 2017/10 Icahn School of Medicine at Mount Sinai Promising Young Investigator Award
   「Rational polypharmacology」 

  受賞者: 園下 将大
• 2016/10 日本癌学会 奨励賞
   「大腸がん悪性化機序と予後診断法・治療薬研究」 

  受賞者: 園下 将大
• 2014/08 京都大学 若手教員海外派遣事業スカラシップ
   「低毒性・高特異性の次世代抗がん薬の創出」 

  受賞者: 園下 将大
• 2014/07 日本がん転移学会 研究奨励賞
   「遺伝学的解析に立脚した大腸がん悪性化機序の解明と新規治療・予防標的の同定」 

  受賞者: 園下 将大
• 2013/08 京都大学 若手教員海外派遣事業スカラシップ
   「ショウジョウバエの遺伝学を用いた、がん転移の関連遺伝子及び治療薬候補の同定」 

  受賞者: 園下 将大

Published Papers

• High-throughput fluorescence lifetime imaging flow cytometry.

  Hiroshi Kanno, Kotaro Hiramatsu, Hideharu Mikami, Atsushi Nakayashiki, Shota Yamashita, Arata Nagai, Kohki Okabe, Fan Li, Fei Yin, Keita Tominaga, Omer Faruk Bicer, Ryohei Noma, Bahareh Kiani, Olga Efa, Martin Büscher, Tetsuichi Wazawa, Masahiro Sonoshita, Hirofumi Shintaku, Takeharu Nagai, Sigurd Braun, Jessica P Houston, Sherif Rashad, Kuniyasu Niizuma, Keisuke Goda

  Nature Communications 15 (1) 7376 - 7376 2024/09/04 

  Flow cytometry is a vital tool in biomedical research and laboratory medicine. However, its accuracy is often compromised by undesired fluctuations in fluorescence intensity. While fluorescence lifetime imaging microscopy (FLIM) bypasses this challenge as fluorescence lifetime remains unaffected by such fluctuations, the full integration of FLIM into flow cytometry has yet to be demonstrated due to speed limitations. Here we overcome the speed limitations in FLIM, thereby enabling high-throughput FLIM flow cytometry at a high rate of over 10,000 cells per second. This is made possible by using dual intensity-modulated continuous-wave beam arrays with complementary modulation frequency pairs for fluorophore excitation and acquiring fluorescence lifetime images of rapidly flowing cells. Moreover, our FLIM system distinguishes subpopulations in male rat glioma and captures dynamic changes in the cell nucleus induced by an anti-cancer drug. FLIM flow cytometry significantly enhances cellular analysis capabilities, providing detailed insights into cellular functions, interactions, and environments.
• Flow zoometry of Drosophila

  Walker Peterson, Joshua Arenson, Soichiro Hata, Laura Kacenauskaite, Tsubasa Kobayashi, Takuya Otsuka, Hanqing Wang, Yayoi Wada, Kotaro Hiramatsu, Zhikai He, Jean-Emmanuel Clement, Chenqi Zhang, Chenglang Hu, Phillip McCann, Hayato Kanazawa, Yuzuki Nagasaka, Hiroyuki Uechi, Yuh Watanabe, Ryodai Yamamura, Mika Hayashi, Yuta Nakagawa, Kangrui Huang, Hiroshi Kanno, Yuqi Zhou, Tianben Ding, Maik Herbig, Shimpei Makino, Shunta Nonaga, Ryosuke Takami, Oguz Kanca, Koji Tabata, Satoshi Amaya, Kotaro Furusawa, Kenichi Ishii, Kazuo Emoto, Fumihito Arai, Ross Cagan, Dino Di Carlo, Tatsushi Igaki, Erina Kuranaga, Shinya Yamamoto, Hugo J Bellen, Tamiki Komatsuzaki, Masahiro Sonoshita, Keisuke Goda

  2024/04/05 

  ABSTRACT Drosophilaserves as a highly valuable model organism across numerous fields including genetics, immunology, neuroscience, cancer biology, and developmental biology. Central toDrosophila-based biological research is the ability to perform comprehensive genetic or chemical screens. However, this research is often limited by its dependence on laborious manual handling and analysis, making it prone to human error and difficult to discern statistically significant or rare events amid the noise of individual variations resulting from genetic and environmental factors. In this article we present flow zoometry, a whole-animal equivalent of flow cytometry for large-scale, individual-level, high-content screening ofDrosophila. Our flow zoometer automatically clears the tissues ofDrosophila melanogaster, captures three-dimensional (3D) multi-color fluorescence tomograms of single flies with single-cell volumetric resolution at an unprecedented throughput of over 1,000 animals within 48 hours (24 hr for clearing; 24 hr for imaging), and performs AI-enhanced data-driven analysis – a task that would traditionally take months or years with manual techniques. To demonstrate its broad applications, we employed the flow zoometer in various laborious screening assays, including those in toxicology, genotyping, and tumor screening. Flow zoometry represents a pivotal evolution in high-throughput screening technology: previously from molecules to cells, now from cells to whole animals. This advancement serves as a foundational platform for “statistical spatial biology”, to improve empirical precision and enable serendipitous discoveries across various fields of biology.
• Concurrent targeting of GSK3 and MEK as a therapeutic strategy to treat pancreatic ductal adenocarcinoma

  Junki Fukuda, Shinya Kosuge, Yusuke Satoh, Sho Sekiya, Ryodai Yamamura, Takako Ooshio, Taiga Hirata, Reo Sato, Kanako C. Hatanaka, Tomoko Mitsuhashi, Toru Nakamura, Yoshihiro Matsuno, Yutaka Hatanaka, Satoshi Hirano, Masahiro Sonoshita

  Cancer Science 1347-9032 2024/02/06 

  Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide. However, drug discovery for PDAC treatment has proven complicated, leading to stagnant therapeutic outcomes. Here, we identify Glycogen synthase kinase 3 (GSK3) as a therapeutic target through a whole‐body genetic screening utilizing a ‘4‐hit’ Drosophila model mimicking the PDAC genotype. Reducing the gene dosage of GSK3 in a whole‐body manner or knocking down GSK3 specifically in transformed cells suppressed 4‐hit fly lethality, similar to Mitogen‐activated protein kinase kinase (MEK), the therapeutic target in PDAC we have recently reported. Consistently, a combination of the GSK3 inhibitor CHIR99021 and the MEK inhibitor trametinib suppressed the phosphorylation of Polo‐like kinase 1 (PLK1) as well as the growth of orthotopic human PDAC xenografts in mice. Additionally, reducing PLK1 genetically in 4‐hit flies rescued their lethality. Our results reveal a therapeutic vulnerability in PDAC that offers a treatment opportunity for patients by inhibiting multiple targets.
• ショウジョウバエを活用した膵がんの創薬研究

  小菅 信哉, 平田 大賀, 関谷 翔, 山村 凌大, 園下 将大

  BIO Clinica 38 (10) 16 - 20 2023/08 [Not refereed][Invited]
  
• Drosophila Screening Identifies Dual Inhibition of MEK and AURKB as an Effective Therapy for Pancreatic Ductal Adenocarcinoma

  Sho Sekiya, Junki Fukuda, Ryodai Yamamura, Takako Ooshio, Yusuke Satoh, Shinya Kosuge, Reo Sato, Kanako C. Hatanaka, Yutaka Hatanaka, Tomoko Mitsuhashi, Toru Nakamura, Yoshihiro Matsuno, Satoshi Hirano, Masahiro Sonoshita

  Cancer Research 8 (16) 2704 - 2715 0008-5472 2023/06/28 [Refereed]
   

  Abstract Significant progress has been made in understanding the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) by generating and using murine models. To accelerate drug discovery by identifying novel therapeutic targets on a systemic level, here we generated a Drosophila model mimicking the genetic signature in PDAC (KRAS, TP53, CDKN2A, and SMAD4 alterations), which is associated with the worst prognosis in patients. The ‘4-hit’ flies displayed epithelial transformation and decreased survival. Comprehensive genetic screening of their entire kinome revealed kinases including MEK and AURKB as therapeutic targets. Consistently, a combination of the MEK inhibitor trametinib and the AURKB inhibitor BI-831266 suppressed the growth of human PDAC xenografts in mice. In patients with PDAC, the activity of AURKB was associated with poor prognosis. This fly-based platform provides an efficient whole-body approach that complements current methods for identifying therapeutic targets in PDAC. Significance: Development of a Drosophila model mimicking genetic alterations in human pancreatic ductal adenocarcinoma provides a tool for genetic screening that identifies MEK and AURKB inhibition as a potential treatment strategy.
• Virtual-freezing fluorescence imaging flow cytometry with 5-aminolevulinic acid stimulation and antibody labeling for detecting all forms of circulating tumor cells

  Hiroki Matsumura, Larina Tzu-Wei Shen, Akihiro Isozaki, Hideharu Mikami, Dan Yuan, Taichi Miura, Yuto Kondo, Tomoko Mori, Yoshika Kusumoto, Masako Nishikawa, Atsushi Yasumoto, Aya Ueda, Hiroko Bando, Hisato Hara, Yuhong Liu, Yunjie Deng, Masahiro Sonoshita, Yutaka Yatomi, Keisuke Goda, Satoshi Matsusaka

  Lab on a Chip 23 (6) 1561 - 1575 1473-0197 2023 [Refereed]
   

  Heterogeneous clusters of cancer cells and leukocytes in blood were visualized by combining high-throughput and high-sensitivity fluorescence imaging flow cytometry with 5-aminolevulinic acid stimulation.
• Drosophila as a toolkit to tackle cancer and its metabolism

  Jiang H, Kimura T, Hai H, Yamamura R, Sonoshita M

  Frontiers in Oncology 12 982751  2022/08/25 [Refereed]
   

  Cancer is one of the most severe health problems worldwide accounting for the second leading cause of death. Studies have indicated that cancers utilize different metabolic systems as compared with normal cells to produce extra energy and substances required for their survival, which contributes to tumor formation and progression. Recently, the fruit fly Drosophila has been attracting significant attention as a whole-body model for elucidating the cancer mechanisms including metabolism. This tiny organism offers a valuable toolkit with various advantages such as high genetic conservation and similar drug response to mammals. In this review, we introduce flies modeling for cancer patient genotypes which have pinpointed novel therapeutic targets and drug candidates in the salivary gland, thyroid, colon, lung, and brain. Furthermore, we introduce fly models for metabolic diseases such as diabetes mellitus, obesity, and cachexia. Diabetes mellitus and obesity are widely acknowledged risk factors for cancer, while cachexia is a cancer-related metabolic condition. In addition, we specifically focus on two cancer metabolic alterations: the Warburg effect and redox metabolism. Indeed, flies proved useful to reveal the relationship between these metabolic changes and cancer. Such accumulating achievements indicate that Drosophila offers an efficient platform to clarify the mechanisms of cancer as a systemic disease.
• ショウジョウバエを活用した計画的な個体レベルのセレンディピティによるがん研究の加速

  佐藤悠介, 園下将大

  医学のあゆみ 282 (9) 798 - 800 2022/08 [Invited]
  
• Tiny Drosophila makes giant strides in cancer research.

  Ryodai Yamamura, Takako Ooshio, Masahiro Sonoshita

  Cancer Science 112 (2) 505 - 514 2021/02 [Refereed]
   

  Cancer burden has been increasing worldwide, making cancer the second leading cause of death in the world. Over the past decades, various experimental models have provided important insights into the nature of cancer. Among them, the fruit fly Drosophila as a whole-animal toolkit has made a decisive contribution to our understanding of fundamental mechanisms of cancer development including loss of cell polarity. In recent years, scalable Drosophila platforms have proven useful also in developing anti-cancer regimens that are effective not only in mammalian models but also in patients. Here, we review studies using Drosophila as a tool to advance cancer study by complementing other traditional research systems.
• 個体を用いた新規抗がん剤創薬基盤 ~既存薬の合理的改変手法の確立~

  園下 将大

  生化学 92 567 - 571 2020/04 [Refereed][Invited]
  
• Integrated computational and Drosophila cancer model platform captures previously unappreciated chemicals perturbing a kinase network.

  Peter M U Ung, Masahiro Sonoshita, Alex P Scopton, Arvin C Dar, Ross L Cagan, Avner Schlessinger

  PLoS Computational Biology 15 (4) e1006878  2019/04 [Refereed][Not invited]
   

  Drosophila provides an inexpensive and quantitative platform for measuring whole animal drug response. A complementary approach is virtual screening, where chemical libraries can be efficiently screened against protein target(s). Here, we present a unique discovery platform integrating structure-based modeling with Drosophila biology and organic synthesis. We demonstrate this platform by developing chemicals targeting a Drosophila model of Medullary Thyroid Cancer (MTC) characterized by a transformation network activated by oncogenic dRetM955T. Structural models for kinases relevant to MTC were generated for virtual screening to identify unique preliminary hits that suppressed dRetM955T-induced transformation. We then combined features from our hits with those of known inhibitors to create a 'hybrid' molecule with improved suppression of dRetM955T transformation. Our platform provides a framework to efficiently explore novel kinase inhibitors outside of explored inhibitor chemical space that are effective in inhibiting cancer networks while minimizing whole body toxicity.
• Transgenic mice that accept Luciferase- or GFP-expressing syngeneic tumor cells at high efficiencies.

  Naoki Aoyama, Hiroyuki Miyoshi, Hitoshi Miyachi, Masahiro Sonoshita, Masaru Okabe, Makoto Mark Taketo

  Genes to Cells 23 (7) 580 - 589 1356-9597 2018/07 [Refereed][Not invited]
   

  Jellyfish green fluorescent protein (GFP) and firefly luciferase can serve as versatile tracking markers for identification and quantification of transplanted cancer cells in vivo. However, immune reactions against these markers can hamper the formation of syngraft tumors and metastasis that follows. Here, we report two transgenic (Tg) mouse lines that express nonfunctional mutant marker proteins, namely modified firefly luciferase (Luc2) or enhanced GFP (EGFP). These mice, named as Tg-mLuc2 and Tg-mEGFP, turned out to be immunologically tolerant to the respective tracking markers and thus efficiently accepted syngeneic cancer cells expressing the active forms of the markers. We then injected intrarectally the F1 hybrid Tg mice (BALB/c × C57BL/6J) with Colon-26 (C26) colon cancer cells that originated from a BALB/c mouse. Even when C26 cells expressed active Luc2 or EGFP, they formed primary tumors in the Tg mice with only 104 cells per mouse compared with more than 106 cells required in the nontransgenic BALB/c hosts. Furthermore, we detected metastatic foci of C26 cells in the liver and lungs of the Tg mice by tracking the specific reporter activities. These results show the usefulness of the Tg mouse lines as recipients for transplantation experiments with the non-self tracking marker-expressing cells.
• A whole-animal platform to advance a clinical kinase inhibitor into new disease space.

  Masahiro Sonoshita, Alex P Scopton, Peter M U Ung, Matthew A Murray, Lisa Silber, Andres Y Maldonado, Alexander Real, Avner Schlessinger, Ross L Cagan, Arvin C Dar

  Nature Chemical Biology 14 (3) 291 - 298 1552-4469 2018/03 [Refereed][Not invited]
   

  Synthetic tailoring of approved drugs for new indications is often difficult, as the most appropriate targets may not be readily apparent, and therefore few roadmaps exist to guide chemistry. Here, we report a multidisciplinary approach for accessing novel target and chemical space starting from an FDA-approved kinase inhibitor. By combining chemical and genetic modifier screening with computational modeling, we identify distinct kinases that strongly enhance ('pro-targets') or limit ('anti-targets') whole-animal activity of the clinical kinase inhibitor sorafenib in a Drosophila medullary thyroid carcinoma (MTC) model. We demonstrate that RAF-the original intended sorafenib target-and MKNK kinases function as pharmacological liabilities because of inhibitor-induced transactivation and negative feedback, respectively. Through progressive synthetic refinement, we report a new class of 'tumor calibrated inhibitors' with unique polypharmacology and strongly improved therapeutic index in fly and human MTC xenograft models. This platform provides a rational approach to creating new high-efficacy and low-toxicity drugs.
• Amino-terminal enhancer of split gene AES encodes a tumor and metastasis suppressor of prostate cancer.

  Yoshiyuki Okada, Masahiro Sonoshita, Fumihiko Kakizaki, Naoki Aoyama, Yoshiro Itatani, Masayuki Uegaki, Hiromasa Sakamoto, Takashi Kobayashi, Takahiro Inoue, Tomomi Kamba, Akira Suzuki, Osamu Ogawa, M Mark Taketo

  Cancer Science 108 (4) 744 - 752 1349-7006 2017/04 [Refereed][Not invited]
   

  A major cause of cancer death is its metastasis to the vital organs. Few effective therapies are available for metastatic castration-resistant prostate cancer (PCa), and progressive metastatic lesions such as lymph nodes and bones cause mortality. We recently identified AES as a metastasis suppressor for colon cancer. Here, we have studied the roles of AES in PCa progression. We analyzed the relationship between AES expression and PCa stages of progression by immunohistochemistry of human needle biopsy samples. We then performed overexpression and knockdown of AES in human PCa cell lines LNCaP, DU145 and PC3, and determined the effects on proliferation, invasion and metastasis in culture and in a xenograft model. We also compared the PCa phenotypes of Aes/Pten compound knockout mice with those of Pten simple knockout mice. Expression levels of AES were inversely correlated with clinical stages of human PCa. Exogenous expression of AES suppressed the growth of LNCaP cells, whereas the AES knockdown promoted it. We also found that AES suppressed transcriptional activities of androgen receptor and Notch signaling. Notably, AES overexpression in AR-defective DU145 and PC3 cells reduced invasion and metastasis to lymph nodes and bones without affecting proliferation in culture. Consistently, prostate epithelium-specific inactivation of Aes in Ptenflox/flox mice increased expression of Snail and MMP9, and accelerated growth, invasion and lymph node metastasis of the mouse prostate tumor. These results suggest that AES plays an important role in controlling tumor growth and metastasis of PCa by regulating both AR and Notch signaling pathways.
• Modeling Human Cancers in Drosophila.

  M Sonoshita, R L Cagan

  Current Topics in Developmental Biology 121 287 - 309 0070-2153 2017 [Refereed][Not invited]
   

  Cancer is a complex disease that affects multiple organs. Whole-body animal models provide important insights into oncology that can lead to clinical impact. Here, we review novel concepts that Drosophila studies have established for cancer biology, drug discovery, and patient therapy. Genetic studies using Drosophila have explored the roles of oncogenes and tumor-suppressor genes that when dysregulated promote cancer formation, making Drosophila a useful model to study multiple aspects of transformation. Not limited to mechanism analyses, Drosophila has recently been showing its value in facilitating drug development. Flies offer rapid, efficient platforms by which novel classes of drugs can be identified as candidate anticancer leads. Further, we discuss the use of Drosophila as a platform to develop therapies for individual patients by modeling the tumor's genetic complexity. Drosophila provides both a classical and a novel tool to identify new therapeutics, complementing other more traditional cancer tools.
• Expression of metastasis suppressor gene AES driven by a Yin Yang (YY) element in a CpG island promoter and transcription factor YY2.

  Fumihiko Kakizaki, Masahiro Sonoshita, Hiroyuki Miyoshi, Yoshiro Itatani, Shinji Ito, Kenji Kawada, Yoshiharu Sakai, M Mark Taketo

  Cancer Science 107 (11) 1622 - 1631 1347-9032 2016/11 [Refereed][Not invited]
   

  We recently found that the product of the AES gene functions as a metastasis suppressor of colorectal cancer (CRC) in both humans and mice. Expression of amino-terminal enhancer of split (AES) protein is significantly decreased in liver metastatic lesions compared with primary colon tumors. To investigate its downregulation mechanism in metastases, we searched for transcriptional regulators of AES in human CRC and found that its expression is reduced mainly by transcriptional dysregulation and, in some cases, by additional haploidization of its coding gene. The AES promoter-enhancer is in a typical CpG island, and contains a Yin-Yang transcription factor recognition sequence (YY element). In human epithelial cells of normal colon and primary tumors, transcription factor YY2, a member of the YY family, binds directly to the YY element, and stimulates expression of AES. In a transplantation mouse model of liver metastases, however, expression of Yy2 (and therefore of Aes) is downregulated. In human CRC metastases to the liver, the levels of AES protein are correlated with those of YY2. In addition, we noticed copy-number reduction for the AES coding gene in chromosome 19p13.3 in 12% (5/42) of human CRC cell lines. We excluded other mechanisms such as point or indel mutations in the coding or regulatory regions of the AES gene, CpG methylation in the AES promoter enhancer, expression of microRNAs, and chromatin histone modifications. These results indicate that Aes may belong to a novel family of metastasis suppressors with a CpG-island promoter enhancer, and it is regulated transcriptionally.
• Characterization of Aes nuclear foci in colorectal cancer cells.

  Yoshiro Itatani, Masahiro Sonoshita, Fumihiko Kakizaki, Katsuya Okawa, Stefano Stifani, Hideaki Itoh, Yoshiharu Sakai, M Mark Taketo

  Journal of Biochemistry 159 (1) 133 - 40 0021-924X 2016/01 [Refereed][Not invited]
   

  Amino-terminal enhancer of split (Aes) is a member of Groucho/Transducin-like enhancer (TLE) family. Aes is a recently found metastasis suppressor of colorectal cancer (CRC) that inhibits Notch signalling, and forms nuclear foci together with TLE1. Although some Notch-associated proteins are known to form subnuclear bodies, little is known regarding the dynamics or functions of these structures. Here, we show that Aes nuclear foci in CRC observed under an electron microscope are in a rather amorphous structure, lacking surrounding membrane. Investigation of their behaviour during the cell cycle by time-lapse cinematography showed that Aes nuclear foci dissolve during mitosis and reassemble after completion of cytokinesis. We have also found that heat shock cognate 70 (HSC70) is an essential component of Aes foci. Pharmacological inhibition of the HSC70 ATPase activity with VER155008 reduces Aes focus formation. These results provide insight into the understanding of Aes-mediated inhibition of Notch signalling.
• Promotion of colorectal cancer invasion and metastasis through activation of NOTCH-DAB1-ABL-RHOGEF protein TRIO.

  Masahiro Sonoshita, Yoshiro Itatani, Fumihiko Kakizaki, Kenji Sakimura, Toshio Terashima, Yu Katsuyama, Yoshiharu Sakai, M Mark Taketo

  Cancer Discovery 5 (2) 198 - 211 2159-8274 2015/02 [Refereed][Not invited]
   

  UNLABELLED: We have recently identified a metastasis suppressor gene for colorectal cancer: AES/Aes, which encodes an endogenous inhibitor of NOTCH signaling. When Aes is knocked out in the adenomatous epithelium of intestinal polyposis mice, their tumors become malignant, showing marked submucosal invasion and intravasation. Here, we show that one of the genes induced by NOTCH signaling in colorectal cancer is DAB1/Dab1. Genetic depletion of DAB1 suppresses cancer invasion and metastasis in the NOTCH signaling-activated mice. DAB1 is phosphorylated by ABL tyrosine kinase, which activates ABL reciprocally. Consistently, inhibition of ABL suppresses cancer invasion in mice. Furthermore, we show that one of the targets of ABL is the RAC/RHOGEF protein TRIO, and that phosphorylation at its Tyr residue 2681 (pY2681) causes RHO activation in colorectal cancer cells. Its unphosphorylatable mutation TRIO Y2681F reduces RHOGEF activity and inhibits invasion of colorectal cancer cells. Importantly, TRIO pY2681 correlates with significantly poorer prognosis of patients with colorectal cancer after surgery. SIGNIFICANCE: These results indicate that TRIO pY2681 is one of the downstream effectors of NOTCH signaling activation in colorectal cancer, and can be a prognostic marker, helping to determine the therapeutic modality of patients with colorectal cancer.
• Molecular mechanisms of liver metastasis.

  Kenji Kawada, Suguru Hasegawa, Teppei Murakami, Yoshiro Itatani, Hisahiro Hosogi, Masahiro Sonoshita, Takanori Kitamura, Teruaki Fujishita, Masayoshi Iwamoto, Takuya Matsumoto, Ryo Matsusue, Koya Hida, Gaku Akiyama, Kae Okoshi, Masahiro Yamada, Junichiro Kawamura, Makoto Mark Taketo, Yoshiharu Sakai

  International Journal of Clinical Oncology 16 (5) 464 - 72 1341-9625 2011/10 [Refereed][Not invited]
   

  Colorectal cancer is the second most common cancer, and is the third leading cause of cancer-related death in Japan. The majority of these deaths is attributable to liver metastasis. Recent studies have provided increasing evidence that the chemokine-chemokine receptor system is a potential mechanism of tumor metastasis via multiple complementary actions: (a) by promoting cancer cell migration, invasion, survival and angiogenesis; and (b) by recruiting distal stromal cells (i.e., myeloid bone marrow-derived cells) to indirectly facilitate tumor invasion and metastasis. Here, we discuss recent preclinical and clinical data supporting the view that chemokine pathways are potential therapeutic targets for liver metastasis of colorectal cancer.
• Suppression of colon cancer metastasis by Aes through inhibition of Notch signaling.

  Masahiro Sonoshita, Masahiro Aoki, Haruhiko Fuwa, Koji Aoki, Hisahiro Hosogi, Yoshiharu Sakai, Hiroki Hashida, Arimichi Takabayashi, Makoto Sasaki, Sylvie Robine, Kazuyuki Itoh, Kiyoko Yoshioka, Fumihiko Kakizaki, Takanori Kitamura, Masanobu Oshima, Makoto Mark Taketo

  Cancer Cell 19 (1) 125 - 37 1535-6108 2011/01/18 [Refereed][Not invited]
   

  Metastasis is responsible for most cancer deaths. Here, we show that Aes (or Grg5) gene functions as an endogenous metastasis suppressor. Expression of Aes was decreased in liver metastases compared with primary colon tumors in both mice and humans. Aes inhibited Notch signaling by converting active Rbpj transcription complexes into repression complexes on insoluble nuclear matrix. In tumor cells, Notch signaling was triggered by ligands on adjoining blood vessels, and stimulated transendothelial migration. Genetic depletion of Aes in Apc(Δ716) intestinal polyposis mice caused marked tumor invasion and intravasation that were suppressed by Notch signaling inhibition. These results suggest that inhibition of Notch signaling can be a promising strategy for prevention and treatment of colon cancer metastasis.
• Chemokine receptor CXCR3 promotes colon cancer metastasis to lymph nodes.

  K Kawada, H Hosogi, M Sonoshita, H Sakashita, T Manabe, Y Shimahara, Y Sakai, A Takabayashi, M Oshima, M M Taketo

  Oncogene 26 (32) 4679 - 88 0950-9232 2007/07/12 [Refereed][Not invited]
   

  Chemokines and their receptors are essential for leukocyte trafficking, and also implicated in cancer metastasis to specific organs. We have recently demonstrated that CXCR3 plays a critical role in metastasis of mouse melanoma cells to lymph nodes. Here, we show that some human colon cancer cell lines express CXCR3 constitutively. We constructed cells that expressed CXCR3 cDNA ('DLD-1-CXCR3'), and compared with nonexpressing controls by rectal transplantation in nude mice. Although both cell lines disseminated to lymph nodes at similar frequencies at 2 weeks, DLD-1-CXCR3 expanded more rapidly than the control in 4 weeks. In 6 weeks, 59% of mice inoculated with DLD1-CXCR3 showed macroscopic metastasis in para-aortic lymph nodes, whereas only 14% of those with the control (P<0.05). In contrast, metastasis to the liver or lung was rare, and unaffected by CXCR3 expression. In clinical colon cancer samples, we found expression of CXCR3 in 34% cases, most of which had lymph node metastasis. Importantly, patients with CXCR3-positive cancer showed significantly poorer prognosis than those without CXCR3, or those expressing CXCR4 or CCR7. These results indicate that activation of CXCR3 with its ligands stimulates colon cancer metastasis preferentially to the draining lymph nodes with poorer prognosis.
• Development of spontaneous tumours and intestinal lesions in Fhit gene knockout mice.

  T Fujishita, Y Doi, M Sonoshita, H Hiai, M Oshima, K Huebner, C M Croce, M M Taketo

  British Journal of Cancer 91 (8) 1571 - 4 0007-0920 2004/10/18 [Refereed][Not invited]
   

  The fragile histidine triad (FHIT) gene is frequently inactivated in various types of tumours. However, the system-wide pathology caused by FHIT inactivation has not been examined in detail. Here we demonstrate that Fhit gene knockout mice develop tumours in the lymphoid tissue, liver, uterus, testis, forestomach and small intestine, together with structural abnormalities in the small intestinal mucosa. These results suggest that Fhit plays important roles in systemic tumour suppression and in the integrity of mucosal structure of the intestines.
• Pivotal role of CXCR3 in melanoma cell metastasis to lymph nodes.

  Kenji Kawada, Masahiro Sonoshita, Hiromi Sakashita, Arimichi Takabayashi, Yoshio Yamaoka, Toshiaki Manabe, Kayo Inaba, Nagahiro Minato, Masanobu Oshima, Makoto Mark Taketo

  Cancer Research 64 (11) 4010 - 7 0008-5472 2004/06/01 [Refereed][Not invited]
   

  Chemokines and their receptors play key roles in leukocyte trafficking and are also implicated in cancer metastasis to specific organs. Here we show that mouse B16F10 melanoma cells constitutively express chemokine receptor CXCR3, and that its ligands CXCL9/Mig, CXCL10/IP-10, and CXCL11/I-TAC induce cellular responses in vitro, such as actin polymerization, migration, invasion, and cell survival. To determine whether CXCR3 could play a role in metastasis to lymph nodes (LNs), we constructed B16F10 cells with reduced CXCR3 expression by antisense RNA and investigated their metastatic activities after s.c. inoculations to syngeneic hosts, C57BL/6 mice. The metastatic frequency of these cells to LNs was markedly reduced to approximately 15% (P < 0.05) compared with the parental or empty vector-transduced cells. On the other hand, pretreatment of mice with complete Freund's adjuvant increased the levels of CXCL9 and CXCL10 in the draining LNs, which caused 2.5-3.0-fold increase (P < 0.05) in the metastatic frequency of B16F10 cells to the nodes with much larger foci. Importantly, such a stimulation of metastasis was largely suppressed when CXCR3 expression in B16F10 cells was reduced by antisense RNA or when mice were treated with specific antibodies against CXCL9 and CXCL10. We also demonstrate that CXCR3 is expressed on several human melanoma cell lines as well as primary human melanoma tissues (5 of 9 samples tested). These results suggest that CXCR3 inhibitors may be promising therapeutic agents for treatment of LN metastasis, including that of melanoma.
• Cooperation of cyclooxygenase 1 and cyclooxygenase 2 in intestinal polyposis.

  Haruna Takeda, Masahiro Sonoshita, Hiroko Oshima, Ken-ichi Sugihara, Patricia C Chulada, Robert Langenbach, Masanobu Oshima, Makoto M Taketo

  Cancer Research 63 (16) 4872 - 7 0008-5472 2003/08/15 [Refereed][Not invited]
   

  Membrane arachidonic acid is converted by cyclooxygenase (COX) into prostaglandin (PG) G(2) and then to PGH(2) which is subsequently metabolized to PGE(2) by PGE synthase (PGES). Both COX-1 and COX-2 play critical roles in intestinal polyp formation, whereas COX-2 is also expressed in cancers of a variety of organs. Likewise, inducible microsomal PGES (mPGES-1) is expressed in several types of cancer, although its role in benign polyp formation has not been investigated. We demonstrated recently that most COX-2-expressing cells in the polyps are stromal fibroblasts. Here we show colocalization of COX-1, COX-2 and mPGES in the intestinal polyp stromal fibroblasts of Apc(Delta 716) mice, a model for familial adenomatous polyposis. Contrary to COX-2 that was induced only in polyps >1 mm in diameter, COX-1 was found in polyps of any size. In polyps >1 mm, not only COX-2 but also mPGES was induced in the stromal fibroblasts where COX-1 had already been expressed. Although polyp number and size were markedly reduced in COX-1 (-/-) or COX-2 (-/-) compound mutant Apc mice, both COX-2 and mPGES were induced in the COX-1 (-/-) polyps, whereas COX-1 was expressed in the COX-2 (-/-) polyps. We found also in human familial adenomatous polyposis polyps that COX-2 and mPGES were induced in the COX-1-expressing fibroblasts. On the basis of these results, we propose that COX-1 expression in the stromal cells secures the basal level of PGE(2) that can support polyp growth to approximately 1 mm, and that simultaneous inductions of COX-2 and mPGES support the polyp expansion beyond approximately 1 mm by boosting the stromal PGE(2) production.
• Phospolipase A2 and apoptosis.

  Makoto Mark Taketo, Masahiro Sonoshita

  Biochimica et Biophysica Acta 1585 (2-3) 72 - 6 0006-3002 2002/12/30 [Refereed][Not invited]
   

  Phospolipase A(2) (PLA(2)) is the esterase activity that cleaves the sn-2 ester bond in glycerophospholipids, releasing free fatty acids and lysophospholipids. The PLA(2) activity is found in a variety of enzymes which can be divided in several types based on their Ca(2+) dependence for their activity; Ca(2+)-dependent secretory phosholipases (sPLA(2)s) and cytosolic phospholipases (cPLA(2)s), and Ca(2+)-independent phospholipase A(2)s (iPLA(2)s). These enzymes also show diverse size and substrate specificity (i.e., in the fatty acid chain length and extent of saturation). Among the fatty acids released by PLA(2), arachidonic acid (AA) is of particular biological importance, because it is subsequently converted to prostanoids and leukotrienes by cyclooxygenases (COX) and lipoxygenases (LOX), respectively. Free AA may also stimulate apoptosis through activation of sphingomyelinase. Alternatively, it is suggested that oxidized metabolites generated from AA by LOX induce apoptosis. Although the precise mechanisms remain to be elucidated, changes are observed in glycerolipid metabolism during apoptotic processes. In some cells induced to undergo apoptosis, AA is released concomitant with loss of cell viability, caspase activation and DNA fragmentation. Such AA releases appear to be mediated by activation of cPLA(2) and/or iPLA(2). For example, tumor necrosis factor-alpha (TNF-alpha)-induced cell death is mediated by cPLA(2), whereas Fas-induced apoptosis appears to be mediated by iPLA(2). Some discrepancies among early experimental results were probably caused by differences in the experimental conditions such as the serum concentration, inhibitors used that are not necessarily specific to a single-type enzyme, or differential expression of each PLA(2) in cells employed in the experiments. Recent studies eliminated such problems, by carefully defining the experimental conditions, and using multiple inhibitors that show different specificities. Accordingly, more convincing data are available that demonstrate involvement of some PLA(2)s in the apoptotic processes. In addition to cPLA(2) and iPLA(2), sPLA(2)s were recently found to play roles in apoptosis. Moreover, new proteins that appear to control PLA(2)s are being discovered. Here, the roles of PLA(2)s in apoptosis are discussed by reviewing recent reports.
• Cyclooxygenase-2 expression in fibroblasts and endothelial cells of intestinal polyps.

  Masahiro Sonoshita, Kazuaki Takaku, Masanobu Oshima, Ken-ichi Sugihara, Makoto M Taketo

  Cancer Research 62 (23) 6846 - 9 0008-5472 2002/12/01 [Refereed][Not invited]
   

  Cyclooxygenase-2 (COX-2), the inducible COX isozyme, plays a key role in intestinal tumorigenesis. We have demonstrated recently that COX-2 protein is induced in the polyp stroma near the intestinal luminal surface in the Apc(Delta716) mouse, a model for human familial adenomatous polyposis, and stimulate tumor angiogenesis. However, the precise cell types that express COX-2 are still to be determined. By immunohistochemical analysis, here we show that the majority of COX-2-expressing cells in the intestinal polyps of Apc(Delta716) mice are fibroblasts and endothelial cells. Furthermore, the COX-2-expressing cells in human familial adenomatous polyposis polyps are also fibroblasts and endothelial cells. In contrast, bone marrow-derived cells such as macrophages and leukocytes express little COX-2 protein in the intestinal polyps. These results clearly indicate that fibroblasts and endothelial cells play important roles in polyp expansion by expressing COX-2, resulting in tumor angiogenesis.
• Acceleration of intestinal polyposis through prostaglandin receptor EP2 in Apc(Delta 716) knockout mice.

  M Sonoshita, K Takaku, N Sasaki, Y Sugimoto, F Ushikubi, S Narumiya, M Oshima, M M Taketo

  Nature medicine 7 (9) 1048 - 51 1078-8956 2001/09 [Refereed][Not invited]
   

  Arachidonic acid is metabolized to prostaglandin H(2) (PGH(2)) by cyclooxygenase (COX). COX-2, the inducible COX isozyme, has a key role in intestinal polyposis. Among the metabolites of PGH(2), PGE(2) is implicated in tumorigenesis because its level is markedly elevated in tissues of intestinal adenoma and colon cancer. Here we show that homozygous deletion of the gene encoding a cell-surface receptor of PGE(2), EP2, causes decreases in number and size of intestinal polyps in Apc(Delta 716) mice (a mouse model for human familial adenomatous polyposis). This effect is similar to that of COX-2 gene disruption. We also show that COX-2 expression is boosted by PGE(2) through the EP2 receptor via a positive feedback loop. Homozygous gene knockout for other PGE(2) receptors, EP1 or EP3, did not affect intestinal polyp formation in Apc(Delta 716) mice. We conclude that EP2 is the major receptor mediating the PGE2 signal generated by COX-2 upregulation in intestinal polyposis, and that increased cellular cAMP stimulates expression of more COX-2 and vascular endothelial growth factor in the polyp stroma.
• Suppression of intestinal polyposis in Apc(delta 716) knockout mice by an additional mutation in the cytosolic phospholipase A(2) gene.

  K Takaku, M Sonoshita, N Sasaki, N Uozumi, Y Doi, T Shimizu, M M Taketo

  The Journal of biological chemistry 275 (44) 34013 - 6 0021-9258 2000/11/03 [Refereed][Not invited]
   

  Arachidonic acid is a precursor for biosynthesis of eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and lipoxins. Cytosolic phospholipase A(2) (cPLA(2)) plays a key role in the release of arachidonic acid as the substrate of cyclooxygenase-1 (COX-1) or COX-2. We found that the level of cPLA(2) mRNA was markedly elevated in the polyps and correlated with the polyp size in the small intestine of the Apc(delta)(716) knockout mouse, a model for human familial adenomatous polyposis. To determine the role of cPLA(2) in intestinal tumorigenesis, we then introduced a cPLA(2) gene mutation into Apc(delta)(716) mice. In the compound mutant mice, the size of the small intestinal polyps was reduced significantly, although the numbers remained unchanged. These results provide direct genetic evidence that cPLA(2) plays a key role in the expansion of polyps in the small intestine rather than in the initiation process. In contrast, colonic polyps were not affected in either size or number. Interestingly, group X sPLA(2) was constitutively expressed in the colon at much higher levels than in the small intestine. These results suggest that in the colon, group X sPLA(2) supplies arachidonic acid in both the normal epithelium and the polyps even in the absence of cPLA(2).

MISC

• Expression of metastasis suppressor gene AES driven by YY element in a CpG island promoter and transcription factor YY2

  Fumihiko Kakizaki, Masahiro Sonoshita, Hiroyuki Miyoshi, Yoshiro Itatani, Shinji Ito, Kenji Kawada, Yoshiharu Sakai, Makoto M. Taketo  CANCER SCIENCE  109-  36  -36  2018/01

Presentations

• ショウジョウバエの活用による膵がんの新規シーズの同定  [Not invited]

  園下将大

  日本薬学会第144年会  2024/03
• ワクワクを探しに宇宙へ！  [Invited]

  園下将大

  宇宙×ライフサイエンス in 神戸  2024/03
• Phenotypic screening of therapeutic seeds for treating pancreatic cancer  [Invited]

  Masahiro Sonoshita

  IISER-B & IGM Inter-Institutional Meeting  2024/03
• 重力変動ががん細胞の薬物応答性に与える影響の解析  [Invited]

  園下将大

  第38回宇宙環境利用シンポジウム  2024/01
• ビタミン代謝経路を標的とする膵がんの新規治療法の開発

  園下将大

  第46回日本分子生物学会年会  2023/12
• 個体表現型スクリーニングによるがん研究の加速  [Invited]

  園下将大

  徳島大学大学院医歯薬研究部 口腔生命科学分野セミナー  2023/11
• 個体レベルの網羅的遺伝学スクリーニングによる膵がんの新規治療標的の同定  [Not invited]

  園下将大

  第96回日本生化学会大会  2023/10
• Drosophila phenotypic screening identifies novel therapeutic candidates for cancer treatment  [Invited]

  Masahiro Sonoshita

  第82回 日本癌学会学術総会  2023/09
• 重力変動ががん細胞の薬物応答性に与える影響  [Invited]

  園下将大

  ヤマト科学主催ウェビナー  2023/09
• 個体モデルの連動による新規がん治療法の開発  [Invited]

  北海道大学遺伝子病制御研究所 生理学研究所 ジョイントシンポジウム  2023/09
• 表現型スクリーニングによる 新規膵がん治療薬の開発  [Invited]

  園下将大

  IGM京大医シンポジウム  2023/08
• 表現型スクリーニングによる新規膵がん治療薬の開発  [Invited]

  第4回SGHがん研究者ワークショップ  2023/07
• ショウジョウバエの個体表現型スクリーニングを活用した膵がん治療薬シーズの同定

  日本ケミカルバイオロジー学会 第17回年会  2023/05
• 表現型スクリーニングによる 新規膵がん治療薬の開発  [Invited]

  北海道がん若手研究者交流会  2023/03
• Whole-animal approaches using Drosophila to develop novel drugs for cancer treatment  [Invited]

  12th AACR-JCA Joint Conference  2022/12
• A Drosophila approach to tackle pancreatic cancer  [Invited]

  金沢大学 がん進展制御研究所 腫瘍遺伝学研究分野セミナー  2022/11
• 意志あるところに道あり  [Invited]

  ニューヨーク野口英世奨学金受賞者が語る留学の魅力  2022/11
• ハエと一緒にがん研究 －創薬から宇宙まで－  [Invited]

  群馬大学重粒子線医学研究センター生物セミナー  2022/11
• A Drosophila approach to tackle pancreatic cancer  [Not invited]

  JDRC15  2022/09
• 異分野融合による疾患研究の加速  [Invited]

  北海道大学病院消化器内科 第3回消化器内科セミナー  2022/08
• Science of FlyWorks  [Invited]

  FlyWorks Workshop 2022  2022/08
• Whole-animal approaches using Drosophila to develop novel therapeutic candidates for pancreatic cancer treatment  [Invited]

  The 7th JCA-AACR Special Joint Conference  2022/07
• Developing novel therapeutics for pancreatic cancer through whole-body phenotypic screening  [Not invited]

  第31回日本がん転移学会学術集会・総会  2022/07
• 個体表現型スクリーニングによる 新規膵がん治療薬の開発  [Not invited]

  第26回日本がん分子標的治療学会  2022/07
• ショウジョウバエの個体表現型スクリーニングによるがん治療薬開発の加速  [Invited]

  東京大学大学院新領域創成科学研究科講義  2022/06
• ハエと一緒にがん研究 -FLY me to drugs!-  [Invited]

  福井大学医学部講義  2022/06
• 個体表現型スクリーニングによるがん治療薬開発の加速  [Invited]

  福井大学大学院セミナー  2022/06
• Drosophila approaches to develop novel cancer drugs  [Invited]

  Serendipity Workshop 2022  2022/05
• 個体表現型スクリーニングによる新規がん治療薬開発の加速  [Invited]

  「感染・免疫・がん・炎症」全国共同研究拠点シンポジウム  2022/03
• Drosophila approaches to develop novel cancer drugs  [Invited]

  The TARA International Symposium  2022/03
• Determining therapeutic vulnerabilities in pancreatic cancer using a whole-animal platform  [Invited]

  第80回日本癌学会学術総会  2021/10
• ショウジョウバエを活用したがん治療薬の探索  [Invited]

  文部科学省科学研究費補助金新学術領域「細胞ダイバース」第６回領域会議  2021/09
• 個体表現型スクリーニングによる新規がん治療薬開発の加速

  第30回日本がん転移学会学術集会  2021/07
• A whole-animal platform to advance drug discovery  [Invited]

  Imperial College London Life Sciences Seminar  2021/06
• 個体表現型スクリーニングが加速する新規がん治療薬開発

  園下 将大

  第25回日本がん分子標的治療学会  2021/05
• 個体ケミカルバイオロジーが加速する高次生命現象の解明と創薬

  第43回日本分子生物学会年会  2020/12
• 個体を使用した新規がん治療薬の創出基盤  [Invited]

  園下将大

  第24回日本がん分子標的治療学会学術集会  2020/10
• Determining therapeutic vulnerabilities in pancreatic cancer using a whole-animal platform  [Not invited]

  Masahiro Sonoshita

  第79回日本癌学会学術総会  2020/10
• Determining therapeutic vulnerabilities in pancreatic cancer using a whole-animal platform  [Not invited]

  Masahiro Sonoshita

  第93回日本生化学会大会  2020/09
• 遺伝学に立脚した新規がん治療法の開発  [Not invited]

  園下将大

  第29回日本がん転移学会学術集会  2020/07
• 個体レベルの遺伝学に立脚した新規創薬手法  [Invited]

  第86回日本生化学会東北支部例会（紙上開催）  2020/05
• 膵臓がんの薬物治療抵抗性の克服に立脚した 新規治療法の開発  [Invited]

  公益財団法人MSD生命科学財団 研究助成４領域合同研究発表会  2020/02
• 個体モデルの連動によるがん研究の加速  [Invited]

  園下 将大

  北海道大学泌尿器科医局特別講演  2019/12
• 個体レベルの化学遺伝学による がん治療薬開発の加速  [Invited]

  園下 将大

  金沢大学がん進展制御研究所・北海道大学遺伝子病制御研究所ジョイントシンポジウム2019  2019/12
• A whole animal platform to generate novel kinase inhibitor drugs  [Invited]

  園下 将大

  第42回日本分子生物学会年会  2019/12
• 個体モデルを駆使したがん創薬研究  [Invited]

  園下将大

  熊本大学大学院生命科学研究部 第5回老化・健康長寿学セミナー  2019/12
• 動物個体を用いた新規創薬基盤  [Invited]

  園下 将大

  東京農工大学セミナー  2019/11
• 計算科学が加速する創薬研究  [Invited]

  園下 将大

  北海道大学共同利用・共同研究拠点アライアンス部局横断シンポジウム「計算科学が拓く汎分野研究」  2019/10
• A whole-animal platform for discovering novel anti-cancer drugs  [Invited]

  園下 将大

  第14回生命医科学研究所ネットワーク国際シンポジウム  2019/10
• A whole animal platform to generate novel kinase inhibitor drugs  [Invited]

  園下 将大

  第78回日本癌学会学術総会  2019/09
• がん個体モデルを使用した論理的創薬  [Not invited]

  園下 将大

  第92回日本生化学会大会  2019/09
• 動物個体を用いた新規創薬基盤  [Invited]

  園下 将大

  第9回生命科学阿波踊りシンポジウム  2019/08
• 個体を使用した新規がん治療薬の創出基盤  [Not invited]

  園下 将大

  第28回日本がん転移学会年会  2019/07
• A whole animal platform to develop novel anti-cancer drugs  [Invited]

  SONOSHITA Masahiro

  The 38th Sapporo International Cancer Symposium  2019/07
• 個体を用いた新規創薬基盤  [Not invited]

  園下 将大

  日本ケミカルバイオロジー学会 第14回年会  2019/06
• がん個体モデルを使用した新規がん治療薬の論理的創出基盤  [Not invited]

  園下 将大

  第23回日本がん分子標的治療学会学術集会  2019/06
• 動物個体を用いた新規創薬基盤  [Invited]

  園下 将大

  国立長寿医療研究センターセミナー  2019/04
• A whole animal platform to advance a clinical kinase inhibitor into new disease space  [Not invited]

  園下 将大

  60th Annual Drosophila Research Conference (Dallas, USA)  2019/03
• ハエが教えてくれる薬の作り方  [Invited]

  園下 将大

  北海道大学病院皮膚科特別講演会  2019/03
• がんに挑む  [Not invited]

  園下 将大

  北海道大学医学研究院新任教授特別セミナー  2019/02
• 動物個体を用いた新規創薬基盤  [Not invited]

  園下 将大

  第41回日本分子生物学会年会  2018/11
• A whole animal platform for anti-cancer drug discovery  [Not invited]

  SONOSHITA Masahiro

  第77回日本癌学会学術総会  2018/10
• A Drosophila platform to generate novel anticancer drug leads  [Not invited]

  SONOSHITA Masahiro

  13th Japanese Drosophila Research Conference  2018/09
• A whole animal platform for anti-cancer drug discovery  [Invited]

  SONOSHITA Masahiro

  第24回京都大学iCeMS国際シンポジウム  2018/09
• 個体モデルが加速するがん創薬研究  [Invited]

  園下 将大

  第442回東京慈恵会医科大学医学研究の基礎を語り合う集い  2018/09
• ハエが教えてくれる抗がん剤のつくり方  [Invited]

  園下 将大

  東京大学薬学部セミナー  2017/10
• 個体を用いたキナーゼ阻害剤の新規創薬基盤  [Not invited]

  園下 将大

  第76回日本癌学会学術総会  2017/09
• ハエが教えてくれる抗がん剤のつくり方  [Invited]

  園下 将大

  北海道大学遺伝病制御研究所セミナー  2017/07
• Understanding colorectal carcinogenesis  [Invited]

  SONOSHITA Masahiro

  第75回日本癌学会学術総会・受賞記念特別講演  2016/10
• A stepwise approach for balancing the polypharmacology of a clinical kinase inhibitor  [Invited]

  SONOSHITA Masahiro

  EMN Collaborative Conference on Drug Discovery (Melbourne, AUS)  2016/10
• ハエが起こす創薬革命  [Invited]

  園下 将大

  国立循環器病研究センターセミナー  2016/08
• ハエと一緒にお薬さがし ～よりよい抗がん剤を目指して～  [Invited]

  園下 将大

  JMSA NY Life Science Forum 2015  2015/04
• Understanding the mechanisms of colorectal carcinogenesis  [Invited]

  SONOSHITA Masahiro

  山形大学医学部セミナー  2014/07
• Stimulation of colon cancer metastasis by Notch signaling  [Invited]

  SONOSHITA Masahiro

  第23回日本がん転移学会学術集会・受賞記念特別講演  2014/07
• 転写因子Rbpjを介したNotchシグナルによる大腸がん転移の促進  [Invited]

  園下 将大

  第22回日本がん転移学会学術集会  2013/07
• Suppression of colon cancer metastasis by Aes through inhibition of notch signaling  [Invited]

  SONOSHITA Masahiro

  第71回日本癌学会学術総会  2012/09
• 大腸がんの悪性化メカニズム  [Invited]

  園下 将大

  第４回生命科学阿波踊りシンポジウム  2012/08
• AesはNotchシグナルを抑制して大腸がん転移を抑制する  [Invited]

  園下 将大

  金沢大学がん進展制御研究所セミナー  2012/02
• Stimulation of colon cancer metastasis by Notch signaling  [Invited]

  SONOSHITA Masahiro

  第70回日本癌学会学術総会  2011/10
• Suppression of colon cancer metastasis by Aes through inhibition of Notch Signaling  [Invited]

  SONOSHITA Masahiro

  第33回日本分子生物学会・第83回日本生化学会合同大会  2010/12
• AesはNotchシグナルを抑制することで大腸がんの転移を抑制する〜がん転移の予防・治療法確立を目指して〜  [Invited]

  園下 将大

  若手生命科学シンポジウム2009  2009/08

Association Memberships

• 宇宙生物科学会   日本がん転移学会   Japanese Medical Society of America   THE JAPANESE BIOCHEMICAL SOCIETY   日本分子生物学会   日本癌学会   THE HOKKAIDO MEDICAL SOCIETY   JAPANESE SOCIETY FOR CHEMICAL BIOLOGY   

Research Projects

• 個体差を活かした計測介入型の迅速スクリーニング計測基盤

  JST：戦略的創造研究推進事業（CREST）

  Date (from‐to) : 2023/10 -2029/03
• 遺伝子型に立脚した膵がん個別化医療開発基盤の創出

  日本学術振興会：科学研究費助成事業

  Date (from‐to) : 2023/04 -2027/03 

  Author : 園下 将大, 五十嵐 学, 小沼 剛, 市川 聡, 合田 圭介
• 遺伝子型に立脚した膵がん個別化医療開発基盤の創出

  日本学術振興会：科学研究費助成事業

  Date (from‐to) : 2023/04 -2027/03 

  Author : 園下 将大, 市川 聡, 五十嵐 学, 小沼 剛
• オートファジーを標的とする膵がんの新規治療法の開発

  日本学術振興会：科学研究費助成事業

  Date (from‐to) : 2023/04 -2026/03 

  Author : 大塩 貴子, 園下 将大, 野田 展生
• 代謝制御因子を標的とする新規膵がん治療法の開発

  AMED：令和5年度次世代がん医療加速化研究事業

  Date (from‐to) : 2023/10 -2026/03
• 重力変動が膵がん形質に与える影響の解明

  日本学術振興会：科学研究費助成事業

  Date (from‐to) : 2023/06 -2026/03 

  Author : 園下 将大
• Development of Oral Cancer Prevention Methods Based on Analysis of Oral Bacterial Flora and Inflammatory Cytokines in Saliva

  Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research

  Date (from‐to) : 2022/04 -2025/03 

  Author : 大賀 則孝, 北川 善政, 坂田 健一郎, 山村 凌大, 佐藤 淳, 園下 将大, 長谷部 晃
• 自律ハイスループット個体解析による膵がんの発生機序解析と新薬開発の変革

  公益財団法人村田学術振興財団：第39回研究助成

  Date (from‐to) : 2023/07 -2024/06
• がん治療薬の効果検証モデルハエによる深宇宙実験システムの確立

  宇宙航空研究開発機構（JAXA）：2023年度フロントローディング研究

  Date (from‐to) : 2023/10 -2024/03
• 個体表現型スクリーニングによる新規膵がん治療法の創出

  公益財団法人高松宮妃癌研究基金：令和４年度研究助成金

  Date (from‐to) : 2023/04 -2024/03
• 補酵素産生系を標的とする新規膵がん治療戦略の創出

  公益財団法人小林がん学術振興会：第17回研究助成金

  Date (from‐to) : 2023/04 -2024/03
• 個体表現型スクリーニングによる新規膵がん治療薬シーズの同定

  公益財団法人G-7奨学財団：令和５年度研究開発助成

  Date (from‐to) : 2023/04 -2024/03
• 個体表現型スクリーニングに立脚した新規治療薬探索基盤の確立

  科学技術振興機構：大学発新産業創出プログラム

  Date (from‐to) : 2021/11 -2024/03
• 強化学習駆動型のショウジョウバエ表現型スクリーニングによる抗腫瘍天然物の開発

  AMED：令和3年度創薬基盤推進研究事業

  Date (from‐to) : 2021/10 -2024/03
• 宇宙環境ががん治療薬の効果に与える影響の解明

  国立研究開発法人宇宙航空研究開発機構：2020年度「きぼう」利用フィジビリティスタディ

  Date (from‐to) : 2021/04 -2024/03
• 抗膵がん効果を持つ天然物の作用機序解明とその治療への応用

  公益財団法人小林財団：令和2年度研究助成

  Date (from‐to) : 2021/02 -2023/12
• リボフラビン経路を標的とした新規膵臓がん治療法の開発

  日本学術振興会：科学研究費助成事業

  Date (from‐to) : 2020/04 -2023/03 

  Author : 大塩 貴子, 園下 将大, 市川 聡, 藤井 清永
• 個体表現型スクリーニングによる新規膵がん治療薬シーズの同定

  公益財団法人G-7奨学財団：令和４年度研究開発助成

  Date (from‐to) : 2022/04 -2023/03
• 膵臓がんの頑健性の分子基盤の解明とその破壊による新規治療法の確立

  日本学術振興会：科学研究費補助金基盤研究（B）

  Date (from‐to) : 2020/04 -2023/03 

  Author : 園下 将大
• 副作用の論理的低減による新規膵臓がん薬物組み合わせ療法の開発

  AMED：令和２年度革新的がん医療実用化研究事業

  Date (from‐to) : 2020/04 -2023/03 

  Author : 園下 将大
• 個体表現型スクリーニングによる新規膵がん治療薬シーズの同定

  公益財団法人G-7奨学財団：令和３年度研究開発助成

  Date (from‐to) : 2021/04 -2022/03
• 膵がんの薬物治療感受性に影響を及ぼす腸内細菌叢の解明

  公益財団法人内藤記念科学振興財団：2020年度研究助成

  Date (from‐to) : 2020/12 -2022/03
• 新規膵がん遺伝子型モデル動物に立脚した膵がん個別化治療法の開発

  公益財団法人日立財団：2020年度倉田奨励金

  Date (from‐to) : 2021/03 -2022/02
• 個体レベルの網羅的な治療標的の同定を基盤とする新規膵がん治療法の開発

  公益財団法人薬理研究会：第22回研究助成

  Date (from‐to) : 2020/09 -2021/08 

  Author : 園下 将大
• 新規膵がん動物モデルに立脚した膵がん組み合わせ療法の開発

  AMED：令和２年度次世代がん医療創生研究事業

  Date (from‐to) : 2020/06 -2021/05 

  Author : 園下 将大
• 代謝反応を標的とする膵がん個別化医療の基盤開発

  公益財団法人秋山記念生命科学振興財団：2020年度研究助成

  Date (from‐to) : 2020/07 -2021/03 

  Author : 園下 将大
• 膵臓がんの発生にコーヒーが及ぼす影響の解明とコーヒーを活用した新規膵臓がん治療法

  一般社団法人全日本コーヒー協会：2020年度研究助成

  Date (from‐to) : 2020/04 -2021/03 

  Author : 園下 将大
• リボフラビン類縁体の創生に立脚した新規膵臓がん治療法の開発

  AMED：橋渡し研究戦略的推進プログラム2020年度シーズA支援

  Date (from‐to) : 2020/04 -2021/03 

  Author : 園下 将大
• 遺伝子変異の多様性が膵臓がん形質に及ぼす影響の解明と新規膵臓がん治療法の開発

  公益財団法人がん研究振興財団：2019年度がん研究助成

  Date (from‐to) : 2020/04 -2021/03 

  Author : 園下 将大
• 新規膵臓がんモデル動物の作出と解析による膵臓がん発生過程の解明と新規治療法の開発

  公益財団法人東京生化学研究会：2019年度研究助成

  Date (from‐to) : 2020/04 -2021/03 

  Author : 園下 将大
• 遺伝子変異の多様性が膵臓がん発生に及ぼす影響の解明と新規膵臓がん治療法の開発

  公益財団法人寿原記念財団：第34回研究助成

  Date (from‐to) : 2019/12 -2021/03 

  Author : 園下 将大
• 化学遺伝学的手法による新規認知症治療法の開発

  日本学術振興会：挑戦的研究（萌芽）

  Date (from‐to) : 2019/08 -2021/03 

  Author : 園下 将大
• 免疫チェックポイントを阻害する新規化合物の探索

  国立大学法人徳島大学：酵素学研究所「共同研究」

  Date (from‐to) : 2019/04 -2021/03 

  Author : 園下 将大
• 少数細胞が規定する膵臓がん発生過程の解明

  日本学術振興会：新学術領域研究「シンギュラリティ生物学」（公募）

  Date (from‐to) : 2019/04 -2021/03 

  Author : 園下 将大
• 膵臓がんの薬物治療抵抗性の克服に立脚した 新規治療法の開発

  公益財団法人MSD生命科学財団：2019年度がん領域スタートアップ研究助成

  Date (from‐to) : 2020/01 -2020/12 

  Author : 園下 将大
• 膵臓がん発生を促進する代謝経路とその調節機序の同定

  公益財団法人SGH財団：第31回SGHがん研究助成

  Date (from‐to) : 2020/01 -2020/12 

  Author : 園下 将大
• 膵臓がん発生を促進する代謝経路の同定とそれに立脚した新規治療法の開発

  公益財団法人鈴木謙三記念医科学応用研究財団：令和元年度研究助成

  Date (from‐to) : 2019/12 -2020/12 

  Author : 園下 将大
• 腸内細菌叢が膵臓がんの形成と薬物応答 に及ぼす影響の解明とそれに立脚した新 規膵臓がん治療戦略の確立

  公益財団法人持田記念医学薬学振興財団：2019年度研究助成

  Date (from‐to) : 2019/12 -2020/12 

  Author : 園下 将大
• 新規膵臓がんモデル動物を用いた薬物療法の開発

  公益財団法人日本対がん協会：2019年度リレー・フォー・ライフ・ジャパン（RFLJ）「プロジェクト未来」研究助成

  Date (from‐to) : 2019/11 -2020/11 

  Author : 園下 将大
• 膵臓がん発生を促進する代謝経路とその調節機序の同定

  公益財団法人金原一郎記念医学医療振興財団：2019年度基礎医学医療研究助成

  Date (from‐to) : 2019/11 -2020/10 

  Author : 園下 将大
• リボフラビン代謝経路による膵臓がん発生促進機序の解明と新規膵臓がん治療法の開発

  公益財団法人武田科学振興財団：2019年度生命科学研究助成

  Date (from‐to) : 2019/11 -2020/10 

  Author : 園下 将大
• ホットスポット変異型RAS群ががん発生を促進する機序の差異の解明と新規治療法の開発

  公益財団法人日本応用酵素協会：2019年度研究助成金

  Date (from‐to) : 2019/05 -2020/03 

  Author : 園下 将大
• 腸内細菌叢が膵臓がんの発生に与える影響の解明とそれに立脚した新規治療法の開発

  国立大学法人金沢大学：がん進展制御研究所「共同研究」

  Date (from‐to) : 2019/04 -2020/03 

  Author : 園下 将大
• 遺伝学に立脚した新規膵臓がん薬物組み合わせ療法の開発

  AMED：北海道大学病院臨床研究開発センター橋渡し研究戦略的推進プログラム2019年度シーズA支援

  Date (from‐to) : 2019/04 -2020/03 

  Author : 園下 将大
• 遺伝子変異の多様性が膵臓がんの発生に及ぼす影響の解析と新規膵臓がん治療法の開発

  公益財団法人高松宮妃癌研究基金：平成30年度研究助成金

  Date (from‐to) : 2019/02 -2020/03 

  Author : 園下 将大
• 60th Annual Drosophila Research Conference (Dallas, TX, USA)

  公益財団法人金原一郎記念医学医療振興財団：第33回研究交流助成金

  Date (from‐to) : 2019/03 

  Author : 園下 将大
• マウスモデルを用いた消化器がん転移の研究

  文部科学省：科学研究費補助金・基盤A

  Date (from‐to) : 2013 -2015 

  Author : 武藤 誠
• 微小環境に注目したがんの治療戦略開発

  文部科学省：次世代がん研究シーズ戦略的育成プログラム

  Date (from‐to) : 2011 -2015 

  Author : 武藤 誠
• 遺伝学的解析に立脚したNotchシグナル伝達経路による大腸がん悪性化メカニズムの解明と新規予防・治療標的の同定

  公益財団法人佐川がん研究振興財団：癌研究助成

  Date (from‐to) : 2012 -2012 

  Author : 園下 将大
• 大腸癌転移におけるNotchシグナル伝達経路の役割の解明

  文部科学省：科学研究費補助金・若手A

  Date (from‐to) : 2011 -2012 

  Author : 園下 将大
• マウスモデルを用いた消化器癌転移の研究

  文部科学省：科学研究費補助金・基盤S

  Date (from‐to) : 2009 -2012 

  Author : 武藤 誠
• 大腸癌の悪性化におけるNotchシグナル転写因子Rbpjの役割の解析

  一般財団法人藤原記念財団：研究奨励金

  Date (from‐to) : 2011 -2011 

  Author : 園下 将大
• Notchシグナルによる大腸癌の悪性化進展促進メカニズムの解明

  公益財団法人かなえ医薬振興財団：第40回研究助成金

  Date (from‐to) : 2011 -2011 

  Author : 園下 将大
• 上皮-間質相互作用の解析と分子標的治療

  文部科学省：特定領域研究

  Date (from‐to) : 2005 -2009 

  Author : 武藤 誠
• 腸癌転移に関わる新規遺伝子の同定、役割の解析、腸自然発癌・転移モデルマウスの作出

  日本学術振興会：特別研究員奨励費

  Date (from‐to) : 2005/04 -2008/03
• 腸管ポリープ形成におけるアラキドン酸代謝経路の役割の解析

  日本学術振興会：特別研究員奨励費

  Date (from‐to) : 2002/04 -2005/03

Industrial Property Rights

• 特許AU Patent 2021226119:Method for screening anticancer agent and combination drug of kinase inhibitors for treatment of pancreatic cancer  

  Masahiro Sonoshita, Sho Sekiya, Satoshi Hirano
• 特許CN Patent ZL2021800048738:Method for screening anticancer agent and combination drug of kinase inhibitors for treatment of pancreatic cancer  

  Masahiro Sonoshita, Sho Sekiya, Satoshi Hirano
• 特許US Patent 11,925,646:がんの治療又は予防剤、及びがんの治療又は予防のためのRF経路阻害剤とMEK阻害剤との組み合わせ  

  大塩貴子, 園下将大, 市川聡, 佐藤悠介, 藤井清永  国立大学法人北海道大学, 学校法人都築学園
• PCT/JP2023/023496:蛍光顕微鏡  2022年/07/06

  園下 将大, 平松光太郎, マクカン フィリップ チャールズ, ピーターソン ヨン ウォーカー, 菅野 寛志, 合田 圭介  国立大学法人北海道大学
• PCT/JP2021/007651:抗がん剤をスクリーニングする方法及び膵がんの治療のためのキナーゼ阻害剤の組み合わせ  2021年/03/01

  園下将大, 関谷翔, 平野聡  国立大学法人北海道大学
• 特許US Patent 10519113:KINASE INHIBITOR COMPOUNDS, COMPOSITIONS, AND METHODS OF TREATING CANCER    2019/12

  Arvin C. Dar, Ross L. Cagan, Alex P. Scopton, Masahiro Sonoshita
• 特許US Patent 9863953B2:METHODS FOR DETERMINING PROGNOSIS OF CANCER    2018/01/09

  武藤誠, 園下将大, 坂井義治, 河田健二, 板谷喜朗
• 特開2008-245522:蛍光性蛋白質の非蛍光性変異体を発現するトランスジェニック非ヒト哺乳動物  2008

  武藤誠, 園下将大

Social Contribution

• がんを制御可能な病気に！

  Date (from-to) : 2023/08/21

  Role : Advisor

  Event, Program, Title : 札幌市向陵中学校科学部 研究室見学
• 「はたらく細胞」から病気の仕組みを知ろう

  Date (from-to) : 2023/06/03

  Role : Advisor

  Event, Program, Title : 北海道大学遺伝子病制御研究所 一般公開
• なぜ、がんは出来るの？

  Date (from-to) : 2023/03/30

  Role : Lecturer

  Event, Program, Title : 北海道大学遺伝子病制御研究所 こども研究所
• エッセイ：あるがん研究者の振り返り

  Date (from-to) : 2021/09

  Role : Contribution

  Sponser, Organizer, Publisher  : 海外日本人研究者ネットワークUJA
• エッセイ：意志あるところに道あり

  Date (from-to) : 2020/07

  Role : Contribution

  Sponser, Organizer, Publisher  : 海外日本人研究者ネットワークUJA
• 職場訪問

  Date (from-to) : 2020/01

  Role : Advisor

  Sponser, Organizer, Publisher  : 北海道札幌北高校
• ハエと一緒にお薬さがし

  Date (from-to) : 2019/06

  Role : Lecturer

  Sponser, Organizer, Publisher  : 北海道大学遺伝子病制御研究所一般公開

  Event, Program, Title : サイエンストーク
• 職場訪問

  Date (from-to) : 2019/01

  Role : Advisor

  Sponser, Organizer, Publisher  : 北海道札幌北高校
• JMSA New York Life Science Forum Kids 2018

  Date (from-to) : 2018/05

  Role : Planner
• JMSA New York Life Science Forum 2018

  Date (from-to) : 2018/04

  Role : Planner
• JMSA New York Life Science Forum Kids 2017

  Date (from-to) : 2017/05

  Role : Planner
• JMSA New York Life Science Forum 2017

  Date (from-to) : 2017

  Role : Planner
• もっと知ってほしい、がんについての基礎知識

  Date (from-to) : 2016/11

  Role : Lecturer

  Sponser, Organizer, Publisher  : 日米ソーシャルサービス（JASSI）

  Event, Program, Title : 第５回ファンドレージングセミナー
• JMSA New York Life Science Forum Kids 2016

  Date (from-to) : 2016/05

  Role : Planner
• JMSA New York Life Science Forum 2016

  Date (from-to) : 2016/04

  Role : Planner
• ハエが教えてくれる抗がん剤の作り方

  Date (from-to) : 2015/10

  Role : Lecturer

  Sponser, Organizer, Publisher  : 日本クラブ／米国日本人医師会

  Event, Program, Title : 第37回ヘルスセミナー
• ハエが教えてくれる抗がん剤の作り方

  Date (from-to) : 2015/07

  Role : Lecturer

  Sponser, Organizer, Publisher  : JASS ニューヨーク日本人理系勉強会

Media Coverage

• 研究留学の技法2023 「留学後、日本のアカデミアで職を得るためにすべきこと」

  Date : 2023/10

  Writer: Myself

  Publisher, broadcasting station: 羊土社

  Program, newspaper magazine: 実験医学10月号

  Paper
• 梅村聡のあの人に会いたい

  Date : 2023/09/19

  Writer: Myself

  Program, newspaper magazine: Lohas Medical

  Paper
• 膵がんモデルハエで薬候補発見

  Date : 2023/08/15

  Program, newspaper magazine: 医薬経済

  医工連携 Paper
• 膵がん治療標的を発見

  Date : 2023/07/07

  Program, newspaper magazine: 科学新聞

  Paper
• 膵臓がん実験モデル ショウジョウバエで

  Date : 2019/12/02

  Publisher, broadcasting station: 日本経済新聞

  Paper
• 研究コラム（全６回）

  Date : 2019/06

  Publisher, broadcasting station: 北海道医療新聞

  Paper
• 個体を用いた新しいがん治療薬の創薬の基盤

  Date : 2018/02

  Publisher, broadcasting station: ライフサイエンス 新着論文レビュー

  Program, newspaper magazine: First Author's

  Internet
• がんとその治療薬

  Date : 2018/01

  Publisher, broadcasting station: ニューヨーク総合コミュニティサイトびびなび

  Program, newspaper magazine: 健康コラム

  Internet
• 一期一会が開いてくれる道

  Date : 2017/06

  Publisher, broadcasting station: 実験医学（羊土社）

  Program, newspaper magazine: ラボレポート

  Paper
• がん治療薬の課題と最新動向

  Date : 2017/02

  Publisher, broadcasting station: NYジャピオン

  Program, newspaper magazine: 心と体のメンテナンス

  Paper
• 大腸がん転移 タンパク質で予測 京大発見

  Date : 2014/12

  Publisher, broadcasting station: 日本経済新聞など6紙
• 大腸がん 転移抑制の遺伝子 京大が発見

  Date : 2011/01

  Publisher, broadcasting station: 報道ステーション（テレビ朝日）、日本経済新聞など6紙

Academic Contribution

• 薬の研究者に聞く、薬がきく仕組みと薬の選び方

  Date (from-to) :2016/02

  Role: Panel chair etc

  Organizer, responsible person: SHARE乳がん患者サポートプログラム
• JMSA New York Life Science Forum 2015

  Date (from-to) :2015/04

  Role: Planning etc