Education 【 display / non-display 】

Education 【 display / non-display 】

• 2009

  -

  2013

  Sapporo Medical University   Graduate School of Medicine   外科腫瘍学・消化器外科治療学  

• 1999

  -

  2005

  Sapporo Medical University   医学部   医学科  

Degree 【 display / non-display 】

Degree 【 display / non-display 】

• 2013.03   Sapporo Medical University   M.D. and Ph.D.

Research Experience 【 display / non-display 】

Research Experience 【 display / non-display 】

• 2025.07

  -

  Now

  Sapporo Medical University   Department of Pathology   Assistant Professor/Lecturer

• 2020.02

  -

  2025.06

  Sapporo Medical University   Department of Pathology   Assistant professor

• 2019.04

  -

  2020.01

  Sapporo Medical University   Department of Surgery, Surcial Oncology and Science   Clinical Associate

• 2018.12

  -

  2019.03

  Sapporo Medical University   Department of Surgery, Surgical Oncology and Science   Clinical Fellow

• 2016.09

  -

  2018.11

  Heidelberg University Hospital   General, Visceral and Transplantation Surgery, Section Surgical Research   Visiting Research Scholar

display all >>

Professional Memberships 【 display / non-display 】

Professional Memberships 【 display / non-display 】

• 2023

  -

  Now

  The Japanese Society for Clinical Molecular Morphology

• 　

  　

  　

  日本消化器外科学会

• 　

  　

  　

  日本病理学会

• 　

  　

  　

  日本外科学会

• 　

  　

  　

  日本癌学会

display all >>

Research Areas 【 display / non-display 】

Research Areas 【 display / non-display 】

• Life sciences   Digestive surgery  

• Life sciences   Tumor diagnostics and therapeutics  

• Life sciences   Experimental pathology  

• Life sciences   General surgery, pediatric surgery  

• Life sciences   Molecular biology  

Affiliation 【 display / non-display 】

Affiliation 【 display / non-display 】

• Sapporo Medical University   Department of Pathology   Assistant Professor/Lecturer  

Papers 【 display / non-display 】

Papers 【 display / non-display 】

• The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation

  Daisuke Kyuno, Hinae Asano, Reona Okumura, Kumi Takasawa, Akira Takasawa, Takumi Konno, Yuna Nakamori, Kazufumi Magara, Yusuke Ono, Masafumi Imamura, Yasutoshi Kimura, Takashi Kojima, Makoto Osanai

  Cancers    2025.04

  DOI

• Concordance of claudin-18.2 expression in biopsy, resection, and recurrent specimens: implications for zolbetuximab therapy in pancreatic ductal adenocarcinoma

  Daisuke Kyuno, Kazuhiko Yanazume, Akira Saito, Yusuke Ono, Tatsuya Ito, Masafumi Imamura, Makoto Osanai

     2025.04

  DOI

• Multilayered proteomics reveals that JAM-A promotes breast cancer progression via regulation of amino acid transporter LAT1.

  Kazufumi Magara, Akira Takasawa, Kumi Takasawa, Tomoyuki Aoyama, Misaki Ota, Daisuke Kyuno, Yusuke Ono, Taro Murakami, Soh Yamamoto, Yuna Nakamori, Naoya Nakahashi, Goro Kutomi, Ichiro Takemasa, Tadashi Hasegawa, Makoto Osanai

  Cancer science    2024.06  [International journal]

  　View Summary

  Recent studies have shown that transmembrane-type tight junction proteins are upregulated in various cancers compared with their levels in normal tissues and are involved in cancer progression, suggesting that they are potential therapeutic targets. Here, we demonstrated the expression profile and a novel role of junctional adhesion molecule-A (JAM-A) in breast cancer. Immunohistochemistry of surgical specimens showed that JAM-A was highly expressed from carcinoma in situ lesions, as in other adenocarcinomas, with higher expression in invasive carcinomas. High expression of JAM-A contributed to malignant aspects such as lymph node metastasis and lymphatic involvement positivity. In breast cancer cells, JAM-A expression status affects malignant potentials including proliferation and migration. Multilayered proteomics revealed that JAM-A interacts with the amino acid transporter LAT1 in breast cancer cells. JAM-A regulates the expression of LAT1 and interacts with it on the whole cell membrane, leading to enhanced amino acid uptake to promote tumor growth. Double high expression of JAM-A and LAT1 predicts poor prognosis in patients with breast cancer. Of note, an antibody against an extracellular domain of JAM-A suppressed the proliferation of breast cancer cells. Our findings indicate the possibility of JAM-A-targeted therapy ideally combined with LAT1-targeted therapy as a new therapeutic strategy against breast cancer.

  DOI PubMed

• Vitamin D-metabolizing enzyme CYP24A1 affects oncogenic behaviors of oral squamous cell carcinoma and its prognostic implication.

  Yuna Nakamori, Akira Takasawa, Kumi Takasawa, Daisuke Kyuno, Yusuke Ono, Kazufumi Magara, Naoya Nakahashi, Shohei Sekiguchi, Kei Tsuchihashi, Akihiro Miyazaki, Makoto Osanai

  Medical molecular morphology    2024.05  [Domestic journal]

  　View Summary

  Vitamin D is an essential molecule for cellular homeostasis, playing a critical role in cell fate decisions including cell proliferation, differentiation, and viability. Accumulating evidence has revealed that expression of the vitamin D-metabolizing enzyme CYP24A1 is dysregulated in different types of human malignancy. CYP24A1 has been shown to be involved in the oncogenic property of a variety of carcinoma cells. However, the pathological relevance of CYP24A1 expression level in human oral malignancy remains to be clarified. In the present study, suppression of CYP24A1 expression in oral squamous cell carcinoma (OSCC) cells increased cell proliferation, invasive activity, colony formation efficacy, and tumor growth in vivo. In addition, knockout of CYP24A1 expression inhibited cell death induced by two different types of anticancer drugs, i.e., fluorouracil and cisplatin. Gene clustering by RNA-sequence analysis revealed that several signaling molecules associated with MYC are involved in CYP24A1-mediated oncogenic behaviors. Furthermore, decreased expression level of CYP24A1 was observed in 124/204 cases (61%) of OSCC and was shown to be associated with short relapse-free and overall survival periods. The results showed that a low expression level of CYP24A1 promotes the oncogenic activity of OSCC and is significantly associated with poor prognosis in patients with this malignancy.

  DOI PubMed

• A case report of carcinoma of the papilla of Vater associated with a hyperplasia-dysplasia-carcinoma sequence by pancreaticobiliary maljunction.

  Takahiro Korai, Yasutoshi Kimura, Kazunori Watanabe, Siew-Kee Low, Masafumi Imamura, Minoru Nagayama, Kazuharu Kukita, Takeshi Murakami, Toru Kato, Yuta Kondo, Daisuke Kyuno, Taro Sugawara, Ayako Murota, Yujiro Kawakami, Yoshiharu Masaki, Hiroshi Nakase, Ichiro Takemasa

  World journal of surgical oncology   22 ( 1 ) 63 - 63  2024.02  [International journal]

  　View Summary

  BACKGROUND: Pancreaticobiliary maljunction (PBM) is a known risk factor for biliary tract cancer. However, its association with carcinoma of the papilla of Vater (PVca) remains unknown. We report a case with PVca that was thought to be caused by the hyperplasia-dysplasia-carcinoma sequence, which is considered a mechanism underlying PBM-induced biliary tract cancer. CASE PRESENTATION: A 70-year-old woman presented with white stool and had a history of cholecystectomy for the diagnosis of a non-dilated biliary tract with PBM. Esophagogastroduodenoscopy revealed a tumor in the papilla of Vater, and PVca was histologically proven by biopsy. We finally diagnosed her with PVca concurrent with non-biliary dilated PBM (cT1aN0M0, cStage IA, according to the Union for International Cancer Control, 8th edition), and subsequently performed subtotal stomach-preserving pancreaticoduodenectomy. Pathological findings of the resected specimen revealed no adenomas and dysplastic and hyperplastic mucosae in the common channel slightly upstream of the main tumor, suggesting a PBM related carcinogenic pathway with hyperplasia-dysplasia-carcinoma sequence. Immunostaining revealed positivity for CEA. CK7 positivity, CK20 negativity, and MUC2 negativity indicated that this PVca was of the pancreatobiliary type. Genetic mutations were exclusively detected in tumors and not in normal tissues, and bile ducts from formalin-fixed paraffin-embedded samples included mutated-ERBB2 (Mutant allele frequency, 81.95%). Moreover, of the cell-free deoxyribonucleic acid (cfDNA) extracted from liquid biopsy mutated-ERBB2 was considered the circulating-tumor deoxyribonucleic acid (ctDNA) of this tumor. CONCLUSIONS: Herein, we report the first case of PVca with PBM potentially caused by a "hyperplasia-dysplasia-carcinoma sequence" detected using immunostaining and next-generation sequencing. Careful follow-up is required if pancreaticobiliary reflux persists, considering the possible development of PVca.

  DOI PubMed

display all >>

Books and Other Publications 【 display / non-display 】

Books and Other Publications 【 display / non-display 】

• インフォームドコンセントのための図説シリーズ 膵がん 改訂3版

  ( Part： Contributor, 術後のフォローアップの方法)

Misc 【 display / non-display 】

Misc 【 display / non-display 】

• 膵癌患者の予後と癌進展におけるJAM-Aの役割(Junctional Adhesion Molecule-A may play a role in the progression of pancreatic cancer)

  及能 大輔, 高澤 啓, 高澤 久美, 真柄 和史, 小山内 誠

  日本癌学会総会記事 ( (一社)日本癌学会 )  81回   J - 2053  2022.09

• 肺多形癌における癌免疫微小環境の組織学的解析(A Histological evaluation of immune microenvironment in pulmonary pleomorphic carcinoma)

  多田 聡法, 廣橋 良彦, 高澤 久美, 真柄 和史, 及能 大輔, 長谷川 匡, 小山内 誠, 高澤 啓, 高澤 久美

  日本癌学会総会記事 ( (一社)日本癌学会 )  83回   P - 1176  2024.09

• 膵癌におけるClaudin 1の機能と予後に与える影響(The Role of Claudin 1 in Pancreatic Cancer Progression: A Study of Expression and Prognosis)

  及能 大輔, 浅野 日南英, 奥村 礼央菜, 真柄 和史, 小野 佑輔, 今村 将史, 高澤 久美, 竹政 伊知朗, 高澤 啓, 小山内 誠

  日本癌学会総会記事 ( (一社)日本癌学会 )  83回   J - 2051  2024.09

• MPNSTで異常高発現するPVRはがん悪性化に寄与し,治療標的となりうる

  中橋 尚也, 高澤 啓, 江森 誠人, 高澤 久美, 真柄 和史, 小野 佑輔, 及能 大輔, 杉田 真太朗, 長谷川 匡, 小山内 誠, 寺本 篤史

  日本整形外科学会雑誌 ( (公社)日本整形外科学会 )  98 ( 8 ) S1750 - S1750  2024.09

• 膵癌がんで高発現する解糖系酵素ALDOAはがん悪性化に関与する(Glycolytic enzyme ALDOA, highly expressed in pancreatic cancer, is involved in malignant potentials)

  高澤 啓, 高澤 久美, 真柄 和史, 及能 大輔, 後藤 正憲, 田中 宏樹, 藤井 裕美子, 小山内 誠

  日本癌学会総会記事 ( (一社)日本癌学会 )  83回   P - 2285  2024.09

display all >>

Awards 【 display / non-display 】

Awards 【 display / non-display 】

• Sapporo Medical University Grants for Programs promoting Academic advancements

  2025.06   Sapporo Medical University   膵癌の進展を促進するタイト結合分子の同定とその機序の解明

• Research grant

  2024   THE SUHARA MEMPRIAL FOUNDATION   膵癌の予後不良サブタイプにおけるタイト結合分子の機能解析と新規治療法を開発するための基盤的研究

• 膵臓病研究奨励賞

  2022   日本膵臓病研究財団   タイト結合分子により促進される膵癌の進展機序の解明

• Young investigator award

  2019.11   Japanese digestive disease week   Exosomes transfer information of cancer cells; reprogramming of nonmetastasizing tumor cells and therapeutic efficacy

  Winner： Daisuke Kyuno

• Young Investigator Award

  2015   国際外科学会日本部会  

  Winner： 及能大輔

display all >>

Research Projects 【 display / non-display 】

Research Projects 【 display / non-display 】

• 膵癌の予後不良サブタイプにおけるタイト結合分子の機能解析と新規治療法を開発するための基盤的研究

  Project Year :

  2025

  -

  2026

   

  Authorship： Principal investigator

• 膵癌の予後不良群に過剰発現するタイト結合分子が促進する癌進展機構の解明

  基盤研究(C)

  Project Year :

  2024.04

  -

  2027.03

   

  及能大輔、今村将史、木村康利、髙澤啓

  Authorship： Principal investigator

• 遺伝子プロファイルとctDNAに基づくサブタイプ別膵癌精密医療実装のための探索的研究

  基盤研究(C)

  Project Year :

  2023.04

  -

  2026.03

   

  木村 康利, 今村 将史, 竹政 伊知朗, 村上 武志, 久木田 和晴, 及能 大輔

• Development of a novel biomarker for postoperative early recurrence of pancreatic cancer by sequential analysis of exosomal miRNAs

  Grant-in-Aid for Scientific Research (C)

  Project Year :

  2023.04

  -

  2026.03

   

  今村 将史, 木村 康利, 永山 稔, 及能 大輔, 久木田 和晴, 村上 武志, 竹政 伊知朗

• イムノヒストグラムを用いた直腸癌に対する術前化学療法の新規治療効果予測法の開発

  基盤研究(C)

  Project Year :

  2022.04

  -

  2025.03

   

  奥谷 浩一, 秋月 恵美, 廣橋 良彦, 竹政 伊知朗, 佐藤 雄, 石井 雅之, 浜部 敦史, 沖田 憲司, 及能 大輔

display all >>