髙濱　隆幸（タカハマ　タカユキ）

医学科医学部講師

Last Updated :2026/02/04

■教員コメント

コメント

がんの診断、治療。特にがんゲノム医療。

報道関連出演・掲載一覧

＜報道関連出演・掲載一覧＞ ●2024/1/27 　NHK Eテレ「ETV特集：肺がんサバイバー第二弾」 　肺がんについて ●2024/1/11 　メディカル＆エスト 　遺伝子検査の調査結果について ●2023/12/16 　NHK「NHK NEWS おはよう日本」、NHK「ウイークエンド関西」 　肺がんの遺伝子検査の普及状況について ●2018/7/20 　化学工業日報 　血液検査による肺がん遺伝子変異の単独診断の有効性を実証

■研究者基本情報

学位

  • 博士（医学）（2018年03月 近畿大学）

ホームページURL

J-Global ID

現在の研究分野（キーワード）

がんの診断、治療。特にがんゲノム医療。

研究分野

  • ライフサイエンス / 腫瘍診断、治療学

■経歴

経歴

  • 2022年04月 - 現在  近畿大学医学部内科学腫瘍内科部門・近畿大学病院ゲノム医療センター兼担
  • 2021年04月 - 2022年03月  近畿大学医学部内科学腫瘍内科部門・近畿大学病院ゲノム医療センター兼担
  • 2020年04月 - 2021年03月  近畿大学奈良病院
  • 2019年04月 - 2020年03月  近畿大学奈良病院
  • 2015年04月 - 2019年03月  近畿大学医学部内科学教室腫瘍内科部門
  • 2013年04月 - 2015年03月  近畿大学大学病院
  • 2012年04月 - 2013年03月  香川大学内分泌代謝血液免疫呼吸器内科学
  • 2011年04月 - 2012年03月  香川県立中央病院呼吸器内科
  • 2009年04月 - 2011年03月  香川県立中央病院

学歴

  • 2015年04月 - 2018年03月   近畿大学   医学部   大学院医学研究科
  • 2003年04月 - 2009年03月   香川大学   医学部   医学科

委員歴

  • 2024年11月 - 現在   日本肺癌学会   広報委員会
  • 2024年11月 - 現在   日本肺癌学会   肺がん医療向上委員会
  • 2024年11月 - 現在   日本肺癌学会   ペイシャント・アドボカシー小委員会 副委員長
  • 2024年11月 - 現在   日本肺癌学会   データベース・利用・審査小委員会
  • 2024年02月 - 現在   日本臨床腫瘍学会   専門医部会
  • 2023年12月 - 現在   IASLC   国際集学的診療基準委員会
  • 2023年05月 - 現在   西日本がん研究機構   教育広報委員会副委員長
  • 2022年04月 - 現在   日本呼吸器学会   成人肺炎診療ガイドライン2022作成委員会SR委員
  • 2019年07月 - 2024年11月   日本肺癌学会   ガイドライン検討委員会 患者向けガイドライン小委員会
  • 2022年03月 - 2024年02月   日本臨床腫瘍学会   指導医審査部会部会員
  • 2017年07月 - 2023年03月   厚生労働省委託事業がんのゲノム医療従事者研修事業   ゲノム医療従事者研修委員会

■研究活動情報

受賞

  • 2020年09月 奈良県医師会 奈良県医師会学術奨励賞
  • 2017年05月 西日本がん研究機構 有吉・福岡賞

論文

  • Satomi Watanabe; Koji Haratani; Tomohiro Nakayama; Takayuki Takahama; Tsutomu Iwasa; Masayuki Takeda; Hidetoshi Hayashi
    The oncologist 2025年07月 
    BACKGROUND: Extramammary Paget's disease (EMPD) is a rare malignancy without established systemic therapy. EMPD shares molecular features with breast cancer, such as human epidermal growth factor receptor 2 (HER2) and hormone receptor (HR) expression, but their clinical relevance remains unclear. MATERIALS AND METHODS: Tumors from 20 metastatic invasive EMPD cases were analyzed for molecular and biological features. Genomic features, transcriptomic profiles, and HER2 and HR expression status were investigated using immunohistochemistry, fluorescence in situ hybridization, and targeted-genome next-generation sequencing and nCounter BC360 panels. Metastatic breast cancer samples were used as a comparison to clarify metastatic EMPD's clinical relevance. RESULTS: Estrogen receptor expression was observed in 45% of EMPD tumors, while only 10% expressed progesterone receptor. HER2 was overexpressed in 30% of cases, and HER2-directed therapies were durably effective. Among 8 patients with NGS data, 63% (5/8) harbored oncogenic ERBB2 alterations independent of HER2 expression. BC360 profiling revealed biological differences between EMPD and breast cancer, particularly poor biological compatibility for HR-positive tumors. Immune profiling showed that a subset of EMPD tumors exhibited CD8+ T-cell signatures and PD-1/PD-L1 gene expression comparable to triple-negative breast cancer. The median overall survival was 22.1 months (95% CI, 12.0-42.2), with 16 patients (80%) treated with systemic therapy including anti-HER2 therapy, hormonal therapy, or cytotoxic therapies based on their molecular features. CONCLUSIONS: This study highlights the unique molecular and biological features of metastatic EMPD, emphasizing the need for tailored treatment approaches. This information should be used to guide future clinical strategies for metastatic EMPD.
  • Luis G Paz-Ares; Oscar Juan-Vidal; Giannis S Mountzios; Enriqueta Felip; Niels Reinmuth; Filippo de Marinis; Nicolas Girard; Vipul M Patel; Takayuki Takahama; Scott P Owen; Douglas M Reznick; Firas B Badin; Irfan Cicin; Sabeen Mekan; Riddhi Patel; Eric Zhang; Divyadeep Karumanchi; Marina Chiara Garassino
    Future oncology (London, England) 1 - 13 2025年05月
  • Shoji Mochizuki; Ryuichi Ohta; Yuki Konya; Kosuke Isomoto; Takayuki Takahama; Junko Tanizaki; Hidetoshi Hayashi
    Cureus 17 3 e81376  2025年03月 
    A 70-year-old male patient presented with fever, polyarthritis, systemic muscle weakness and pain, and skin rash, initially suspected to be an autoimmune disorder. Imaging revealed right supraclavicular and paratracheal lymphadenopathy, and a right supraclavicular lymph node biopsy confirmed squamous cell carcinoma. Still, the primary site remained unidentified, leading to a diagnosis of cancer of unknown primary origin (CUP). Laboratory tests showed no positive autoantibodies such as anti-Jo-1, anti-ribonucleoprotein (RNP), anti-Smith (Sm), and anti-SS-A antibodies, and a skin biopsy of the back indicated panniculitis with neutrophilic infiltration. Given the absence of infectious or autoimmune causes, the symptoms were attributed to paraneoplastic syndrome (PNS) associated with CUP, mimicking dermatomyositis and remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome. Treatment with prednisolone (15 mg/day) led to the rapid resolution of joint pain, rash, and fever. Chemotherapy with carboplatin and paclitaxel for CUP was initiated with minimal adverse effects, allowing for continued outpatient management. This case highlights the importance of considering PNS when collagen disease-like symptoms are present in malignancy, particularly in CUP. Early recognition and corticosteroid therapy can improve performance status, enabling timely cancer treatment. Identifying atypical PNS presentations in CUP remains challenging, but a multidisciplinary approach can aid in diagnosis and management.
  • Naoki Shiraishi; Takayuki Takahama; Kazuko Sakai; Kaoru Tanaka; Yuzuki Nakagawa; Hiroaki Kanemura; Tomohiro Nakayama; Yusuke Kawanaka; Takashi Kurosaki; Shinichiro Suzuki; Tsutomu Iwasa; Junko Tanizaki; Chiaki Inagaki; Kimio Yonesaka; Kazuya Fukuoka; Tetsuya Mitsudomi; Kazuto Nishio; Hidetoshi Hayashi; Kazuhiko Nakagawa
    Thoracic Cancer 16 3 e70007  2025年02月 [査読有り]
     
    BACKGROUND: Recognizing rare molecular variants of driver mutations poses a challenge in precision oncology, particularly for treatment of non-small cell lung cancer (NSCLC). In this study, we aimed to determine whether Oncomine Dx Target Test Multi-CDx System (ODxTT), the most widely used genetic test for NSCLC in Japan, potentially overlooks druggable EGFR mutations. MATERIALS AND METHODS: Among 418 patients who underwent molecular testing using ODxTT at our hospital, 267 were diagnosed with adenocarcinoma. No mutations were reported in 82 of these cases. For these 82 cases, we searched for EGFR mutations in exons 18-21 by examining the binary alignment map file. Once a mutation was identified, its pathological significance was evaluated using the ClinVar database to determine whether ODxTT had overlooked any actionable EGFR mutations. RESULTS: Mutations in EGFR exons 19 and 18 were identified in six and four cases, respectively. Three, six, and none of these variants were detectable using the Cobas EGFR Mutation Test v2, Lung Cancer Compact Panel, and Amoy Dx, respectively. Of the 10 patients, five were subsequently treated with EGFR TKI; three showed partial response, one had stable disease, and one had progressive disease. CONCLUSIONS: ODxTT failed to identify 10 actionable EGFR mutations, accounting for 12.2% (10/82) of the cases initially reported as not carrying actionable mutations. Therefore, comprehensive genomic profiling should be actively performed early in cases with high clinical suspicion of EGFR mutations.
  • Yoshihiko Fujita; Hiromichi Matsuoka; Yasutaka Chiba; Junji Tsurutani; Takeshi Yoshida; Kiyohiro Sakai; Miki Nakura; Ryo Sakamoto; Chihiro Makimura; Yoichi Ohtake; Kaoru Tanaka; Hidetoshi Hayashi; Takayuki Takahama; Junko Tanizaki; Atsuko Koyama; Kazuto Nishio; Kazuhiko Nakagawa
    Molecular and clinical oncology 22 2 14 - 14 2025年02月 
    We have been exploring biomarkers that could help physicians select the appropriate opioid for individualized treatment of cancer pain. Recently, we identified a single nucleotide polymorphism (SNP) of CCL11 (rs17809012) as one such biomarker that was significantly associated with the analgesic effect of morphine. The current study measured the plasma concentrations of chemokines/cytokines in pre-treatment plasma samples of a total of 138 patients who were randomized to receive morphine (n=70) or oxycodone (n=68). Based on the results, one cytokine, IL-16, was identified whose plasma concentrations showed a clear bias between patients with cancer pain who responded well and responded poorly to oxycodone. A genotypic analysis also identified a SNP of the IL-16 gene (rs4778889) as being significantly associated with the analgesic effect of oxycodone. Whether both of the SNPs identified as being significant (CCL11 rs17809012 and IL-16 rs4778889) could be used in combination to accurately predict which opioid might be the most suitable to provide pain relief in patients with cancer was assessed. Morphine tended to provide superior analgesic effect over oxycodone in patients with the IL-16 rs4778889 TT genotype and the CCL11 rs17809012 AG/GG genotype (n=45), while a trend towards a greater analgesic effect of oxycodone was observed in patients with other genotype combinations of these SNPs (n=93) (P=0.0012 for the interaction), suggesting that the IL-16 rs4778889 and CCL11 rs17809012 SNPs could serve as a potential dual-biomarker combination for personalized analgesic therapy in patients with cancer pain.
  • Akiho Nagayama; Chiho Miyagawa; Yoko Kashima; Mamiko Ohta; Tomoyuki Otani; Takashi Kurosaki; Kohsuke Isomoto; Chiaki Inagaki; Takayuki Takahama; Kimio Yonesaka; Hidetoshi Hayashi; Kazuko Sakai; Kazuto Nishio; Kazuhiko Nakagawa; Noriomi Matsumura
    International Cancer Conference Journal 14 2 85 - 90 2024年12月 [査読有り]
     
    UNLABELLED: A 69-year-old multiparous postmenopausal woman had undergone bilateral total hip arthroplasty 17 years ago. Computed tomography showed a mature teratoma of 10 cm in the pelvis. Subsequently, she presented with symptoms of hoarseness and weight loss, along with evidence of malignant transformation of the same tumor in the pelvis and multiple enlarged lymph nodes. Bilateral adnexectomy was performed via laparotomy, yet peritoneal dissemination persisted. The ovarian tumor's histopathological diagnosis was mature teratoma with squamous cell carcinoma. Additionally, the mediastinal lymph nodes biopsy revealed poorly differentiated carcinoma. Comprehensive genomic profiling testing of the ovarian tumor showed pathogenic variants of TP53 and PTEN, a high tumor mutational burden, homologous recombination deficiency and the absence of human papilloma virus. The similar genomic testing of the mediastinal tumor revealed three variants of uncertain significance that were common to the ovarian tumor. However, no variants of TP53 or PTEN were identified. Following surgery, she demonstrated a partial response to six cycles of conventional paclitaxel and carboplatin. She then received maintenance treatment with niraparib; however, disease progression subsequently occurred. The patient was treated with pembrolizumab and is currently receiving treatment with a partial response. Previous reports have demonstrated the efficacy of immune checkpoint inhibitors in 5 out of 6 cases of malignant transformation of mature teratomas, and this treatment appears to be a promising strategy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13691-024-00740-z.
  • Masayuki Takeda; Masahide Ota; Eiji Iwama; Shunichi Sugawara; Takehito Shukuya; Shigeki Umemura; Hiroshi Tanaka; Masahide Oki; Takayuki Takahama; Takeshi Masuda; Naoyuki Nogami; Mototsugu Shimokawa
    Clinical lung cancer 26 3 e232-e235  2024年12月 
    BACKGROUND: MET gene exon 14 skipping was identified as a potential driver mutation that occurs in approximately 3%-4% of patients with nonsmall cell lung cancer (NSCLC), typically in the absence of other driver mutations. Capmatinib and tepotinib were the first MET- tyrosine kinase inhibitors (MET-TKIs) approved by the FDA and PMDA, specifically for patients with metastatic NSCLC. Several studies have reported acquired resistance after MET-TKI treatment for MET mutation-positive NSCLC. Sequencing of the MET kinase region of resistant cell lines revealed secondary mutations at residues D1228 and Y1230 that were sensitive to type II MET-TKIs, such as cabozantinib. This suggested that sequential administration of other MET-TKIs may overcome the development of secondary mutations after acquired resistance in MET exon 14 mutation-positive NSCLC. METHODS: We designed the single arm phase II study CAPTURE Trial to assess the efficacy of cabozantinib in patients with advanced/metastatic NSCLC with activating MET exon 14 alterations who developed acquired resistance to tepotinib or capmatinib, as well as after 2 prior chemotherapy regimens that included platinum and docetaxel. The primary endpoint was objective response rate by independent review committees. The sample size (n = 30) is calculated by assuming a threshold response rate of 5% and an expected response rate of 25%. Recruitment began in August 2024. RESULTS: This ongoing study aimed to evaluate the safety and efficacy of cabozantinib after acquired resistance to tepotinib or capmatinib.
  • Tomohiro Nakayama; Takayuki Takahama; Yasutaka Chiba; Naoki Shiraishi; Hisato Kawakami; Kimio Yonesaka; Kazuhiko Nakagawa; Hidetoshi Hayashi
    Journal for ImmunoTherapy of Cancer 12 12 2024年12月 [査読有り]
     
    BACKGROUND: Amplification of the programmed cell death-ligand 1 gene (CD274) is highly prevalent and associated with a high response rate to immune checkpoint inhibitors (ICIs) in lymphomas, and is also a potential biomarker for ICI treatment of solid tumors. However, the efficacy of ICIs for solid tumors with CD274 amplification identified by comprehensive genomic profiling (CGP) has been unclear. We here examined ICI efficacy for solid tumors with CD274 amplification identified by CGP in a national database. METHODS: We retrospectively analyzed data from the Center for Cancer Genomics and Advanced Therapeutics database containing 60,155 CGP test results for individuals with solid tumors. Only clinical data from patients treated with ICIs alone (not those undergoing concomitant therapy with molecularly targeted or cytotoxic chemotherapeutic agents) were evaluated. We matched 48 patients in the CD274 amplification-positive group with 170 patients in the CD274 amplification-negative group in a 1:4 ratio based on tumor type, histology, treatment, and age. Overall survival (OS), time to next treatment (TTNT), and response rate were evaluated as treatment outcomes in the two groups. RESULTS: OS was similar in the CD274-amplified and matched CD274-non-amplified groups (median of 22.1 vs 26.3 months, respectively; HR of 0.92 with a 95% CI of 0.55 to 1.54; p=0.075). TTNT tended to be longer in the CD274-amplified group than in the matched CD274-non-amplified group (median of 16.5 vs 14.0 months; HR of 0.63 with a 95% CI of 0.37 to 1.08; p=0.091). The objective response rate was 33.3% and 18.4% (difference of 14.9%, with a 95% CI of -0.2% to 31.6%), and the disease control rate was 63.9% and 41.1% (difference of 22.8%, with a 95% CI of 5.1% to 40.4%), in the CD274-amplified and matched CD274-non-amplified groups, respectively. CONCLUSIONS: The number of patients with solid tumors positive for CD274 amplification in this analysis is the largest to date, and our results suggest that such gene amplification may be associated with the outcome of ICI treatment in such individuals. CD274 amplification identified by CGP may therefore be a predictor of ICI efficacy for solid tumors. TRIAL REGISTRATION NUMBER: UMIN000029779.
  • Satoshi Ikeda; Kazuo Hasegawa; Kenta Kachi; Akihiro Yanagisawa; Sachiko Kawakami; Shinsuke Hamasaki; Sachiko Watanabe; Aki Yoshikawa; Takayuki Takahama; Kazuhiko Nakagawa
    Cancer medicine 13 21 e70375  2024年11月 
    BACKGROUND: Previous reports indicated still low implementation rates of multigene testing for advanced non-small cell lung cancer (NSCLC) in Japan. METHODS: This is a retrospective study launched at the initiative of lung cancer patients. Patients with stage IV NSCLC from January 2019 to December 2022 were investigated for testing of 8 actionable oncogenic drivers with targeted therapies available as of 2022. RESULTS: A total of 15,719 patients were included. Between 2019 and 2022, the percentage of patients who were not tested for any actionable oncogenic drivers remained the same, ranging from 21.5% to 33.1%. However, since late 2021, the percentage of patients tested for five or more actionable oncogenic drivers has increased. Across hospital categories and regions, the number of actionable oncogenic drivers tested was similar. CONCLUSIONS: This patient-initiated national survey in Japan reveals the recent nationwide increase in testing rates for actionable oncogenic drivers in Advanced NSCLC.
  • Luis G. Paz-Ares; Oscar Juan-Vidal; Giannis S. Mountzios; Enriqueta Felip; Niels Reinmuth; Filippo de Marinis; Nicolas Girard; Vipul M. Patel; Takayuki Takahama; Scott P. Owen; Douglas M. Reznick; Firas B. Badin; Irfan Cicin; Sabeen Mekan; Riddhi Patel; Eric Zhang; Divyadeep Karumanchi; Marina Chiara Garassino; Elizabeth Ahern; Venessa Chin; Stephen Della-Fiorentina; Kevin Jasas; Christos Karapetis; Jeremy Long; Louise Nott; Kenneth O'Byrne; Craig Underhill; Richard Greil; Maximilian Hochmair; Andreas Pircher; Wim Demey; Paul Germonpré; Elke Govaerts; Thierry Pieters; Reinier Wener; Alan Azambuja; Giuliano Borges; Gilberto Castro; Suellen Castro; Felipe Cruz; Fábio Franke; Eduardo Silva; Parneet Cheema; Robert El-Maraghi; Swati Kulkarni; Rami Nassabein; Scott Owen; Clarisse Audigier Valette; Jaafar Bennouna; Christos Chouaid; Alexis Cortot; Sebastien Couraud; Didier Debieuvre; Fabrice Denis; Patrick Dumont; Radj Gervais; Nicolas Girard; Etienne Giroux Leprieur; Florian Guisier; Sandrine Hiret; Henri Janicot; Corinne Lamour; Jeannick Madelaine; Marie Marcq; Emilie Pluquet; Jean Louis Pujol; Magali Ravoire; Marielle Sabatini; Alain Vergnenegre; Sabine Bohnet; Martin Faehling; Melanie Janning; Eckart Laack; Niels Reinmuth; Achim Rittmeyer; Claas Wesseler; Sofia Baka; George Fountzilas; Panagiotis Katsaounis; Athanasios Kotsakis; Ioannis Mountzios; Konstantinos Syrigos; Julia Dudnik; Fink Carmel; Ofer Merimsky; Hovav Nechushtan; Julia Sobolev; Franceso Agustoni; Anna Cecilia Bettini; Matteo Brighenti; Giulio Cerea; Filippo De Marinis; Salvatore Grisanti; Francesco Grossi; Andrea Luciani; Evaristo Maiello; Hector Soto Parra; Pierfrancesco Tassone; Giuseppe Tonini; Yoko Agemi; Koichi Azuma; Tomohisa Baba; Yuka Fujita; Eiki Ichihara; Takashi Kasai; Terufumi Kato; Haruki Kobayashi; Shoichi Kuyama; Kazumi Nishino; Masahide Oki; Kyoichi Okishio; Tomohiro Sakamoto; Yuki Sato; Yuki Shinno; Takayuki Takahama; Koichi Takayama; Yasutaka Watanabe; Noriko Yanagitani; Yoshitaka Zenke; Daniel Motola Kuba; Tomas Daniel Pineda Razo; Robin Cornelissen; Lizza Hendriks; Jeroen Kloover; Klaar Maas; Cor van der Leest; Lubomir Bodnar; Boguslawa Karaszewska; Andrzej Mruk; Paula Alves; Antonio Araujo; Isabel Domingues; Ana da Conceicao Fernandes Rodrigues; Nuno Gil; Helena Magalhaes; Barbara Parente; Marcia Correa; Hector Velez-Cortes; Andres Aguilar Hernandez; Ruben Alonso Calderon; Joaquim Barrera; David Baz; Antonio Calles; Maria Campelo; Francisco Carpeno; Enric Costa; Manuel Dols; Manuel Domine Gomez; Miguel Fernandez de Sanmamed; Enriqueta Font; Jose Fuentes; Maria Pilar Garrido Lopez; Oscar Juan Vidal; Jose Larriba; Laia Martinez; Ramon Palmero Sanchez; Silverio Ros Martinez; Jon Zugazagoitia Fraile; Ahmet Bilici; Irfan Cicin; Umut Demirci; Yesim Eralp; Mahmut Gumus; Ozan Yazici; Shobhit Baijal; Katy Clarke; Farah Lim; Dakshinamoorthy Muthukumar; Nicola Steele; Yvonne Summers; Ahmed Abdelaziz; Eric Avery; Firas Badin; Charles Connor; Davey Daniel; Amir Faridi; January Fields-Meehan; Marina Garassino; Todd Gersten; Daniel Haggstrom; David Hakimian; William Houck; Henrik Illum; Roger Keresztes; Charles Kurkul; Charles Kuzma; Rachel Lerner; Steven Liu; Smitha Menon; Rami Owera; Vipul Patel; Ivor Percent; Andrew Piper; Sucharu Prakash; Douglas Reznick; Jorge Rios-Perez; Jun Sun; Restituto Tibayan; Anne Traynor; William Walsh; Donald Wender
    Journal of Clinical Oncology 42 24 JCO2400733 - 2872 2024年05月 
    PURPOSE: The open-label, phase III EVOKE-01 study evaluated sacituzumab govitecan (SG) versus standard-of-care docetaxel in metastatic non-small cell lung cancer (mNSCLC) with progression on/after platinum-based chemotherapy, anti-PD-(L)1, and targeted treatment for actionable genomic alterations (AGAs). Primary analysis is reported. METHODS: Patients were randomly assigned 1:1 (stratified by histology, best response to last anti-PD-(L)1-containing regimen, and AGA treatment received or not) to SG (one 10 mg/kg intravenous infusion on days 1 and 8) or docetaxel (one 75 mg/m2 intravenous infusion on day 1) in 21-day cycles. Primary end point was overall survival (OS). Key secondary end points were investigator-assessed progression-free survival (PFS), objective response rate, patient-reported symptom assessment, and safety. RESULTS: In the intention-to-treat population (SG, n = 299; docetaxel, n = 304), 55.4% had one previous line of therapy. Median follow-up was 12.7 months (range, 6.0-24.0). The primary end point was not met. There was a numerical OS improvement for SG versus docetaxel (median, 11.1 v 9.8 months; hazard ratio [HR], 0.84 [95% CI, 0.68 to 1.04]; one-sided P = .0534), consistent across squamous and nonsquamous histologies. Median PFS was 4.1 versus 3.9 months (HR, 0.92 [95% CI, 0.77 to 1.11]). An OS benefit was observed for SG (n = 192) versus docetaxel (n = 191) in mNSCLC nonresponsive to last anti-PD-(L)1-containing regimen (3.5-month median OS increase; HR, 0.75 [95% CI, 0.58 to 0.97]); this was consistent across histologies. Among patients receiving SG and docetaxel, 6.8% and 14.2% discontinued because of treatment-related adverse events (TRAEs), respectively; 1.4% and 1.0%, respectively, had TRAEs leading to death. CONCLUSION: Although statistical significance was not met, OS numerically improved with SG versus docetaxel, which was consistent across histologies. Clinically meaningful improvement in OS was noted in mNSCLC nonresponsive to last anti-PD-(L)1-containing regimen. SG was better tolerated than docetaxel and consistent with its known safety profile, with no new safety signals.
  • Hidetoshi Hayashi; Kenji Chamoto; Ryusuke Hatae; Takashi Kurosaki; Yosuke Togashi; Kazuya Fukuoka; Megumi Goto; Yasutaka Chiba; Shuta Tomida; Takayo Ota; Koji Haratani; Takayuki Takahama; Junko Tanizaki; Takeshi Yoshida; Tsutomu Iwasa; Kaoru Tanaka; Masayuki Takeda; Tomoko Hirano; Hironori Yoshida; Hiroaki Ozasa; Yuichi Sakamori; Kazuko Sakai; Keiko Higuchi; Hitoshi Uga; Chihiro Suminaka; Toyohiro Hirai; Kazuto Nishio; Kazuhiko Nakagawa; Tasuku Honjo
    Journal of Clinical Investigation 134 7 2024年04月 
    BACKGROUNDPrecise stratification of patients with non-small cell lung cancer (NSCLC) is needed for appropriate application of PD-1/PD-L1 blockade therapy.METHODSWe measured soluble forms of the immune-checkpoint molecules PD-L1, PD-1, and CTLA-4 in plasma of patients with advanced NSCLC before PD-1/PD-L1 blockade. A prospective biomarker-finding trial (cohort A) included 50 previously treated patients who received nivolumab. A retrospective observational study was performed for patients treated with any PD-1/PD-L1 blockade therapy (cohorts B and C), cytotoxic chemotherapy (cohort D), or targeted therapy (cohort E). Plasma samples from all patients were assayed for soluble immune-checkpoint molecules with a highly sensitive chemiluminescence-based assay.RESULTSNonresponsiveness to PD-1/PD-L1 blockade therapy was associated with higher concentrations of these soluble immune factors among patients with immune-reactive (hot) tumors. Such an association was not apparent for patients treated with cytotoxic chemotherapy or targeted therapy. Integrative analysis of tumor size, PD-L1 expression in tumor tissue (tPD-L1), and gene expression in tumor tissue and peripheral CD8+ T cells revealed that high concentrations of the 3 soluble immune factors were associated with hyper or terminal exhaustion of antitumor immunity. The combination of soluble PD-L1 (sPD-L1) and sCTLA-4 efficiently discriminated responsiveness to PD-1/PD-L1 blockade among patients with immune-reactive tumors.CONCLUSIONCombinations of soluble immune factors might be able to identify patients unlikely to respond to PD-1/PD-L1 blockade as a result of terminal exhaustion of antitumor immunity. Our data suggest that such a combination better predicts, along with tPD-L1, for the response of patients with NSCLC.TRIAL REGISTRATIONUMIN000019674.FUNDINGThis study was funded by Ono Pharmaceutical Co. Ltd. and Sysmex Corporation.
  • Daisuke Hazama; Kenji Nakahama; Hiroaki Kodama; Akito Miyazaki; Koichi Azuma; Yosuke Kawashima; Yuki Sato; Kentaro Ito; Yoshimasa Shiraishi; Keita Miura; Takayuki Takahama; Satoshi Oizumi; Yoshinobu Namba; Satoshi Ikeda; Hiroshige Yoshioka; Asuka Tsuya; Yuichiro Yasuda; Yoshiki Negi; Ayako Hara; Michihito Toda; Motoko Tachihara
    JTO clinical and research reports 5 1 100613 - 100613 2024年01月 
    INTRODUCTION: Pulmonary sarcomatoid carcinoma (PSC) is a rare subtype of lung cancer associated with poor prognosis and resistance to conventional chemotherapy. Immune checkpoint inhibitors (ICIs), alone or in combination with chemotherapy, were found to have clinical benefits in PSC in recent studies. Nevertheless, because these studies included a small number of patients owing to disease rarity, larger studies are needed to evaluate the effectiveness and safety of ICI-based therapy for PSC. METHODS: This multicenter retrospective study evaluated patients with ICI-naive advanced or metastatic PSC who were treated with ICI-based therapy at 25 hospitals in Japan. RESULTS: A total of 124 patients were evaluated. The overall response rate, median progression-free survival (PFS), and median overall survival (OS) were 59.0%, 10.5 months, and 32.8 months, respectively. The PFS and OS rates at 24 months were 35.3% and 51.5%, respectively. Programmed death-ligand 1 expression, concomitant chemotherapy, and the treatment line were not significantly associated with PFS or OS. Immune-related adverse events (irAEs) were observed in 70 patients (56.5%), including 30 (24.2%) with grade 3 to 5 events. Patients with mild irAEs (grades 1-2) had longer PFS and OS than did those with severe (grades 3-5) or no irAEs. In a multivariate analysis, any-grade irAEs and the absence of liver metastases were independently associated with PFS, whereas any-grade irAEs and Eastern Cooperative Oncology Group performance status less than or equal to 1 were independently associated with OS. CONCLUSIONS: ICI-based therapy was found to have promising effectiveness in patients with advanced or metastatic PSC, regardless of programmed death-ligand 1 expression, concomitant chemotherapy, or treatment line.
  • Tomohiro Sakamoto; Taichi Matsubara; Takayuki Takahama; Toshihide Yokoyama; Atsushi Nakamura; Takaaki Tokito; Tatsuro Okamoto; Hiroaki Akamatsu; Masahide Oki; Yuki Sato; Kazunori Tobino; Satoshi Ikeda; Masahide Mori; Chihiro Mimura; Ken Maeno; Satoru Miura; Toshiyuki Harada; Kunihiro Nishimura; Manabu Hiraoka; Hirotsugu Kenmotsu; Junya Fujimoto; Mototsugu Shimokawa; Nobuyuki Yamamoto; Kazuhiko Nakagawa
    JAMA network open 6 12 e2347700  2023年12月 [査読有り]
     
    IMPORTANCE: Biomarker testing for driver mutations is essential for selecting appropriate non-small cell lung cancer (NSCLC) treatment but is insufficient. OBJECTIVE: To investigate the status of biomarker testing and drug therapy for NSCLC in Japan for identifying problems in treatment. DESIGN, SETTING, AND PARTICIPANTS: The REVEAL cohort study included retrospective data collection and prospective follow-up from 29 institutions across Japan. Of 1500 patients diagnosed with advanced or recurrent NSCLC between January 1 and March 18, 2021, 1479 were eligible. Cases recognized at the wrong clinical stage (n = 12), diagnosed outside the study period (n = 6), not treated according to eligibility criteria before recurrence (n = 2), and with deficient consent acquisition procedure (n = 1) were excluded. MAIN OUTCOMES AND MEASURES: The primary end point was the biomarker testing status. Treatment-related factors were examined. RESULTS: Among the 1479 patients included in the analysis, the median age was 72 (range, 30-95) years; 1013 (68.5%) were men; 1161 (78.5%) had an Eastern Cooperative Oncology Group performance status 0 or 1; 1097 (74.2%) were current or past smokers; and 947 (64.0%) had adenocarcinoma. Biomarker status was confirmed in 1273 patients (86.1%). Multigene testing was performed in 705 cases (47.7%); single-gene testing, in 847 (57.3%); and both, in 279 (18.9%). Biomarker testing was performed for EGFR in 1245 cases (84.2%); ALK, in 1165 (78.8%); ROS1, in 1077 (72.8%); BRAF, in 803 (54.3%); and MET, in 805 (54.4%). Positivity rates among 898 adenocarcinoma cases included 305 (34.0%) for EGFR, 29 (3.2%) for ALK, 19 (2.1%) for ROS1, 11 (1.2%) for BRAF, and 14 (1.6%) for MET. Positivity rates among 375 nonadenocarcinoma cases were 14 (3.7%) for EGFR, 6 (1.6%) for ALK, 1 (0.3%) for ROS1, 3 (0.8%) for BRAF, and 8 (2.1%) for MET. Poor physical status, squamous cell carcinoma, and other comorbidities were associated with hampered multigene testing. Targeted therapy was received as first-line treatment by 263 of 278 cases (94.6%) positive for EGFR, 25 of 32 (78.1%) positive for ALK, 15 of 24 (62.5%) positive for ROS1, 9 of 12 (75.0%) positive for BRAF, and 12 of 19 (63.2%) positive for MET. Median overall survival of patients with positive findings for driver gene alteration and who received targeted therapy was 24.3 (95% CI, not reported) months; with positive findings for driver gene alteration and who did not receive targeted therapy, 15.2 (95% CI, 7.7 to not reported) months; and with negative findings for driver gene alteration, 11.0 (95% CI, 10.0-12.5) months. Multigene testing for nonadenocarcinomas and adenocarcinomas accounted for 705 (47.7%) of all NSCLC cases. CONCLUSIONS AND RELEVANCE: These findings suggest that multigene testing has not been sufficiently implemented in Japan and should be considered prospectively, even in nonadenocarcinomas, to avoid missing rare driver gene alterations.
  • 高濱 隆幸; 米阪 仁雄; 谷崎 潤子; 田中 薫; 鈴木 慎一郎; 金村 宙昌; 磯本 晃佑; 白石 直樹; 坂井 和子; 福岡 和也; 西尾 和人; 中川 和彦; 林 秀敏
    肺癌 63 5 372 - 372 (NPO)日本肺癌学会 2023年10月
  • Yasushi Goto; Hirotsugu Kenmotsu; Motohiro Tamiya; Shuji Murakami; Takayasu Kurata; Noriko Yanagitani; Hirokazu Taniguchi; Shoichi Kuyama; Junichi Shimizu; Toshihide Yokoyama; Naoko Shimada; Tadashi Maeda; Akihiro Tamiya; Ayumi Uchiyama; Kazuyoshi Imaizumi; Takayuki Takahama; Terufumi Kato; Hidetoshi Hayashi; Naoko Shiraiwa; Shigeyuki Toyoizumi; Hironori Kikkawa; Despina Thomaidou; Makoto Nishio
    JTO Clinical and Research Reports 4 5 100508 - 100508 2023年05月
  • Yasuo Otsuka; Yoriaki Komeda; Masayuki Takeda; Takayuki Takahama; Masashi Kono; Mamoru Takenaka; Satoru Hagiwara; Naoshi Nishida; Hiroshi Kashida; Masatoshi Kudo
    Case Reports in Medicine 2023 1 - 4 2023年02月 
    A 76-year-old woman presented with lower abdominal pain and nausea and was referred to the gastroenterology department in our institution. Previous contrast-enhanced computed tomography (CE-CT) for follow-up after breast cancer surgery had indicated a soft tissue mass below the right diaphragm, which was considered a benign change. CE-CT performed at the first visit to our department revealed further thickening of the soft tissue mass with extension to the liver surface. In addition, ascites and nodules were observed in the abdominal cavity. Histopathological examination of a biopsy specimen revealed peritoneal invasion of atypical epithelioid cells with trabecular and glandular patterns. The tumor cells were positive for AE1/AE2, calretinin, WT-1, D2-40, HEG1, EMA, BAP1, and MTAP and negative for carcinoembryonic antigen, MOC-31, Ber-Ep4, ER, PgR, TTF-1, claudin 4, and desmin. A diagnosis of epithelioid mesothelioma was made. The patient received chemotherapy with cisplatin (75 mg/m2) and pemetrexed (500 mg/m2). After six courses of combined chemotherapy, pemetrexed was administered as a single agent. At the time of writing this report, she was undergoing over the 30th course of chemotherapy without any significant side effects. Diffuse malignant peritoneal mesothelioma is a rare, fatal, and progressive disease. Our patient achieved long-term survival of more than 5 years with maintenance therapy using single-agent pemetrexed.
  • Fujita, Y.; Matsuoka, H.; Chiba, Y.; Tsurutani, J.; Yoshida, T.; Sakai, K.; Nakura, M.; Sakamoto, R.; Makimura, C.; Ohtake, Y.; Tanaka, K.; Hayashi, H.; Takeda, M.; Okuno, T.; Takegawa, N.; Haratani, K.; Takahama, T.; Tanizaki, J.; Koyama, A.; Nishio, K.; Nakagawa, K.
    Oncology Letters 26 2 355 - 355 2023年
  • Kana Fujimoto; Satomi Watanabe; Yuto Yasuda; Emi Date; Yasuhiro Kawabata; Hiroaki Kanemura; Takayuki Takahama; Kimio Yonesaka; Norishige Iizuka; Ken-Ichi Takahashi; Osamu Kawakami; Tomohiro Ozaki; Kazuhiko Nakagawa
    Thoracic cancer 14 2 214 - 217 2023年01月
  • Tsukamoto, S.; Takahama, T.; Mavrogenis, A.F.; Tanaka, Y.; Tanaka, Y.; Errani, C.
    Musculoskeletal Surgery 107 1 2023年
  • 阪本 智宏; 松原 太一; 高濱 隆幸; 横山 俊秀; 中村 敦; 時任 高章; 岡本 龍郎; 赤松 弘朗; 沖 昌英; 佐藤 悠城; 飛野 和則; 西村 邦裕; 平岡 学; 釼持 広知; 藤本 淳也; 下川 元継; 山本 信之; 中川 和彦
    肺癌 62 6 491 - 491 (NPO)日本肺癌学会 2022年11月
  • がん遺伝子パネル検査FoundationOneによる肺癌の遺伝子変異の測定
    米阪 仁雄; 高濱 隆幸; 黒崎 隆; 川中 雄介; 金村 宙昌; 磯本 晃佑; 鈴木 慎一郎; 三谷 誠一郎; 中川 和彦; 白石 直樹; 小田 いつき; 西郷 和真; 池川 敦子; 福岡 和也; 武田 真幸; 西尾 和人
    肺癌 62 5 439 - 439 (NPO)日本肺癌学会 2022年10月
  • がん遺伝子パネル検査FoundationOneによる肺癌の遺伝子変異の測定
    米阪 仁雄; 高濱 隆幸; 黒崎 隆; 川中 雄介; 金村 宙昌; 磯本 晃佑; 鈴木 慎一郎; 三谷 誠一郎; 中川 和彦; 白石 直樹; 小田 いつき; 西郷 和真; 池川 敦子; 福岡 和也; 武田 真幸; 西尾 和人
    肺癌 62 5 439 - 439 (NPO)日本肺癌学会 2022年10月
  • Hiroaki Kanemura; Hidetoshi Hayashi; Shuta Tomida; Junko Tanizaki; Shinichiro Suzuki; Yusuke Kawanaka; Asuka Tsuya; Yasushi Fukuda; Hiroyasu Kaneda; Keita Kudo; Takayuki Takahama; Ryosuke Imai; Koji Haratani; Yasutaka Chiba; Tomoyuki Otani; Akihiko Ito; Kazuko Sakai; Kazuto Nishio; Kazuhiko Nakagawa
    JTO clinical and research reports 3 8 100373 - 100373 2022年08月
  • 高濱 隆幸; 米阪 仁雄; 白石 直樹; 小田 いつき; 池川 敦子; 西郷 和真; 福岡 和也; 中川 和彦
    近畿大学医学雑誌 47 1-2 19 - 25 近畿大学医学会 2022年06月
  • Daichi Fujimoto; Satoru Miura; Kenichi Yoshimura; Kazushige Wakuda; Yuko Oya; Koji Haratani; Shoichi Itoh; Takehiro Uemura; Ryotaro Morinaga; Takayuki Takahama; Kazuhisa Nakashima; Motoko Tachihara; Go Saito; Junko Tanizaki; Kohei Otsubo; Satoshi Ikeda; Hirotaka Matsumoto; Satoshi Hara; Akito Hata; Takeshi Masuda; Nobuyuki Yamamoto
    JTO clinical and research reports 3 2 100265 - 100265 2022年02月
  • Takahiro Kimura; Takayuki Takahama; Tomoko Wakasa; Shiori Adachi; Yusaku Akashi; Takao Tamura; Katsunari Yane
    Molecular and clinical oncology 16 1 2 - 2 2022年01月
  • Yoshinori Imamura; Kaoru Tanaka; Naomi Kiyota; Hidetoshi Hayashi; Ichiro Ota; Akihito Arai; Shigemichi Iwae; Shujiro Minami; Katsunari Yane; Tomoko Yamazaki; Yoshiaki Nagatani; Masanori Toyoda; Takayuki Takahama; Kazuko Sakai; Kazuto Nishio; Naoki Otsuki; Ken-ichi Nibu; Hironobu Minami
    Medical Oncology 38 11 128 - 128 2021年11月
  • Kazuko Sakai; Toshiharu Sakurai; Marco A. De Velasco; Tomoyuki Nagai; Takaaki Chikugo; Kazuomi Ueshima; Yurie Kura; Takayuki Takahama; Hidetoshi Hayashi; Kazuhiko Nakagawa; Masatoshi Kudo; Kazuto Nishio
    Frontiers in Oncology 11 763468 - 763468 2021年10月
  • T. Takahama; H. Shimizu; H. Kaneda; H. Horinouchi; K. Watanabe; T. Yoshida; K. Hasegawa; K. Onishi; K. Yoshimura; T. Sawa; A. Gemma
    Journal of Thoracic Oncology 16 10 S1133 - S1133 2021年10月
  • 白石 直樹; 田中 薫; 高濱 隆幸; 鈴木 慎一郎; 金村 宙昌; 磯本 晃佑; 林 秀敏; 米阪 仁雄; 中川 和彦
    肺癌 61 6 649 - 649 (NPO)日本肺癌学会 2021年10月
  • 高濱 隆幸; 清水 秀文; 堀之内 秀仁; 吉田 健史; 渡邊 清高; 金田 裕靖; 長谷川 一男; 大西 幸次; 吉村 健一; 澤 祥幸; 弦間 昭彦
    肺癌 61 6 586 - 586 (NPO)日本肺癌学会 2021年10月
  • 金村 宙昌; 林 秀敏; 大谷 知之; 冨田 秀太; 鈴木 慎一郎; 原谷 浩司; 谷崎 潤子; 津谷 あす香; 福田 泰; 金田 裕靖; 工藤 慶太; 高濱 隆幸; 今井 亮介; 千葉 康敬; 西尾 和人; 伊藤 彰彦; 中川 和彦
    肺癌 61 6 499 - 499 (NPO)日本肺癌学会 2021年10月
  • Ryoji Kato; Hidetoshi Hayashi; Kazuko Sakai; Shinichiro Suzuki; Koji Haratani; Takayuki Takahama; Junko Tanizaki; Yoshikane Nonagase; Kaoru Tanaka; Takeshi Yoshida; Masayuki Takeda; Kimio Yonesaka; Hiroyasu Kaneda; Kazuto Nishio; Kazuhiko Nakagawa
    International journal of clinical oncology 26 9 1628 - 1639 2021年09月
  • Esuteru Hirokawa; Satomi Watanabe; Kazuko Sakai; Masayuki Takeda; Chihiro Sato; Takayuki Takahama; Kazuto Nishio; Kazuhiko Nakagawa
    Thoracic cancer 12 16 2283 - 2287 2021年08月
  • Hidefumi Shimizu; Takayuki Takahama; Hiroyasu Kaneda; Hidehito Horinouchi; Takeshi Yoshida; Kiyotaka Watanabe; Kazuo Hasegawa; Kouji Onishi; Kenichi Yoshimura; Toshiyuki Sawa; Akihiko Gemma
    Annals of Oncology 32 S306 - S306 2021年07月
  • Tomoya Fukui; Kazuko Sakai; Jiichiro Sasaki; Mikiko Ishihara Kakegawa; Satoshi Igawa; Hisashi Mitsufuji; Masayuki Takeda; Takayuki Takahama; Kazuhiko Nakagawa; Kazuto Nishio; Katsuhiko Naoki
    Cancer biomarkers : section A of Disease markers 31 2 119 - 126 2021年
  • Kazuko Sakai; Takayuki Takahama; Mototsugu Shimokawa; Koichi Azuma; Masayuki Takeda; Terufumi Kato; Haruko Daga; Isamu Okamoto; Hiroaki Akamatsu; Shunsuke Teraoka; Akira Ono; Tatsuo Ohira; Toshihide Yokoyama; Nobuyuki Yamamoto; Kazuhiko Nakagawa; Kazuto Nishio
    Molecular oncology 15 1 126 - 137 2021年01月
  • Masayuki Takeda; Takayuki Takahama; Kazuko Sakai; Shigeki Shimizu; Satomi Watanabe; Hisato Kawakami; Kaoru Tanaka; Chihiro Sato; Hidetoshi Hayashi; Yoshikane Nonagase; Kimio Yonesaka; Naoki Takegawa; Tatsuya Okuno; Takeshi Yoshida; Soichi Fumita; Shinichiro Suzuki; Koji Haratani; Kazumasa Saigoh; Akihiko Ito; Tetsuya Mitsudomi; Hisashi Handa; Kazuya Fukuoka; Kazuhiko Nakagawa; Kazuto Nishio
    The oncologist 26 4 e588-e596 - e596 2020年12月
  • CAPP-Seqを用いたLiquid biopsyによるT790M陽性非小細胞肺癌のオシメルチニブ耐性因子の検討
    加藤 了資; 林 秀敏; 原谷 浩司; 高濱 隆幸; 谷崎 潤子; 野長瀬 祥兼; 田中 薫; 吉田 健史; 武田 真幸; 米阪 仁雄; 中川 和彦; 坂井 和子; 西尾 和人; 金田 裕靖
    肺癌 60 2 148 - 148 (NPO)日本肺癌学会 2020年04月
  • Kurosaki, T.; Kawakami, H.; Mitani, S.; Kawabata, R.; Takahama, T.; Nonagase, Y.; Fumita, S.; Ozaki, T.; Chiba, Y.; Tamura, T.; Nakagawa, K.
    In vivo (Athens, Greece) 34 4 1921 - 1929 2020年 [査読有り]
  • Masayuki Takeda; Kazuko Sakai; Hidetoshi Hayashi; Kaoru Tanaka; Koji Haratani; Takayuki Takahama; Ryoji Kato; Kimio Yonesaka; Kazuto Nishio; Kazuhiko Nakagawa
    Lung cancer (Amsterdam, Netherlands) 139 28 - 34 2020年01月 [査読有り]
  • Takayuki Takahama; Koichi Azuma; Mototsugu Shimokawa; Masayuki Takeda; Hidenobu Ishii; Terufumi Kato; Haruhiro Saito; Haruko Daga; Yuko Tsuboguchi; Isamu Okamoto; Kohei Otsubo; Hiroaki Akamatsu; Shunsuke Teraoka; Toshiaki Takahashi; Akira Ono; Tatsuo Ohira; Toshihide Yokoyama; Kazuko Sakai; Nobuyuki Yamamoto; Kazuto Nishio; Kazuhiko Nakagawa
    Cancer 126 9 1940 - 1948 2020年01月 [査読有り]
  • Kimio Yonesaka; Eiji Iwama; Hidetoshi Hayashi; Shinichiro Suzuki; Ryoji Kato; Satomi Watanabe; Takayuki Takahama; Junko Tanizaki; Kaoru Tanaka; Masayuki Takeda; Kazuko Sakai; Koichi Azuma; Yasutaka Chiba; Shinji Atagi; Kazuto Nishio; Isamu Okamoto; Kazuhiko Nakagawa
    Scientific reports 9 1 19501 - 19501 2019年12月 [査読有り]
  • Satomi Watanabe; Tomoyuki Otani; Tsutomu Iwasa; Takayuki Takahama; Masayuki Takeda; Kazuko Sakai; Kazuto Nishio; Akihiko Ito; Kazuhiko Nakagawa
    Clinical breast cancer 19 5 e589-e592 - e592 2019年10月 [査読有り]
  • Koji Haratani; Hidetoshi Hayashi; Takayuki Takahama; Yasushi Nakamura; Shuta Tomida; Takeshi Yoshida; Yasutaka Chiba; Takahiro Sawada; Kazuko Sakai; Yoshihiko Fujita; Yosuke Togashi; Junko Tanizaki; Hisato Kawakami; Akihiko Ito; Kazuto Nishio; Kazuhiko Nakagawa
    Journal for immunotherapy of cancer 7 1 251 - 251 2019年09月 [査読有り]
  • Kazuko Sakai; Masayuki Takeda; Shigeki Shimizu; Takayuki Takahama; Takeshi Yoshida; Satomi Watanabe; Tsutomu Iwasa; Kimio Yonesaka; Shinichiro Suzuki; Hidetoshi Hayashi; Hisato Kawakami; Yoshikane Nonagase; Kaoru Tanaka; Junji Tsurutani; Kazumasa Saigoh; Akihiko Ito; Tetsuya Mitsudomi; Kazuhiko Nakagawa; Kazuto Nishio
    Scientific reports 9 1 11340 - 11340 2019年08月 [査読有り]
  • Masayuki Takeda; Kazuko Sakai; Takayuki Takahama; Kazuya Fukuoka; Kazuhiko Nakagawa; Kazuto Nishio
    Cancers 11 6 2019年05月 [査読有り]
  • Shinichiro Suzuki; Koji Haratani; Takayuki Takahama; Satomi Watanabe; Naoki Takegawa; Hidetoshi Hayashi; Masayuki Takeda; Kimio Yonesaka; Kazuhiko Nakagawa
    Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 14 3 e50-e52 - e52 2019年03月 [査読有り]
  • Hiroto Ueda; Hisato Kawakami; Yoshikane Nonagase; Naoki Takegawa; Tatsuya Okuno; Takayuki Takahama; Masayuki Takeda; Yasutaka Chiba; Takao Tamura; Kazuhiko Nakagawa
    The oncologist 24 2 163-e76 - e76 2019年02月 [査読有り]
  • Fujita Etsuo; Ohya Daichi; Kitamura Yousuke; Yamamura Risa; Ishikawa Kana; Sagimori Miki; Ohta Fuminori; Kiyoi Megumi; Kawabata Yoshitaka; Hashimoto Tadayuki; Aoki Tatsuya; Kayama Yuta; Mukai Yosuke; Nakamura Ryo; Yabuuchi Toshinobu; Furuta Katsuyuki; Hikimoto Shigetoshi; Takahata Masahiro; Sougawa Hiromichi; Kobayashi Katsunobu; Hoshiya Hironobu; Nakachi Kenichiro; Ikejima Miwa; Furukawa Kenichi; Kawahara Masaaki; Takahama Takayuki; Nishikawa Yusaku; Tohda Yuji; Shimada Kousuke; Yamamoto Katsuhiro
    日本臨床生理学会雑誌 48 3 127 - 133 2018年08月 
    肺癌の診断に気管支肺胞洗浄液(BAL)のサイトケラチンフラグメント(CYFRA)を使用できるか検討するため、患者39名(男31名、女8名、平均年齢73.2±1.6歳)のBALにおけるCYFRA濃度を測定した。全員のBALのCYFRA値は49.4±21.8ng/mLで、そのうち悪性と診断された患者27名の値は38.0±12.9ng/mL、良性病変の患者12名の値は75.0±66.0ng/mLで、有意差は認めなかった。一方、血清中のCYFRA値は、全員、悪性、良性の患者でそれぞれ、4.5±0.8ng/mL、5.5±1.1ng/mL、2.3±0.6ng/mLであった。BALのCYFRAの平均値は悪性の症例よりも良性の症例で高く、血清CYFRA値では悪性の症例のほうが高い傾向がみられた。
  • Kimio Yonesaka; Koji Haratani; Shiki Takamura; Hitomi Sakai; Ryoji Kato; Naoki Takegawa; Takayuki Takahama; Kaoru Tanaka; Hidetoshi Hayashi; Masayuki Takeda; Sigeki Kato; Osamu Maenishi; Kazuko Sakai; Yasutaka Chiba; Takafumi Okabe; Keita Kudo; Yoshikazu Hasegawa; Hiroyasu Kaneda; Michiko Yamato; Kenji Hirotani; Masaaki Miyazawa; Kazuto Nishio; Kazuhiko Nakagawa
    Clinical cancer research : an official journal of the American Association for Cancer Research 24 11 2653 - 2664 2018年06月 [査読有り]
  • Takahama, T.; Sakai, K.; Nakagawa, K.; Nishio, K.
    Annals of Oncology 29 2018年
  • Takahama, T.; Azuma, K.; Shimokawa, M.; Kato, T.; Daga, H.; Okamoto, I.; Akamatsu, H.; Takahashi, T.; Ohira, T.; Yokoyama, T.; Hirano, K.; Shiraishi, Y.; Himeji, D.; Yamamoto, N.; Nishio, K.; Nakagawa, K.
    Annals of Oncology 29 2018年 [査読有り]
  • Fujita Etsuo; Shojima Kensaku; Nishimura Hideko; Hattori Maiko; Takahata Masahiro; Sougawa Hiromichi; Kobayashi Katsunobu; Hoshiaya Hironobu; Ohta Fuminori; Kiyoi Megumi; Nakai Takeo; Tsunoi Kazuyuki; Sakanaka Keiichiro; Tanaka Akio; Deguchi Yoko; Horiuchi Yuko; Iwahashi Naoyuki; Furukawa Kenichi; Hirabayashi Yasuo; Inagaki Takashi; Kawahara Masaaki; Takahama Takayuki; Nakanishi Yuya; Nishikawa Yusaku; Tohda Yuji; Shimada Kousuke; Yamamoto Katsuhiro
    日本臨床生理学会雑誌 47 2 105 - 111 2017年05月 
    BAL中のSCCを測定して肺癌の診断を行い、血清SCC測定結果と比較した。肺癌の疑いのある患者68名(男48名、女20名、平均71.4名)に、PETとGaシンチグラフィーを行い、経気管支鏡肺生検、経気管支鏡生検またはBALを含む組織検査または細胞診を行った。肺癌患者ではBAL中のSCC抗原マーカー(435.5±61.1ng/mL)は、良性病変(354.2±86.9ng/mL)よりもわずかに高値を示した。血清のSCC抗原マーカー(3.3±0.9ng/mL)も良性病変(1.3±0.1ng/mL)よりもわずかに高値を示した。以上より、この測定値を他の放射線画像診断と併用すると、肺癌の診断の信頼性が高くなると考えられた。
  • Yoshikane Nonagase; Kimio Yonesaka; Hisato Kawakami; Satomi Watanabe; Koji Haratani; Takayuki Takahama; Naoki Takegawa; Hiroto Ueda; Junko Tanizaki; Hidetoshi Hayashi; Takeshi Yoshida; Masayuki Takeda; Yasutaka Chiba; Takao Tamura; Kazuhiko Nakagawa; Junji Tsurutani
    Oncotarget 7 51 84860 - 84871 2016年12月 [査読有り]
  • Takayuki Takahama; Kazuko Sakai; Masayuki Takeda; Koichi Azuma; Toyoaki Hida; Masataka Hirabayashi; Tetsuya Oguri; Hiroshi Tanaka; Noriyuki Ebi; Toshiyuki Sawa; Akihiro Bessho; Motoko Tachihara; Hiroaki Akamatsu; Shuji Bandoh; Daisuke Himeji; Tatsuo Ohira; Mototsugu Shimokawa; Yoichi Nakanishi; Kazuhiko Nakagawa; Kazuto Nishio
    Oncotarget 7 36 58492 - 58499 2016年09月 [査読有り]
  • Satomi Watanabe; Masayuki Takeda; Takayuki Takahama; Tsutomu Iwasa; Junji Tsurutani; Junko Tanizaki; Toshio Shimizu; Kazuko Sakai; Yoshitaka Wada; Noritaka Isogai; Kazuto Nishio; Kazuhiko Nakagawa
    Investigational new drugs 34 3 394 - 6 2016年06月 [査読有り]
  • M. Takeda; K. Sakai; M. Terashima; H. Kaneda; H. Hayashi; K. Tanaka; K. Okamoto; T. Takahama; T. Yoshida; T. Iwasa; T. Shimizu; Y. Nonagase; K. Kudo; S. Tomida; T. Mitsudomi; K. Saigo; A. Ito; K. Nakagawa; K. Nishio
    ANNALS OF ONCOLOGY 26 12 2477 - 2482 2015年12月
  • Kimio Yonesaka; Keita Kudo; Satomi Nishida; Takayuki Takahama; Tsutomu Iwasa; Takeshi Yoshida; Kaoru Tanaka; Masayuki Takeda; Hiroyasu Kaneda; Isamu Okamoto; Kazuto Nishio; Kazuhiko Nakagawa
    Oncotarget 6 32 33602 - 11 2015年10月 [査読有り]
  • Takayuki Takahama; Masayuki Takeda; Shinichi Nishina; Kazuhiko Nakagawa
    BMC research notes 8 1 100 - 100 2015年03月 [査読有り]
  • Naoki Watanabe; Tomoya Ishii; Takayuki Takahama; Akira Tadokoro; Nobuhiro Kanaji; Hiroaki Dobashi; Shuji Bandoh
    Internal medicine (Tokyo, Japan) 53 23 2711 - 5 2014年 [査読有り]
  • Nobuhiro Kanaji; Yoshio Kushida; Shuji Bandoh; Tomoya Ishii; Reiji Haba; Akira Tadokoro; Naoki Watanabe; Takayuki Takahama; Nobuyuki Kita; Hiroaki Dobashi; Takuya Matsunaga
    American Journal of Case Reports 14 543 - 547 2013年12月 [査読有り]
  • Nobuhiro Kanaji; Yoshio Kushida; Shuji Bandoh; Tomoya Ishii; Reiji Haba; Akira Tadokoro; Naoki Watanabe; Takayuki Takahama; Nobuyuki Kita; Hiroaki Dobashi; Takuya Matsunaga
    The American journal of case reports 14 543 - 7 2013年 [査読有り]
  • Akira Tadokoro; Tomoya Ishii; Takayuki Takahama; Naoki Watanabe; Koshiro Takano; Nobuhiro Kanaji; Osamu Imataki; Hiroaki Dobashi; Shuji Bandoh; Takuya Matsunaga
    Internal medicine (Tokyo, Japan) 52 17 1953 - 6 2013年 [査読有り]
  • Nobuhiro Kanaji; Shuji Bandoh; Tomoya Ishii; Akira Tadokoro; Naoki Watanabe; Takayuki Takahama; Reiji Haba; Osamu Imataki; Hiroaki Dobashi; Takuya Matsunaga
    LUNG CANCER 77 2 293 - 298 2012年08月 [査読有り]

MISC

所属学協会

  • 日本がん分子標的治療学会   日本呼吸器内視鏡学会   日本感染症学会   日本肺癌学会   日本呼吸器学会   日本癌学会   日本臨床腫瘍学会   日本内科学会   

共同研究・競争的資金等の研究課題

  • 日本学術振興会：科学研究費助成事業 基盤研究(C)
    研究期間 : 2022年04月 -2026年03月 
    代表者 : 北島 一宏; 山門 亨一郎; 甲斐田 勇人; 大崎 洋充; 渡部 直史; 木島 貴志; 南 俊行; 高濱 隆幸
  • 日本学術振興会：科学研究費助成事業 基盤研究(C)
    研究期間 : 2019年04月 -2022年03月 
    代表者 : 林 秀敏; 冨田 秀太; 坂井 和子; 伊藤 彰彦; 高濱 隆幸; 原谷 浩司
     
    研究実施計画書を近畿大学・複数施設にて倫理委員会による審査の承認後、各施設から症例登録・臨床情報収集を行い、自施設含む4施設から計125例の症例登録が得られた。 登録症例のうち解析可能な90症例について、生検または手術で得た腫瘍組織検体（FFPE）を収集、当施設にてRNA/DNAを抽出し、nCounter, PanCancer, IO360Panelにて腫瘍免疫関連遺伝子発現の評価を行った。現在も一部解析中で、最終解析対象症例は60例となる見込みである。免疫チェックポイント阻害薬と化学療法の併用療法の奏効がPD-L1の発現および一部の免疫関連遺伝子発現と相関している可能性があることを見出した。

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