2026/06/27 更新

写真a

ハラ　ナオフミ
原　尚史
Hara Naofumi
所属
学術研究院医療開発領域 助教（特任）
職名
助教（特任）
外部リンク
 

論文

  • Afatinib Overcomes Osimertinib Resistance via Egfr V804F Mutation in a Syngeneic Egfr-Mutant Lung Cancer Mouse Model. 国際誌

    Takaaki Tanaka, Masato Fujitani, Masataka Taoka, Iwao Shimomura, Sachi Okawa, Shunta Mori, Tadahiro Kuribayashi, Jun Nishimura, Tomoka Nishimura, Ayako Morita, Naofumi Hara, Kiichiro Ninomiya, Go Makimoto, Hisao Higo, Kammei Rai, Eiki Ichihara, Shuta Tomida, Katsuyuki Hotta, Yosuke Togashi, Yoshinobu Maeda, Katsuyuki Kiura, Ryohei Katayama, Kadoaki Ohashi

    Cancer science   2026年6月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Osimertinib is the standard first-line treatment for advanced EGFR-mutant non-small cell lung cancer. However, acquired resistance invariably develops, and identifying novel resistance pathways is clinically important as a substantial portion remains undefined. We used an immunocompetent syngeneic lung cancer mouse model harboring an Egfr exon 19 deletion (mDEL tumors) to establish acquired resistance. Osimertinib-resistant tumors were generated in vivo using a drug-holiday/re-challenge protocol. The resistance mechanism was identified using Sanger sequencing, receptor tyrosine kinase arrays, and western blotting. Egfr V804F knock-in cells were generated using CRISPR/Cas9, and their sensitivity to osimertinib and afatinib was assessed in vitro and in vivo. We established two distinct osimertinib-resistant tumor lines in a syngeneic lung cancer mouse model (mDEL OsiR #1/#3). The analysis revealed an on-target secondary Egfr V804F mutation (corresponding to human EGFR V802F) in both tumor lines. Importantly, Egfr V804F knock-in cells demonstrated significant osimertinib resistance, with a 5.7-10.5-fold increase in in vitro IC50 (mean, 8.2-fold), but remained highly sensitive to afatinib. Furthermore, afatinib effectively overcame osimertinib resistance in the V804F knock-in cell-derived mouse model. Consistently, afatinib treatment resulted in marked tumor shrinkage and suppression of EGFR signaling in the established mDEL OsiR #1/#3 in vivo. These findings establish secondary Egfr V804F/EGFR V802F as an on-target osimertinib resistance mechanism, providing a preclinical rationale for evaluating afatinib in biomarker-selected patients harboring this alteration.

    DOI： 10.1111/cas.70431

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  • TGF-β Inhibitor Potentiates Osimertinib-Induced Anti-Tumor Immunity in Egfr-Mutant Lung Cancer. 国際誌

    Tadahiro Kuribayashi, Jun Nishimura, Sachi Okawa, Masataka Taoka, Shunta Mori, Takaaki Tanaka, Tomoka Nishimura, Ayako Morita, Naofumi Hara, Kiichiro Ninomiya, Go Makimoto, Kammei Rai, Eiki Ichihara, Katsuyuki Hotta, Yosuke Togashi, Yoshinobu Maeda, Katsuyuki Kiura, Kadoaki Ohashi

    Cancer science   2026年2月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Immunotherapy for epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) remains challenging. We previously found that EGFR-tyrosine kinase inhibitors induced antitumor immunity but also triggered immunosuppressive cytokines, including transforming growth factor-β (TGF-β), in Egfr-mutant lung cancer. Here, we investigate whether TGF-β inhibition potentiates osimertinib-induced antitumor immunity using a syngeneic mouse model of Egfr-mutated lung cancer, with cancer cells subcutaneously transplanted into wild-type C57BL/6J mice. We evaluated the antitumor effect of the combination therapy with osimertinib and either nintedanib (an indirect TGF-β inhibitor) or vactosertib (a specific TGF-β type I receptor kinase inhibitor). Changes in the tumor microenvironment during treatment were assessed using immunohistochemical staining, western blot analysis, and flow cytometry. We found that TGF-β expression was upregulated in the tumor treated with osimertinib. Nintedanib monotherapy showed no significant antitumor effect, whereas osimertinib combined with nintedanib significantly potentiates the antitumor effect compared with osimertinib monotherapy in vivo. Crucially, no additive effect of nintedanib on osimertinib monotherapy was observed in vitro. Combination therapy with osimertinib and nintedanib significantly increased effector T cells (CD8+CD44+CD62L-) and Granzyme B+ areas and decreased CD206+ cells, while significantly decreasing TGF-β and SMAD2/3 expression. Similar effects were observed with vactosertib but not with a vascular endothelial growth factor receptor 2 inhibitor. In conclusion, combination therapy with osimertinib and TGF-β inhibitors potentiates osimertinib-induced antitumor immunity. These findings highlight a novel therapeutic strategy for EGFR-mutated NSCLC and warrant further clinical investigation.

    DOI： 10.1111/cas.70352

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  • A Prompt Diagnosis of Ascites and Dramatic Effect of Alectinib for Advanced Lung Adenocarcinoma Harboring EML4-ALK Fusion.

    Takahiro Baba, Hirofumi Inoue, Hiromi Matsuoka, Mio Kyakuno, Yusuke Yoshinaga, Tetsuya Takeguchi, Miho Fujiwara, Kotaro Yamada, Eri Nakamura, Ayako Morita, Naofumi Hara, Kiichiro Ninomiya, Hisao Higo, Masanori Fujii, Eiki Ichihara, Kammei Rai, Kadoaki Ohashi, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Yosuke Togashi, Go Makimoto

    Internal medicine (Tokyo, Japan)   64 ( 23 )   3413 - 3418   2025年12月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    A 75-year-old never-smoker woman presented with dyspnea and loss of appetite. A mass was identified in the left upper lobe of the lung, and the patient was referred to our hospital. Despite the diagnosis of lung adenocarcinoma via bronchoscopy, anaplastic lymphoma kinase (ALK) immunostaining was negative. Rapid weight gain and abdominal distension caused by ascites prompted fluid testing using the AmoyDx® Pan Lung Cancer PCR Panel. EML4-ALK fusion was confirmed, and alectinib therapy was initiated immediately. The tumor size had decreased significantly, and the patient was discharged on day 34. This case highlights the necessity of multiplex genetic testing even when ALK immunostaining is negative.

    DOI： 10.2169/internalmedicine.5397-25

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  • Colony-Stimulating Factor-1 Receptor Inhibitor Augments Osimertinib-Induced Antitumor Immunity via Suppression of Macrophages in Lung Cancer Harboring EGFR Mutation. 国際誌

    Sachi Okawa, Shuta Tomida, Tadahiro Kuribayashi, Jun Nishimura, Takamasa Nakasuka, Atsuko Hirabae, Naofumi Hara, Hirofumi Inoue, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Katuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura, Kadoaki Ohashi

    Molecular cancer therapeutics   24 ( 11 )   1763 - 1774   2025年11月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Persister cancer cells, which reversibly adapt to survive EGFR-tyrosine kinase inhibitor (TKI) treatment, contribute to the incurability of EGFR-mutant lung cancer. We previously reported that gefitinib induces CD8+ T cell-related tumor immunity in a genetically engineered mouse model. This study investigates the tolerance of persister cancer cells to EGFR-TKI-induced tumor immunity in this model. EGFR-mutated lung cancer cells (C57BL/6/EgfrdelE748-A752) from the genetically engineered mouse model were transplanted subcutaneously into wild-type C57BL/6J mice. Persistent tissues under osimertinib treatment were analyzed using digital spatial transcriptional profiling, IHC staining, and flow cytometry. The antitumor effect of osimertinib peaked at 14 days, leaving a small population of persister cancer cells. The number of PD-1+ CD8+ cells increased in the tumor microenvironment (TME), and CD8+ cell depletion attenuated the antitumor effect of osimertinib. Digital spatial transcriptional profiling revealed upregulated expression of M2 macrophage-related genes in the TME of persister cancer cells. Consistently, IHC and flow cytometry confirmed an increased number of CD206+ macrophages in the TME. Combining osimertinib with the colony-stimulating factor-1 receptor inhibitor pexidartinib reduced CD206+ macrophages and enhanced the efficacy of osimertinib. Elevated Granzyme B or CD107 expression on CD8+ cells in the TME suggests that macrophages negatively affect osimertinib-induced antitumor immunity. M2-like macrophages may contribute to the immune tolerance of persister cancer cells against EGFR-TKI-induced tumor immunity. A clinical trial evaluating combined osimertinib and colony-stimulating factor-1 receptor inhibitor therapy is warranted for EGFR-mutated lung cancer.

    DOI： 10.1158/1535-7163.MCT-25-0002

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  • Endotracheal and Endobronchial Metastases in Epidermal Growth Factor Receptor Exon 19 Deletion Lung Adenocarcinoma: A Case Successfully Managed with Bronchoscopic Therapy and Sequential Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.

    Miho Fujiwara, Takahiro Baba, Kotaro Yamada, Eri Nakamura, Tetsuya Takeguchi, Yuki Takigawa, Ayako Morita, Naofumi Hara, Hiromi Watanabe, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Kadoaki Ohashi, Katsuyuki Hotta, Ken Sato, Yoshinobu Maeda, Yosuke Togashi, Go Makimoto

    Internal medicine (Tokyo, Japan)   2025年10月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Endotracheal and endobronchial metastases from peripheral lung adenocarcinoma are rare, and optimal clinical management remains unclear. We herein report a 60-year-old woman with epidermal growth factor receptor (EGFR) exon 19 deletion-positive early-stage lung adenocarcinoma who underwent surgical resection followed by osimertinib treatment for recurrence. She later developed oligoprogressive disease with airway metastases. Bronchoscopic tumor removal was performed, and next-generation sequencing of the resected specimen revealed an acquired EGFR C797S mutation, along with exon 19 deletion. Gefitinib treatment was initiated, which led to a partial response. This case underscores the utility of repeated molecular profiling and local intervention in managing acquired resistance in EGFR-mutant non-small-cell lung cancer.

    DOI： 10.2169/internalmedicine.6220-25

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  • Efficacy of amivantamab, a bi-specific antibody targeting EGFR and MET, in ALK-rearranged non-small-cell lung cancer cell lines. 国際誌

    Tatsuya Nishi, Ayako Morita, Naofumi Hara, Go Makimoto, Kiichiro Ninomiya, Masanori Fujii, Kammei Rai, Kadoaki Ohashi, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Eiki Ichihara

    Lung cancer (Amsterdam, Netherlands)   201   108415 - 108415   2025年3月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    BACKGROUND: Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) are highly effective in treating ALK-rearranged non-small-cell lung cancer (NSCLC). However, at least 40% of patients develop acquired resistance during treatment. Adaptive or acquired resistance to ALK TKIs could be mediated through epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET) signaling. Sixteen percent of acquired resistance cases are linked to bypass signaling. METHODS: In this study, we evaluated the effects of amivantamab, a bi-specific antibody targeting both EGFR and MET, on ALK-rearranged NSCLC cells. We investigated the effect of amivantamab on the ALK-rearranged NSCLC cell lines H3122, ABC-19, and ABC-11. RESULTS: Combining alectinib with amivantamab resulted in greater inhibition of cell growth inhibition in H3122 and ABC-19 cells compared to alectinib alone, but not in ABC-11 cells. EGFR TKI erlotinib showed similar efficacy in H3122 and ABC-19 cells, whereas MET TKI tepotinib was ineffective in both, suggesting that the efficacy of amivantamab is through EGFR inhibition. Unlike H3122 and ABC-19 cells, ABC-11 cells were resistant to EGFR/MET signaling inhibition. Interestingly, amivantamab enhanced alectinib efficacy against ABC-11 cells in the presence of peripheral blood mononuclear cells (PBMCs), despite showing no effect alone without PBMCs, suggesting action through non-signal inhibitory mechanisms. Finally, we treated alectinib-resistant cellswith alectinib, with or without amivantamab, and found that amivantamab restored the sensitivity of these cells to alectinib. CONCLUSION: The bi-specific antibody amivantamab, which targets EGFR and MET, enhanced the efficacy of alectinib through both signal and non-signal inhibitory mechanisms in ALK-rearranged NSCLC cells.

    DOI： 10.1016/j.lungcan.2025.108415

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  • A randomized, open-label phase II study on the preventive effect of goshajinkigan against peripheral neuropathy induced by paclitaxel-containing chemotherapy: The OLCSG2101 study protocol. 国際誌

    Naoki Nakamura, Go Makimoto, Takaaki Tanaka, Yuka Kato, Isao Oze, Toshiyuki Kozuki, Toshihide Yokoyama, Hirohisa Ichikawa, Shoichi Kuyama, Naofumi Hara, Yoshinobu Maeda, Katsuyuki Hotta

    Respiratory investigation   62 ( 5 )   897 - 900   2024年9月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    BACKGROUND: Paclitaxel (PTX) is an essential cytotoxic anticancer agent and a standard treatment regimen component for various malignant tumors, including advanced unresectable non-small cell lung cancer, thymic cancer, and primary unknown cancers. However, chemotherapy-induced peripheral neuropathy (CIPN) caused by PTX is a significant adverse event that may lead to chemotherapy discontinuation and deterioration of the quality of life (QOL). Although treatment modalities such as goshajinkigan (GJG), pregabalin, and duloxetine are empirically utilized for CIPN, there is no established evidence for an agent as a preventive measure. We designed a randomized phase II trial (OLCSG2101) to investigate whether prophylactic GJG administration can prevent the onset of CIPN induced by PTX. METHODS: This study was designed as a two-arm, prospective, randomized, multicenter phase II trial. The patients will be randomly assigned to either the GJG prophylaxis arm (Arm A) or the GJG non-prophylaxis arm (Arm B), using cancer type (lung cancer or not) and age (<70 years or not) as adjustment factors. A total of 66 patients (33 in each arm) will be enrolled. DISCUSSION: The results of this study may contribute to better management of CIPN, which can enable the continuation of chemotherapy and maintenance of the patient's QOL. ETHICS AND DISSEMINATION: Ethical approval was obtained from the certified review board of Okayama University (approval no. CRB21-005) on September 28, 2021. Results will be published in peer-reviewed journals and presented at national and international conferences. TRIAL REGISTRATION: Japan Registry of Clinical Trials (registration number jRCTs061210047).

    DOI： 10.1016/j.resinv.2024.07.017

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  • CDK4/6 signaling attenuates the effect of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in EGFR-mutant non-small cell lung cancer

    Naofumi Hara, Eiki Ichihara, Hirohisa Kano, Chihiro Ando, Ayako Morita, Tatsuya Nishi, Sachi Okawa, Takamasa Nakasuka, Atsuko Hirabae, Masaya Abe, Noboru Asada, Kiichiro Ninomiya, Go Makimoto, Masanori Fujii, Toshio Kubo, Kadoaki Ohashi, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Translational Lung Cancer Research   12 ( 10 )   2098 - 2112   2023年10月

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    掲載種別：研究論文（学術雑誌）   出版者・発行元：AME Publishing Company  

    DOI： 10.21037/tlcr-23-99

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  • Efficacy of gilteritinib in comparison with alectinib for the treatment of ALK-rearranged non-small cell lung cancer. 国際誌

    Chihiro Ando, Eiki Ichihara, Tatsuya Nishi, Ayako Morita, Naofumi Hara, Kenji Takada, Takamasa Nakasuka, Hiromi Watanabe, Hirohisa Kano, Kazuya Nishii, Go Makimoto, Takumi Kondo, Kiichiro Ninomiya, Masanori Fujii, Toshio Kubo, Kadoaki Ohashi, Ken-Ichi Matsuoka, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Cancer science   114 ( 11 )   4343 - 4354   2023年9月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Gilteritinib is a multitarget tyrosine kinase inhibitor (TKI), approved for the treatment of FLT3-mutant acute myeloid leukemia, with a broad range of activity against several tyrosine kinases including anaplastic lymphoma kinase (ALK). This study investigated the efficacy of gilteritinib against ALK-rearranged non-small cell lung cancers (NSCLC). To this end, we assessed the effects of gilteritinib on cell proliferation, apoptosis, and acquired resistance responses in several ALK-rearranged NSCLC cell lines and mouse xenograft tumor models and compared its efficacy to alectinib, a standard ALK inhibitor. Gilteritinib was significantly more potent than alectinib, as it inhibited cell proliferation at a lower dose, with complete attenuation of growth observed in several ALK-rearranged NSCLC cell lines and no development of drug tolerance. Immunoblotting showed that gilteritinib strongly suppressed phosphorylated ALK and its downstream effectors, as well as mesenchymal-epithelial transition factor (MET) signaling. By comparison, MET signaling was enhanced in alectinib-treated cells. Furthermore, gilteritinib was found to more effectively abolish growth of ALK-rearranged NSCLC xenograft tumors, many of which completely receded. Interleukin-15 (IL-15) mRNA levels were elevated in gilteritinib-treated cells, together with a concomitant increase in the infiltration of tumors by natural killer (NK) cells, as assessed by immunohistochemistry. This suggests that IL-15 production along with NK cell infiltration may constitute components of the gilteritinib-mediated antitumor responses in ALK-rearranged NSCLCs. In conclusion, gilteritinib demonstrated significantly improved antitumor efficacy compared with alectinib against ALK-rearranged NSCLC cells, which can warrant its candidacy for use in anticancer regimens, after further examination in clinical trial settings.

    DOI： 10.1111/cas.15958

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  • Efficacy of immune checkpoint inhibitor monotherapy in elderly patients with non-small-cell lung cancer. 国際誌

    Toshio Kubo, Eiki Ichihara, Daijiro Harada, Koji Inoue, Keiichi Fujiwara, Sinobu Hosokawa, Daizo Kishino, Haruyuki Kawai, Nobuaki Ochi, Naohiro Oda, Naofumi Hara, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Respiratory investigation   61 ( 5 )   643 - 650   2023年9月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    BACKGROUND: Limited information on anticancer therapy for super-elderly patients with non-small-cell lung cancer is available. Immune checkpoint inhibitors offer long-term survival to elderly patients aged ≥65 years with non-small-cell lung cancer. However, the efficacy and safety of immune checkpoint inhibitors in more elderly patients are not well understood. METHODS: We retrospectively evaluated the efficacy and safety of immune checkpoint inhibitors in patients aged ≥85 years with advanced non-small-cell lung cancer at nine centers using the Okayama Lung Cancer Study Group-Immunotherapy Database. RESULTS: Among 531 patients who received immune checkpoint inhibitors, 16 were aged ≥85 years (median, 86.5 years; range, 85-93 years). Many had high programmed death-ligand 1 expression and received pembrolizumab as first-line therapy. The objective response rate, median progression-free survival, and median survival time were 25% (95% confidence interval: 1-49), 2.8 months (95% confidence interval: 1.7-4.5), and not reached (95% confidence interval: 4.7-not reached), respectively. Moreover, the 4-year overall survival rate was 60.8% (95% confidence interval: 29.3-81.7), and a long-lasting effect of immune checkpoint inhibitors was observed even in patients aged ≥85 years. The incidence of immune-related and grade ≥3 immune-related adverse events was 32% and 6%, respectively. CONCLUSIONS: The effect and toxicity of immune checkpoint inhibitors for patients aged ≥85 years were acceptable. Immune checkpoint inhibitors may be a treatment option for patients aged ≥85 years.

    DOI： 10.1016/j.resinv.2023.06.005

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  • VEGFR2 blockade augments the effects of tyrosine kinase inhibitors by inhibiting angiogenesis and oncogenic signaling in oncogene-driven non-small-cell lung cancers. 国際誌

    Hiromi Watanabe, Eiki Ichihara, Hiroe Kayatani, Go Makimoto, Kiichiro Ninomiya, Kazuya Nishii, Hisao Higo, Chihiro Ando, Sachi Okawa, Takamasa Nakasuka, Hirohisa Kano, Naofumi Hara, Atsuko Hirabae, Yuka Kato, Takashi Ninomiya, Toshio Kubo, Kammei Rai, Kadoaki Ohashi, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Cancer science   112 ( 5 )   1853 - 1864   2021年5月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    DOI： 10.1111/cas.14801

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  • Randomized study comparing mannitol with furosemide for the prevention of cisplatin-induced renal toxicity in non-small cell lung cancer: The OLCSG1406 trial. 国際誌

    Go Makimoto, Katsuyuki Hotta, Isao Oze, Kiichiro Ninomiya, Masamoto Nakanishi, Naofumi Hara, Hirohisa Kano, Hiromi Watanabe, Yusuke Hata, Kazuya Nishii, Takamasa Nakasuka, Junko Itano, Takashi Ninomiya, Toshio Kubo, Kadoaki Ohashi, Eiki Ichihara, Daisuke Minami, Akiko Sato, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Asia-Pacific journal of clinical oncology   17 ( 1 )   101 - 108   2021年2月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    AIM: Evidence is lacking on the best standard method for forced diuresis to prevent cisplatin-induced nephrotoxicity. We compared the cisplatin-induced nephrotoxicity prevention effect of furosemide or mannitol in patients with advanced non-small cell lung cancer. METHODS: Patients with advanced non-small cell lung cancer suitable to receive cisplatin-containing regimen were randomly assigned to receive furosemide or mannitol with appropriate hydration. The primary endpoint was the proportion of ≥ grade 1 serum creatinine elevation in the first cycle. RESULTS: The trial was terminated early with 44 (22 per arm) of the planned 66 patients because of slow accrual. Patients' characteristics were well balanced with median baseline creatinine clearance of 98.0 and 95.1 mL/min in the furosemide and mannitol arms, respectively. In the first cycle, two (9%) and four (18%) patients developed grade 1 creatinine elevation (P = .66), respectively, despite no ≥ grade 2 toxicity. The median times to develop the worst creatinine score were 10 and 8 days, respectively. For all cycles, median times to recover to grade 0 were 56 and 20 days, respectively. The furosemide arm was characterized by relatively high urine output after cisplatin administration (900 vs 550 mL/h), low frequency of unplanned additional hydration (14% vs 32%), and high incidence of hyponatremia (18% and 5%) compared with the mannitol arm. Both arms showed similar progression-free survival and overall survival. CONCLUSION: The preventive effect of the two forced diuretics on cisplatin-induced nephrotoxicity was not significantly different. However, the two diuretics have some distinct types of clinical presentations.

    DOI： 10.1111/ajco.13423

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  • Utility of immune checkpoint inhibitors in non-small-cell lung cancer patients with poor performance status. 国際誌

    Hirohisa Kano, Eiki Ichihara, Daijiro Harada, Koji Inoue, Hiroe Kayatani, Shinobu Hosokawa, Daizo Kishino, Kazuhiko Watanabe, Nobuaki Ochi, Naohiro Oda, Naofumi Hara, Kiichiro Ninomiya, Katsuyuki Hotta, Yoshinobu Maeda, Katsuyuki Kiura

    Cancer science   111 ( 10 )   3739 - 3746   2020年10月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    DOI： 10.1111/cas.14590

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  • Patients' preferences and perceptions of lung cancer treatment decision making: results from Okayama lung cancer study group trial 1406. 国際誌

    Go Makimoto, Katsuyuki Hotta, Isao Oze, Kiichiro Ninomiya, Masamoto Nakanishi, Naofumi Hara, Hirohisa Kano, Hiromi Watanabe, Yusuke Hata, Kazuya Nishii, Takamasa Nakasuka, Junko Itano, Takashi Ninomiya, Toshio Kubo, Kadoaki Ohashi, Eiki Ichihara, Daisuke Minami, Akiko Sato, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Acta oncologica (Stockholm, Sweden)   59 ( 3 )   324 - 328   2020年3月

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  • Efficacy of afatinib treatment for lung adenocarcinoma harboring exon 18 delE709_T710insD mutation. 国際誌

    Yoshitaka Iwamoto, Eiki Ichihara, Naofumi Hara, Takamasa Nakasuka, Chihiro Ando, Takahiro Umeno, Atsuko Hirabae, Yoshinobu Maeda, Katsuyuki Kiura

    Japanese journal of clinical oncology   49 ( 8 )   786 - 788   2019年8月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    DOI： 10.1093/jjco/hyz086

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  • Osimertinib Depletes EGFR T790M in the Spinal Fluid of Patients with Carcinomatous Meningitis of Lung Adenocarcinoma Harboring De Novo EGFR T790M. 国際誌

    Satoru Senoo, Kadoaki Ohashi, Kazuya Nishii, Naofumi Hara, Hirohisa Kano, Kiichiro Ninomiya, Yoshinobu Maeda, Katsuyuki Kiura

    Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer   13 ( 8 )   e140-e142 - E142   2018年8月

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MISC

  • 甲状腺がんの加療中に発症した,柴胡加竜骨牡蛎湯による薬剤性肺障害の一例

    北内真衣, 大森洋樹, 槇本剛, 高橋侑子, 森田絢子, 原尚史, 二宮貴一朗, 肥後寿夫, 藤井昌学, 頼冠名, 市原英基, 堀田勝幸, 宮原信明, 田端雅弘, 大橋圭明, 冨樫庸介, 冨樫庸介

    日本呼吸器学会誌(Web)   14   2025年

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  • Egfr改変肺癌マウスモデルを用いたpersisterがん細胞に対する根治的薬物療法の開発

    大川 祥, 大橋 圭明, 原 尚史, 西井 和也, 中須賀 崇匡, 平生 敦子, 安東 千裕, 狩野 裕久, 渡邉 洋美, 二宮 貴一朗, 加藤 有加, 久保 寿夫, 頼 冠名, 市原 英基, 堀田 勝幸, 田端 雅弘, 前田 嘉信, 木浦 勝行

    肺癌   60 ( 6 )   644 - 644   2020年10月

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    記述言語：日本語   出版者・発行元：(NPO)日本肺癌学会  

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  • Egfr改変肺癌マウスモデルを用いたEGFR-TKI、抗VEGFR-2抗体と抗PD-1抗体併用療法の検討

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