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<Review> Driver oncogene mutations and personalized treatment of lung cancer
https://kindai.repo.nii.ac.jp/records/10555
https://kindai.repo.nii.ac.jp/records/10555cfd9ee1d-90c7-4a33-8332-c0b558ab79b8
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AA0050842X-20130600-0007.pdf (4.3 MB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2013-09-16 | |||||||||
| タイトル | ||||||||||
| タイトル | <Review> Driver oncogene mutations and personalized treatment of lung cancer | |||||||||
| 言語 | en | |||||||||
| 著者 |
Mitsudomi, Tetsuya
× Mitsudomi, Tetsuya
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| 言語 | ||||||||||
| 言語 | eng | |||||||||
| キーワード | ||||||||||
| 主題 | targeted therapy, oncogene addiction | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 著者 所属 | ||||||||||
| 値 | Division of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine | |||||||||
| 著者所属(翻訳) | ||||||||||
| 値 | 近畿大学医学部 | |||||||||
| 版 | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | The Kinki University Medical Association | |||||||||
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY 巻 38, 号 1, p. 7-24, 発行日 2013-06-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 03866092 | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | [Abstract] Discovery of activating mutation of the EGFR gene in 2004 opened the era of personalized therapy in thoracic oncology. These tumors are highly dependent on the EGFR pathway and inhibition of this pathway results in dramatic induction of apoptosis in vitro, even though cancer cells may have various genetic alterations (oncogene addiction). These observations were soon translated into clinical trials, which reproducibly showed significantly longer progression free survival for those treated with EGFR-tyrosine kinase inhibitors (TKI) than those treated with platinum doublet chemotherapy in patients with lung cancer harboring EGFR mutation. In 2007, it was found that —5％ of adenocarcinoma of the lung harbors EML4- ALK translocation and that these tumors are also addicted to the ALK pathway. We have learned how effective the targeted therapy is, when "addicted oncogene" is pharmacologically inhibited. List of addicted oncogenes is expanding continuously and now it includes HER2, ROS1 or RET in adenocarcinoma of the lung.Efforts are also being made to identify addicted oncogenes in squamous cell carcinoma. These continued efforts for personalization of lung cancer treatment would further improve patient outcome. However, even in patients with a dramatic initial response in these addicted tumors, resistance almost inevitably develops typically after less than one year. Mechanisms of the resistance include secondary mutations of the targeted gene and activation of alternative pathways. To develop effective treatment against the acquired resistance, extensive efforts are being made worldwide. At the dawn of personalized medicine of lung cancer, there is a great need for all patients with lung cancer to have a multimodality, team-based treatment approach to assist decision making. This close collaboration will allow personalized therapeutic approaches to lung cancer treatment to help convert this fatal disease into a more-chronic disorder, and eventually cure it. | |||||||||
| フォーマット | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | application/pdf | |||||||||
