Abstract |
While lung cancer is the leading cause of cancer deaths worldwide, the molecular mechanism underlying its carcinogenesis is mainly unknown. We have discovered a small, fusion-type tyrosine kinase EML4-ALK that is generated through a tiny inversion within the short arm of human chromosome 2. Transgenic mice expressing EML4-ALK in lung developed hundreds of lung cancer nodules soon after birth, but such nodules were readily eradicated upon treatment with an ALK inhibitor. Clinical trials for EML4-ALK-positive lung cancer with an ALK inhibitor is ongoing, with its interim results being highly promising.
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Authors | Hiroyuki Mano |
Journal | Gan to kagaku ryoho. Cancer & chemotherapy
(Gan To Kagaku Ryoho)
Vol. 38
Issue 1
Pg. 27-30
(Jan 2011)
ISSN: 0385-0684 [Print] Japan |
PMID | 21368458
(Publication Type: Journal Article)
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Chemical References |
- EML4-ALK fusion protein, human
- Oncogene Proteins, Fusion
- Protein Kinase Inhibitors
- ALK protein, human
- Alk protein, mouse
- Anaplastic Lymphoma Kinase
- Protein-Tyrosine Kinases
- Receptor Protein-Tyrosine Kinases
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Topics |
- Anaplastic Lymphoma Kinase
- Animals
- Humans
- Lung Neoplasms
(drug therapy, enzymology, genetics)
- Molecular Targeted Therapy
- Oncogene Proteins, Fusion
(genetics, metabolism)
- Protein Kinase Inhibitors
(therapeutic use)
- Protein-Tyrosine Kinases
(antagonists & inhibitors, genetics, metabolism)
- Receptor Protein-Tyrosine Kinases
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