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- Anh T. Le
- Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado.
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- Robert C. Doebele
- Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado.
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- Aria Vaishnavi
- Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado.
書誌事項
- 公開日
- 2015-01-01
- DOI
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- 10.1158/2159-8290.cd-14-0765
- 公開者
- American Association for Cancer Research (AACR)
この論文をさがす
説明
<jats:title>Abstract</jats:title> <jats:p>The use of high-throughput next-generation sequencing techniques in multiple tumor types during the last few years has identified NTRK1, 2, and 3 gene rearrangements encoding novel oncogenic fusions in 19 different tumor types to date. These recent developments have led us to revisit an old oncogene, Trk (originally identified as OncD), which encodes the TPM3–NTRK1 gene fusion and was one of the first transforming chromosomal rearrangements identified 32 years ago. However, no drug has yet been approved by the FDA for cancers harboring this oncogene. This review will discuss the biology of the TRK family of receptors, their role in human cancer, the types of oncogenic alterations, and drugs that are currently in development for this family of oncogene targets.</jats:p> <jats:p>Significance: Precision oncology approaches have accelerated recently due to advancements in our ability to detect oncogenic mutations in tumor samples. Oncogenic alterations, most commonly gene fusions, have now been detected for the genes encoding the TRKA, TRKB, and TRKC receptor tyrosine kinases across multiple tumor types. The scientific rationale for the targeting of the TRK oncogene family will be discussed here. Cancer Discov; 5(1); 25–34. ©2014 AACR.</jats:p>
収録刊行物
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- Cancer Discovery
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Cancer Discovery 5 (1), 25-34, 2015-01-01
American Association for Cancer Research (AACR)
