Identification of Targetable ALK Rearrangements in Pancreatic Ductal Adenocarcinoma
| Autor: | Anil K. Dasyam, Inderpal S. Sarkaria, Siraj M. Ali, Jeffrey S. Ross, Khanh Nguyen, Jon Chung, Marina N. Nikiforova, Jill Lacy, Nathan Bahary, Jamie Koo, Andrew Eugene Hendifar, Aatur D. Singhi, Herbert J. Zeh, Joel R. Greenbowe |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Oncology medicine.medical_specialty endocrine system diseases medicine.drug_class Chromosomal translocation medicine.disease_cause Fusion gene 03 medical and health sciences Exon 0302 clinical medicine hemic and lymphatic diseases Internal medicine medicine Carcinoma Anaplastic lymphoma kinase business.industry Gene rearrangement medicine.disease digestive system diseases ALK inhibitor 030104 developmental biology 030220 oncology & carcinogenesis KRAS business |
| Zdroj: | Journal of the National Comprehensive Cancer Network. 15:555-562 |
| ISSN: | 1540-1413 1540-1405 |
| Popis: | Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, with a 5-year survival of 8%. Current therapeutic regimens are largely ineffective and underscore the need for novel treatment strategies. Chromosomal rearrangements involving the anaplastic lymphoma kinase (ALK) gene have been identified in several neoplasms. In addition, ALK protein inhibitors have proven efficacy in patients with ALK-rearranged tumors. However, ALK translocations in PDAC have not been described. Through comprehensive genomic profiling of 3,170 PDACs, we identified 5 cases (0.16%) that harbored an ALK fusion gene: an exon 6 EML4-exon 20 ALK translocation (n=3), an exon 13 EML4-exon 20 ALK translocation (n=1), and an exon 3 STRN-exon 20 ALK translocation (n=1). Among the most prevalent PDAC-related genes, activating KRAS mutations were absent in all 5 cases, who were |
| Databáze: | OpenAIRE |
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