Targeted inhibition in tumors with ALK dependency
Eunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: The oncogenic function of gene translocations involving the anaplastic lymphoma kinase (ALK) was first reported in rare subtypes of non-Hodgkin's lymphoma almost two decades...
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Dove Medical Press
2013
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oai:doaj.org-article:47647a89cdb9463a8e88b0b7ed4428452021-12-02T00:04:56ZTargeted inhibition in tumors with ALK dependency1179-2728https://doaj.org/article/47647a89cdb9463a8e88b0b7ed4428452013-01-01T00:00:00Zhttp://www.dovepress.com/targeted-inhibition-in-tumors-with-alk-dependency-a11914https://doaj.org/toc/1179-2728Eunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: The oncogenic function of gene translocations involving the anaplastic lymphoma kinase (ALK) was first reported in rare subtypes of non-Hodgkin's lymphoma almost two decades ago. More recently, aberrant ALK signaling was found to be an oncogenic driver in subsets of non-small cell lung cancer (NSCLC), particularly in patients with little or no tobacco smoking history. The advent of molecularly targeted therapies that inhibit ALK has allowed the pairing of ALK inhibitors such as crizotinib as treatment for ALK-positive NSCLC, yielding dramatic responses and long-term disease control. The clinicopathologic features of ALK-driven NSCLC, the clinical development of ALK inhibitors, and the genetic determinants of acquired resistance to ALK inhibition are among the topics covered in this review.Keywords: targeted inhibition, tumors, ALK dependencyKwak ELClark JWShaw ATDove Medical PressarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENLung Cancer: Targets and Therapy, Vol 2013, Iss default, Pp 1-8 (2013) |
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DOAJ |
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DOAJ |
| language |
EN |
| topic |
Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 |
| spellingShingle |
Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Kwak EL Clark JW Shaw AT Targeted inhibition in tumors with ALK dependency |
| description |
Eunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: The oncogenic function of gene translocations involving the anaplastic lymphoma kinase (ALK) was first reported in rare subtypes of non-Hodgkin's lymphoma almost two decades ago. More recently, aberrant ALK signaling was found to be an oncogenic driver in subsets of non-small cell lung cancer (NSCLC), particularly in patients with little or no tobacco smoking history. The advent of molecularly targeted therapies that inhibit ALK has allowed the pairing of ALK inhibitors such as crizotinib as treatment for ALK-positive NSCLC, yielding dramatic responses and long-term disease control. The clinicopathologic features of ALK-driven NSCLC, the clinical development of ALK inhibitors, and the genetic determinants of acquired resistance to ALK inhibition are among the topics covered in this review.Keywords: targeted inhibition, tumors, ALK dependency |
| format |
article |
| author |
Kwak EL Clark JW Shaw AT |
| author_facet |
Kwak EL Clark JW Shaw AT |
| author_sort |
Kwak EL |
| title |
Targeted inhibition in tumors with ALK dependency |
| title_short |
Targeted inhibition in tumors with ALK dependency |
| title_full |
Targeted inhibition in tumors with ALK dependency |
| title_fullStr |
Targeted inhibition in tumors with ALK dependency |
| title_full_unstemmed |
Targeted inhibition in tumors with ALK dependency |
| title_sort |
targeted inhibition in tumors with alk dependency |
| publisher |
Dove Medical Press |
| publishDate |
2013 |
| url |
https://doaj.org/article/47647a89cdb9463a8e88b0b7ed442845 |
| work_keys_str_mv |
AT kwakel targetedinhibitionintumorswithalkdependency AT clarkjw targetedinhibitionintumorswithalkdependency AT shawat targetedinhibitionintumorswithalkdependency |
| _version_ |
1718403924311932928 |