| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5888257 | Experimental and Molecular Pathology | 2013 | 5 Pages |
Abstract
Intratumoral heterogeneity of KRAS mutational status is rare in NSCLC but highly sensitive tools are required to reliably identify these mutations. This finding is in line with the hypothesis that oncogenic activation of KRAS is an early event and a bona fide “driver mutation” in NSCLC. Furthermore, future therapies targeting KRAS will not be limited by intratumoral heterogeneity.
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Authors
Winfried H. Alsdorf, Till S. Clauditz, Tobias Hoenig, Alexander Quaas, Hüseyin Sirma, Alexandra M. Koenig, Jakob Izbicki, Guido Sauter, Andreas H. Marx, Tobias J. Grob,