BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors.

@article{Banerji2008BRAFAN,
  title={BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors.},
  author={Udai Banerji and Annette Affolter and Ian Judson and Richard Marais and Paul Workman},
  journal={Molecular cancer therapeutics},
  year={2008},
  volume={7 4},
  pages={737-9}
}
Oncogenic BRAF and NRAS mutations are frequent in malignant melanoma. BRAF that is activated by the common V600E and other mutations, as well as by upstream NRAS mutations, has been shown to require the molecular chaperone heat shock protein 90 (HSP90) for stabilization and is depleted by the HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG)]. Here, we explore the possible relationship between tumor BRAF and NRAS mutations and clinical response to 17-AAG in six patients with… CONTINUE READING

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Phase I trial of 17allylamino17demethoxygeldanamycin in patients with advanced cancer

  • DB Solit, SP Ivy, C Kopil
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