Quick Search:

uzh logo
Browse by:
bullet
bullet
bullet
bullet

Zurich Open Repository and Archive

Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-48819

Zipser, M C; Eichhoff, O M; Widmer, D S; Schlegel, N C; Schoenewolf, N L; Stuart, D; Liu, W; Gardner, H; Smith, P D; Nuciforo, P; Dummer, R; Hoek, K S (2011). A proliferative melanoma cell phenotype is responsive to RAF/MEK inhibition independent of BRAF mutation status. Pigment Cell & Melanoma Research, 24(2):326-333.

[img]Published Version
PDF - Registered users only
1MB

View at publisher

Abstract

Oncogenic mutations within the MAPK pathway are frequent in melanoma, and targeting of MAPK signaling has yielded spectacular responses in a significant number of patients that last for several months before relapsing. We investigated the effects of two different inhibitors of MAPK signaling in proliferative and invasive melanoma cell cultures with various mutations in the MAPK pathway. Proliferative melanoma cells were more susceptible to pathway inhibition than invasive phenotype cells, irrespective of BRAF mutation status, while invasive phenotype cell response was dependent on BRAF mutation status. Critically, MAPK pathway inhibition of proliferative phenotype cells resulted in acquisition of invasive phenotype characteristics. These results show that melanoma cell phenotype is an important factor in MAPK pathway inhibition response. This suggests that while current therapeutic strategies target proliferative melanoma cells, future approaches should also account for the invasive phenotype population.

Citations

12 citations in Web of Science®
14 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

2 downloads since deposited on 27 Jul 2011
0 downloads since 12 months

Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
DDC:610 Medicine & health
Language:English
Date:2011
Deposited On:27 Jul 2011 13:08
Last Modified:27 Nov 2013 22:24
Publisher:Wiley-Blackwell
ISSN:1755-1471
Publisher DOI:10.1111/j.1755-148X.2010.00823.x
PubMed ID:21176117

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page