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research
Response of Merkel cell polyomavirus-positive Merkel cell carcinoma xenografts to a survivin inhibitor
Authors
A Guastafierro
A Kita
+54 more
Anna Guastafierro
AW Tolcher
B Kumar
BD Cheson
D Schrama
D Schrama
Daniel Normolle
EA Engels
F Lamers
G Giaccone
H Ahrens
H Feng
H Xie
I Prieto Muñoz
J Albores-Saavedra
J Cheng
J Kaae
J Li
K Yamanaka
KD Lewis
L Zhao
LD Shultz
Lindsay R. Dresang
M Agelli
M Heath
M Plummer
M Shuda
M Shuda
M Shuda
M Van Gele
M Veness
N Nakamura
NC Hodgson
Patrick S. Moore
PJ Allen
PW Harms
R Arora
R Houben
R Houben
Reety Arora
S Kuwamoto
Shou-Jiang Gao
ST Rosen
T Iwasa
T Nakahara
T Nakahara
T Nakahara
T Nakamura
T Satoh
T Yamauchi
TY Eng
Y Aoyama
Y Chang
Yuan Chang
Publication date
18 November 2013
Publisher
'Public Library of Science (PLoS)'
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PubMed
Abstract
Merkel cell carcinoma (MCC) is a neuroendocrine skin cancer associated with high mortality. Merkel cell polyomavirus (MCV), discovered in 2008, is associated with ∼80% of MCC. The MCV large tumor (LT) oncoprotein upregulates the cellular oncoprotein survivin through its conserved retinoblastoma protein-binding motif. We confirm here that YM155, a survivin suppressor, is cytotoxic to MCV-positive MCC cells in vitro at nanomolar levels. Mouse survival was significantly improved for NOD-Scid-Gamma mice treated with YM155 in a dose and duration dependent manner for 3 of 4 MCV-positive MCC xenografts. One MCV-positive MCC xenograft (MS-1) failed to significantly respond to YM155, which corresponds with in vitro dose-response activity. Combination treatment of YM155 with other chemotherapeutics resulted in additive but not synergistic cell killing of MCC cell lines in vitro. These results suggest that survivin targeting is a promising therapeutic approach for most but not all MCV-positive MCCs. © 2013 Dresang et al
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