Merkel Cell Carcinoma Expresses Vasculogenic Mimicry: Demonstration in Patients and Experimental Manipulation in Xenografts

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Merkel Cell Carcinoma Expresses Vasculogenic Mimicry: Demonstration in Patients and Experimental Manipulation in Xenografts

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Title: Merkel Cell Carcinoma Expresses Vasculogenic Mimicry: Demonstration in Patients and Experimental Manipulation in Xenografts
Author: Lezcano, Cecilia; Kleffel, Sonja; Lee, Nayoung; Larson, Allison R.; Zhan, Qian; DoRosario, Andrew; Wang, Linda C.; Schatton, Tobias; Murphy, George F.

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Citation: Lezcano, Cecilia, Sonja Kleffel, Nayoung Lee, Allison R. Larson, Qian Zhan, Andrew DoRosario, Linda C. Wang, Tobias Schatton, and George F. Murphy. 2014. “Merkel Cell Carcinoma Expresses Vasculogenic Mimicry: Demonstration in Patients and Experimental Manipulation in Xenografts.” Laboratory investigation; a journal of technical methods and pathology 94 (10): 1092-1102. doi:10.1038/labinvest.2014.99. http://dx.doi.org/10.1038/labinvest.2014.99.
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Abstract: Merkel cell carcinoma (MCC) is a highly virulent cutaneous neoplasm that, like melanoma, is a frequent cause of patient morbidity and mortality. The cellular mechanisms responsible for the aggressive behavior of MCC remain unknown. Vasculogenic mimicry (VM) is a phenomenon associated with cancer virulence, including in melanoma, whereby anastomosing laminin networks form in association with tumor cells that express certain endothelial genes. To determine whether VM is a factor in MCC, we employed a relevant xenograft model using two independent human MCC lines. Experimentally induced tumors were remarkably similar histologically to patient MCC, and both contained laminin networks associated with vascular endothelial-cadherin (CD144) and vascular endothelial growth factor receptor 1 (VEGFR-1) as well as Nodal expression typical of VM in melanoma. Moreover, two established chemotherapeutic agents utilized for human MCC, etoposide and carboplatin, induced necrosis in xenografts upon systemic administration while enriching for laminin networks in apparently resistant viable tumor regions that persisted. These findings for the first time establish VM-like laminin networks as a biomarker in MCC, demonstrate the experimental utility of the MCC xenograft model, and suggest that VM-rich regions of MCC may be refractory to conventional chemotherapeutic agents.
Published Version: doi:10.1038/labinvest.2014.99
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236190/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:15034897
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