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Hypoxia, metabolism, and growth factor signaling in head and neck squamous cell carcinoma: Correlation between primary and xenograft tumors
Author(s) -
Stegeman Hanneke,
Rademakers Saskia E.,
Span Paul N.,
Takes Robert P.,
Kogel Albert J.,
Kaanders Johannes H.A.M.,
Bussink Johan
Publication year - 2014
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.23446
Subject(s) - head and neck squamous cell carcinoma , hypoxia (environmental) , epidermal growth factor receptor , cancer research , primary tumor , glucose transporter , biology , carcinoma , tumor hypoxia , pathology , medicine , head and neck cancer , chemistry , cancer , metastasis , radiation therapy , organic chemistry , oxygen , insulin
Background Hypoxia, metabolism, and growth factor signaling are important prognostic features in most solid tumors. The purpose of this study was to determine whether head and neck squamous cell carcinoma (HNSCC) xenografts show similar biological and molecular characteristics as the primary tumor they originate from. Methods Eighteen HNSCC primary tumor‐xenograft pairs were immunofluorescently stained for pimonidazole (hypoxia), carbonic anhydrase IX (CAIX), glucose transporter‐1 (GLUT‐1), monocarboxylate transporter‐1 (MCT‐1), monocarboxylate transporter‐4 (MCT‐4), epidermal growth factor receptor (EGFR), and phosphorylated protein kinase B (pAKT). Results Although no correlation was found for the amount of hypoxia, significant correlations between primary tumors and xenografts were observed for both the percentage of cells positive for expression and the hypoxia‐related expression pattern of CAIX, GLUT‐1, and MCT‐1. For EGFR and MCT‐4, the intensity of expression was correlated. No correlation was observed for pAKT. Conclusion Xenografts did not always resemble the primary tumor they originate from, but the xenografts did represent the variability in expression levels and patterns observed in the primary tumors. © 2013 Wiley Periodicals, Inc. Head Neck 36: 1288–1295, 2014