%0 Journal Article
%T EGFR protein overexpression correlates with chromosome 7 polysomy and poor prognostic parameters in clear cell renal cell carcinoma
%A Gordana £¿or£¿evi£¿
%A Koviljka Matu£¿an Ilija£¿
%A Ita Had£¿isejdi£¿
%A Anton Mari£¿i£¿
%A Bla£¿enka Grahovac
%A Nives Jonji£¿
%J Journal of Biomedical Science
%D 2012
%I BioMed Central
%R 10.1186/1423-0127-19-40
%X The protein EGFR expression was analyzed immunohistochemically on 94 CCRCC, and gene copy number alterations of EGFR by FISH analysis on 41 CCRCC selected according to distinct membrane EGFR staining.Membrane EGFR expression in tumor cells was heterogeneous with respect to the proportion of positive cells and staining intensity. FISH analysis did not reveal EGFR gene amplification, while polysomy of chromosome 7 found in 41% was associated with higher EGFR membrane expression. Moreover, EGFR overexpression was associated with a higher nuclear grade, larger tumor size and shorter patient's survival, while there was no connection with pathological stage.In conclusion, the protein expression of EGFR had an impact on prognosis in patients with CCRCC, while an increased copy number of chromosome 7 could be the possible reason for EGFR protein overexpression in the absence of gene amplification.The role of growth factors in the pathogenesis and progression of various malignant tumors has long been known [1-3]. Among them, epidermal growth factor (EGF) and its receptor (EGFR) play a central role. Specific ligands, EGF and related growth factors such as TGF ¦Á, ampiregulin, betacellulin, neuregulins, epiregulin and heparin binding growth factor bind to the extracellular domain of EGFR resulting in receptor conformational change. This structural change allows for receptor dimerization and autophosphorylation of tyrosine kinase residues within the intracellular domain leading to activation of the signal transduction pathways. EGFR tyrosine phosphorylation triggers several signaling cascades, including the RAS-MAPK, PI3K-Akt and STAT pathways. Together, these EGFR-induced signaling pathways control gene transcription, cell cycle progression, cell proliferation and survival, adhesion, angiogenesis, migration, and invasion [4].EGFR may be deregulated following point mutations occurring in the tyrosine kinase (TK) domain or protein overexpression. Both mechanisms can constitutivel
%K Carcinoma
%K Renal cell
%K Chromosome 7
%K EGFR
%K In Situ Hybridization
%K Fluorescence
%K Prognosis
%U http://www.jbiomedsci.com/content/19/1/40