Hypoxia related growth factors and p53 in preoperative sera from patients with colorectal cancer – evaluation of the prognostic significance of these agents
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Stanislaw Sulkowski
, Andrzej Wincewicz , Bogdan Zalewski , Waldemar Famulski , Joanna Maria Lotowska , Mariusz Koda , Maria Elzbieta Sobaniec-Lotowska , Michal Mysliwiec , Marek Baltaziak , Krystyna Pawlak and Mariola Sulkowska
Abstract
Background: Insulin-like growth factor-I (IGF-I) and vascular endothelial growth factor (VEGF) belong to a group of hypoxia related proteins. IGF-I induces expression of VEGF and decomposes wild type p53 in cancer cell lines. The goal of our study was to evaluate serum IGF-I, VEGF and p53 with respect to overall and disease free survival of patients with colorectal cancer (CRC) patients compared with healthy volunteers.
Methods: Preoperative blood samples from 125 patients with CRC and 16 healthy volunteers were examined using ELISA for serum IGF-I, p53 and VEGF concentrations.
Results: Concentrations of p53 and VEGF were significantly higher in CRC patients than in controls (p<0.0006 and p<0.0001, respectively). IGF-I was not statistically different between both groups. Serum IGF-I showed negative correlation with p53 in CRC patients (p<0.04, r=−0.193). IGF-I and VEGF showed negative correlation in poorly differentiated cancers (G3) (p<0.03, r=−0.339). Patients with VEGF concentrations that were above average for the cancer population survived for a shorter period of time (p=0.065 in evaluation of overall survival and 0.071 in estimation of disease-free survival during a 3-year follow-up) compared with patients with serum VEGF lower than the highest values seen in controls.
Conclusions: Comparisons between serum IGF-I and p53 appear to confirm the metabolism of p53 by IGF-I. Serum VEGF showed prognostic significance in our study. Serum concentrations of IGF-I and VEGF did not show positive correlation, as expected due to IGF-I induction of VEGF in malignant colon cell lines.
Clin Chem Lab Med 2009;47:1439–45.
©2009 by Walter de Gruyter Berlin New York
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