Immunohistochemical study of VEGF-A, VEGFR-1, VEGFR-2 and CD34 expression in сolorectal adenocarcinoma progression

Abstract

Aim – to study VEGF-A, VEGFR-1, VEGFR-2 and CD34 immunohistochemical expression on the I, II, III, IV stages (pTNM) of colorectal adenocarcinoma development.Materials and methods. Pathomorphological and immunohistochemical studies of surgical material of colorectal adenocarcinoma (CRA) from 40 patients (I, II, III and IV stages, 10 cases in each group) were conducted.Results. There is a tendency to increasing expression of VEGF-A and VEGFR-2 during the CRA progression from I to IV stage (VEGF-A 37.80 (30.22; 56.89) CUOD on I stage, 88.50 (63.00 ; 115.00) CUOD on II stage, 79.34 (63.14; 84.99) CUOD on III stage, 84.69 (80.66; 110.28) CUOD on IV stage; VEGFR-2 – 52.75 (39.14; 70.22) CUOD on I stage, 82.71 (63.14; 111.19) CUOD on II stage, 104.17 (96.04; 111.02) CUOD on III stage, 99.91 (86.15; 120.29) CUOD on IV stage). The expression indices of these markers correlate in CRA stages I, II and III (r = 0.95, r = 0.69, r = 0.85). It is established that VEGFR-1 is not expressed in unchanged mucous membrane of the large intestine, as well as in samples of CRA stage I. On subsequent II, III and IV stages of CRA progresson the marker is expressed by stromal cells, but there is an absence of statistically significant difference between the expression indices. There are no correlations between expression indices of VEGFR-1 and other studied markers. The microvascular density assessed by CD34 expression is not significantly different on each of CRA progression stages. There are direct correlations between microvascular density and VEGF-A expression (r = 0.70), and VEGFR-2 expression (r = 0.69) in CRA III stage, microvascular density and VEGF-A expression in CRA IV stage (r = 0.69).Conclusions. Expression of VEGF-A and VEGFR-2 increases with the progression of colorectal adenocarcinoma from stage I to stage IV, with a maximum “jump” of the expression levels from stage I to stage II of colorectal adenocarcinoma, which may be due to abnormally increasing KRAS activity.