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Immunohistochemical evaluation of pRb2/p130, VEGF, EZH2, p53, p16, p21waf-1, p27, and PCNA in Barrett's esophagus

✍ Scribed by Elettra Merola; Eliseo Mattioli; Corrado Minimo; Weineng Zuo; Carla Rabitti; Michele Cicala; Renato Caviglia; Lucio Pollice; Armando Gabbrielli; Antonio Giordano; Pier Paolo Claudio


Publisher
John Wiley and Sons
Year
2006
Tongue
English
Weight
486 KB
Volume
207
Category
Article
ISSN
0021-9541

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✦ Synopsis


Abstract

Control of the G1/S‐phase transition as well as angiogenic switch are two of the most studied mechanisms in cancer. The current study examined the correlation between the immunohistochemical expression of pRb2/p130, VEGF, EZH2, p53, p16, p21^waf‐1^, p27, and PCNA in Barrett's esophagus (BE). Overall, p53 showed a much higher expression in BE patients (up to 50%) than in controls (1–10%) (P < 0.005). Also p21 showed a downregulation in BE when compared to normal esophagus (70% of cells vs. 65%), but the difference did not show any statistical significance (P = 0.45). pRb2/p130 was detected in 80% of cells in normal controls, but showed positive in only 20% of cells in BE biopsies. Additionally, Rb2/p130 expression was inversely correlated to that of VEGF, EZH2, and PCNA (P < 0.0001, P = 0.0032, P < 0.001, respectively). p27 stained more intensely and in a widespread manner (70%) cells in normal esophageal tissues but about only 30% in BE samples (P < 0.001). Lastly, in accordance with other reports, we also found p16 expressed by immunohistochemistry at high levels in normal controls and at low levels in BE (P < 0.001). In conclusion, p16, p21, p27, and p53 staining confirmed previously published data. Interestingly, pRb2/p130 expression was found significantly decreased in metaplastic epithelium compared to normal controls and showed significant inverse correlation with the expression of other markers, such as VEGF, EZH2, and PCNA. These data, taken together, indicate that these molecular events occurring in Barrett's metaplasia (BM) may represent one of the many steps taking place during esophageal malignant progression such as impairment of cell‐cycle control, altered differentiation, and unbalanced angiogenesis. J. Cell. Physiol. 207: 512–519, 2006. Β© 2006 Wiley‐Liss, Inc.


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## Abstract Although the considerable progress against gastric cancer, it remains a complex lethal disease defined by peculiar histological and molecular features. The purpose of the present study was to investigate pRb2/p130, VEGF, EZH2, p53, p16^INK4A^, p27^KIP1^, p21^WAF1^, Ki‐67 expressions, an