Premium
Immunohistochemical and molecular analysis of PI3K/ AKT /m TOR pathway in esophageal carcinoma
Author(s) -
Tasioudi Konstantia E.,
Sakellariou Stratigoula,
Levidou Georgia,
Theodorou Dimitrios,
Michalopoulos Nikolaos V.,
Patsouris Efstratios,
Korkolopoulou Penelope,
Saetta Angelica A.
Publication year - 2015
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12398
Subject(s) - immunohistochemistry , pi3k/akt/mtor pathway , carcinoma , chemistry , cancer research , biology , microbiology and biotechnology , pathology , medicine , signal transduction , biochemistry
Among the numerous signaling pathways involved in tumorigenesis, PI3K‐ AKT ‐m TOR is a key one that regulates diverse cellular functions. However, its prognostic value in esophageal carcinoma remains unclear. In our study, we examined the immunohistochemical expression of phosphorylated (p‐) AKT , m TOR , p70S6K and 4E‐BP1 along with the mutational status of PIK 3CA and AKT 1 genes by High Resolution Melting Analysis and Pyrosequencing in 44 esophageal carcinomas. The results were correlated with the clinicopathological characteristics of the patients in an effort to define their possible prognostic significance. Total p‐m TOR cytoplasmic expression, assessed in 10 random areas, was positively correlated with tumor stage (Kruskal–Wallis ANOVA, I/II vs III/IV, p = 0.0500). Μoreover, maximum p‐mTOR cytoplasmic immunoexpression, estimated in hot spot areas, was positively associated with tumor grade (Mann–Whitney U test, I/II vs III, p = 0.0565). Interestingly, p‐4E‐BP1 immunoreactivity was negatively correlated with tumor histological grade (Mann–Whitney U test, I/II vs III, p = 0.0427). No mutation was observed in exons 9 and 20 of PIK 3CA gene and in exon 4 of AKT 1 gene. In conclusion, our findings depict the presence of activated PI3K/ AKT /m TOR pathway in esophageal cancer bringing forward p‐m TOR and p‐4E‐BP1 for their potential role in esophageal carcinogenesis. Additional studies are warranted to validate our findings.