3 - Role of Immunohistochemical Expression of p53 and Vascular Endothelial Growth Factor in Gastric Carcinoma

This chapter describes the technique for immunohistochemical detection of p53 and vascular endothelial growth factors (VEGF) in gastric carcinomas and the possible role of their expression, as prognostic factors of survival, recurrence, and response to treatments. TP53 is the most commonly mutated gene in human tumors. TP53 encodes for a nuclear protein that plays a key role in tumor progression, by regulating deoxyribonucleic acid (DNA) repair, cell division, and apoptosis. The gene spans 20 Kb of genomic DNA located at 17p13 contains 11 exons and encodes a 53-kd phosphoprotein that is a transcription factor for genes that induce cell cycle arrest or apoptosis. The p53 is also a genomic stabilizer and an inhibitor of angiogenesis. More than 50% of human cancers contain mutations in p53 and these mutations can affect the angiogenic balance. The result of the mutational inactivation of TP53, by single-amino-acid substitutions, is that many tumor cells retain the ability to express the mutant p53 protein. These proteins are often more stable than the wild-type p53 and are present at very high levels in the tumor cell.