Journal of Molecular Biomarkers and Clinical Trials

In Non-Small Cell Lung Carcinomas, 18f-Fdg Suvmax Values are Independent of P63 Immunohistochemical Expression

*Dr. Pablo Aguiar
Department Of Medicine, IDIS And Molecular Imaging Group, University Hospital Santiago Compostela, Spain

*Corresponding Author:
Dr. Pablo Aguiar
Department Of Medicine, IDIS And Molecular Imaging Group, University Hospital Santiago Compostela, Spain
Email:pablo.aguiar.fernandez@sergas.es

Published on: 2016-07-20

Abstract

Objective: to study the possible relation between immunohistochemical expression of p63 and the maximum standardised uptake value (max SUV) of 18F-FDG PET in patients with non-small cell lung cancer (NSCLC) Material and Methods: The study group included 49 patients (42 males), ranged between 41 to 82 years old with pretreatment NSCLC (26 squamous, 15 adenocarcinomas and 8 large cell carcinomas) of whom the diagnosis was found in our centre. According to the clinical stage the classification was the following: 2 IA, 9 IB, 1 IIA, 5 IIB, 9 IIIA, 10 IIIB and 13 IV. Immunohistochemical expression of p63 was studied through the technique of tissue-matrix using Tissue Arrayer Device (Beecher Instruments, Sun Prairie, WI), using the Mab Clone 4A4 from Dako (Denmark). Results: Positive p63 immunohistochemical expression was more frequent (p:0,0007) in squamous cell carcinomas (21/26; 80,7%) than in adenocarcinomas (2/15; 13,3 %), but not than in large cell carcinomas (4/8; 50%). There were not statistically significant differences on SuV max values in the patients classified according to p63 expression. The same findings were noted using different maxSuV qualitative cut-offs. When we considered exclusively the squamous cell carcinomas, we didn’t observe statistically significant differences between the maxSuV values (qualitative and quantitative) of patients classified according to p63 expression also. Conclusions: These results led us to consider that SuV max values are not correlated with immunohistochemical expression of p63 neither in patients with NSCLC considered as a whole nor in squamous cell carcinoma subtype, strong related to p63.

Keywords

p63, Non-Small Cell Carcinomas, maxSuV-18F-FDG-PET

Introduction

P63 is a member of p53 family [1] , mapping to 3q27 and it is deregulated in a broader range of tumors [2]. It is expressed in benign bronchial stem cells, in neoplastic cells with either squamous differentiation or squamous differentiating potential, as well as in a subpopulation of adenocarcinomas [3]. It is up-regulated in the early phase of epithelial abnormality in idiopathic pulmonary fibrosis [4] and also is involved in the control of maspin expression in non-small cell lung carcinomas (NSCLC), a member of the serpin family of protease inhibitors that inhibits tumor growth and suppresses metastasis in some malignancies, including lung cancer [5]. Massion et al. [6], analyzing p63 gene copy number, observed amplification in 88% of squamous carcinomas, in 42% of large cell carcinomas and in 11% of adenocarcinomas of the lung. Likewise, the predominant splice variant of p63 expressed was DeltaNp63alpha.