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Phosphorylated Extracellular Signal-regulated Kinases Are Significantly Increased in Malignant Mesothelioma

Merivane de Melo, Margaret W. Gerbase, Joseph Curran and Jean-Claude Pache

Division of Clinical Pathology (MdM,J-CP), Department of Pulmonary Medicine (MWG), University Hospital of Geneva, Geneva, Switzerland, and Department of Microbiology and Molecular Medicine, University of Geneva, Geneva, Switzerland (JC)

Correspondence to: Jean-Claude Pache, MD, Division of Clinical Pathology, Centre Medical Universitaire (CMU), 1 Rue Michel-Servet, 1211 Geneva 4, Switzerland. E-mail: Jean-Claude.Pache{at}hcuge.ch

Tumorigenesis is associated with the activation of mitogenic signal transduction pathways. The expression of activated extracellular signal-regulated kinase (p-ERK) may play an important role in cell proliferation of malignant mesothelioma (MM). We compare the expression of p-ERK in 50 biopsy specimens of MM, non-small-cell lung cancer (NSCLC), and normal lung tissue. We hypothesized that phosphorylated extracellular signal-regulated kinase is increased in MM. We stained the sections by immunohistochemistry for activated ERK-1 and -2 and performed the quantification of the stained nuclei. Quantitative analysis of p-ERK showed a high percentage score in MM (30.3 ± 4.6%) as compared with NSCLC (12.2 ± 2.1%) (p<0.01) and control lung tissue (6.4 ± 1.3%) (p=0.0002). Furthermore, p-ERK was found significantly higher in poorly differentiated NSCLC (17.7 ± 3.1%) as compared with well-differentiated NSCLC (5.4 ± 1.2%) (p<0.01). Our data show that the nuclear quantification of p-ERK is significantly increased in MM and poorly differentiated NSCLC in comparison to well-differentiated NSCLC and normal lung tissue. These results corroborate previous experimental studies that suggest a critical role of p-ERK in cell proliferation of malignant disease and may represent new targets for therapeutic agents. (J Histochem Cytochem 54:855–861, 2006)

Key Words: human malignant mesothelioma • non-small-cell lung carcinoma • ERK1/2 • PI3K/AKT

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