Analysis of expression of PTEN/PI3K pathway and programmed cell death ligand 1 (PD-L1) in malignant pleural mesothelioma (MPM)

•PI3K pathway and PD-L1 are frequently expressed in MPM.•PD-L1 is a negative prognostic factor.•There is no association between PI3K pathway and PD-L1 in MPM. Malignant pleural mesothelioma (MPM) frequently express elevated AKT/mTOR activity. Previous reports in gliomas, colon, breast and prostate c...

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Published inLung cancer (Amsterdam, Netherlands) Vol. 96; pp. 1 - 6
Main Authors Cedrés, S., Ponce-Aix, S., Pardo-Aranda, N., Navarro-Mendivil, A., Martinez-Marti, A., Zugazagoitia, J., Sansano, I., Montoro, M.A., Enguita, A., Felip, E.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 01.06.2016
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Summary:•PI3K pathway and PD-L1 are frequently expressed in MPM.•PD-L1 is a negative prognostic factor.•There is no association between PI3K pathway and PD-L1 in MPM. Malignant pleural mesothelioma (MPM) frequently express elevated AKT/mTOR activity. Previous reports in gliomas, colon, breast and prostate cancer suggest that PTEN/PI3K pathway may be important for the induction of PD-L1 expression. This study explored the expression of PTEN/PI3K pathway and PD-L1 in MPM and its relationship with the patient́s prognosis Twenty seven consecutive MPM patients were reviewed. Formalin-fixed, paraffin-embedded tissue biopsies were used for immunohistochemical analysis of PTEN/PI3K pathway and PD-L1 Expression of PTEN, mTOR, pAKT, p4EBP1, peif4E, pS6 and FOXO3a was found in 88.5%, 92.3%, 78.3%, 38.5%, 100%, 52.2% and 100% of tumors and PD-L1 in 23%. We found a significant correlation between pAKT, FOXO3a and PD-L1 expression and longer overall survival (p <0.05). We did not identify significant association between the level of PD-L1 expression and alterations in PI3K pathway This study shows PTEN/PI3K pathway and PD-L1 in MPM are frequently activated. Our results suggests that there is not association between PD-L1 and the involvement of the PI3K pathway in MPM.
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ISSN:0169-5002
1872-8332
DOI:10.1016/j.lungcan.2016.03.001