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PTEN Loss and Cyclin A2 Upregulation Define a PI3K/AKT Pathway Activation in Helicobacter pylori–induced MALT and DLBCL Gastric Lymphoma With Features of MALT

Abstract : Helicobacter pylori infection is strongly associated with primary gastric diseases, such as extranodal mucosa-associated lymphoid tissue (MALT) lymphoma, diffuse large B-cell lymphoma (DLBCL) with histologic evidence of MALT origin, and gastric carcinoma. The cytotoxin-associated gene A (CagA) protein behaves as a bacterial oncoprotein, promoting tumorigenesis via dysregulation of the phosphatidylinositol 3-kinase/AKT pathway (PI3K/AKT). We investigated the molecular mechanisms of PI3K/AKT pathway dysregulation in H. pylori-induced MALT and DLBCL gastric lymphoma. Immunohistochemical assays for CagA, phospho(p)-S473-AKT, PTEN, SHIP, and cyclin A2 proteins were performed on samples from 23 patients with H. pylori-positive MALT lymphoma and 16 patients with H. pylori-positive gastric DLBCL. We showed that CagA localization is correlated with the activation of the AKT pathway in both MALT and DLBCL lymphoma cells. Interestingly, we found a close association between the loss of PTEN, the overexpression of cyclin A2, and the phosphorylation of AKT in gastric MALT and DLBCL tumor cells.
Keywords : AKT CagA cyclin A2 MALT DLBCL
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https://hal-normandie-univ.archives-ouvertes.fr/hal-02971489
Contributor : Brigitte Sola <>
Submitted on : Monday, October 19, 2020 - 3:15:39 PM
Last modification on : Wednesday, October 28, 2020 - 9:52:06 AM

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Khaoula Ben Younes, Raoudha Doghri, Karima Mrad, Walid Bedhiafi, Amel Benammar-Elgaaied, et al.. PTEN Loss and Cyclin A2 Upregulation Define a PI3K/AKT Pathway Activation in Helicobacter pylori–induced MALT and DLBCL Gastric Lymphoma With Features of MALT. Applied Immunohistochemistry and Molecular Morphology, Lippincott, Williams & Wilkins, 2020, Publish Ahead of Print, ⟨10.1097/PAI.0000000000000839⟩. ⟨hal-02971489⟩

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