Publications by authors named "Anezka Rajmonova"

T-cell lymphomas (TCLs) are a rare and heterogeneous subgroup of non-Hodgkin lymphomas (NHLs), forming only 10 % of all NHL cases in Western countries. Resulting from their low incidence and heterogeneity, the current treatment outcome is generally unfavorable, with limited availability of novel therapeutic approaches. Therefore, the recent success of immune checkpoint inhibitors (ICIs) in cancer treatment motivated their clinical investigation in TCLs as well.

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The phosphatidylinositol 3‑kinase/protein kinase B (PI3K/AKT) signaling pathway is critically active in many cell types, both normal and neoplastic. Many small-molecule inhibitors targeting different levels of the PI3K/AKT pathway have been developed for cancer therapy, but their efficacy is reduced by compensatory pathway re-activation mechanisms, and their tolerability by toxic side effects. We studied this problem using cell lines representing diffuse large B-cell lymphoma (SUDHL-4 and OCI-Ly7), a genetically-encoded live-cell reporter of AKT activity, and 3 small-molecule inhibitors targeting different levels of the pathway: idelalisib (PI3Kδ), GSK2334470 (PDPK1), and ipatasertib (AKT).

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Article Synopsis
  • Mantle cell lymphoma (MCL) shows recurring genetic changes in key regulators of the phosphoinositol-3-kinase (PI3K) pathway, particularly involving PIK3CA amplifications and PTEN losses.
  • In vitro studies using modified MCL cell lines revealed that PIK3CA overexpression reduces reliance on B-cell receptor (BCR) signaling, alters metabolic processes, and leads to therapy resistance without affecting AKT signaling.
  • Conversely, PTEN knockout resulted in notable changes, including heightened AKT activation, greater resistance to various inhibitors, and decreased reliance on BCR signaling, indicating how these genetic alterations may promote therapy resistance and adaptive survival mechanisms in MCL.
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