Publications by authors named "M Entezam"

Background: In this study, we investigate the impact of a multi-targeted therapeutic approach that includes camptothecin (CPT), a potent chemotherapeutic topoisomerase inhibitor; metformin (Met), a metabolic modulator with emerging anti-tumor effects; and GW280264X, an inhibitor of ADAM 10/ADAM 17 enzymes, which are associated with tumor invasion and immune response. The study aims to assess the combined effects of these agents in enhancing CD8 T cell-mediated anti-tumor immunity and suppressing cancer cell growth in triple-negative breast cancer (TNBC) models, both in vitro and in vivo.

Methods: Cell viability was performed on the 4 T1 human TNBC cell line.

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Background: gene mutations are responsible for more than 95% of Congenital Adrenal Hyperplasia (CAH) disorders with autosomal recessive inheritance. Most of these pathogenic mutations originate from the , a neighboring pseudogene with 98% homology, due to unequal crossing over or gene conversion events. Mutation identification of the gene could be beneficial for accurate diagnosis and outcome prediction.

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Scientific research over the past decades has proven the pivotal role of long non-coding RNAs (LncRNAs) in regulating gene expression. The immune responses are controlled through the interaction of pro-inflammatory (predominance of T helper 17 cells (Th17)) and anti-inflammatory cytokines excretion (predominance of Regulatory T cells (Treg)). Recent studies have marked the impact of many diverse LncRNAs on Treg/Th17 imbalances.

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Article Synopsis
  • BATF3 is a key transcription factor essential for developing conventional type 1 dendritic cells (cDC1), which help activate CD8+ T cells to fight off infections and cancer.
  • It plays a role in regulating immunity, including promoting tolerance, combating pathogens, and enhancing cancer immunotherapy by improving immune monitoring in tumors.
  • BATF3 also influences the fate of T cells, inhibiting regulatory T cell (Treg) development while enhancing CD8+ T cell survival and memory formation, and has been implicated in cancer-related processes like proliferation and invasion.
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Article Synopsis
  • This study explores the potential of targeting the BATF3 transcription factor in chronic myeloid leukemia (CML) cells using siRNA to improve treatment outcomes, as CML is currently considered incurable due to resistance issues.
  • Researchers performed various assays to evaluate the effects of BATF3 downregulation on K562 CML cells, discovering that this approach significantly promoted cell apoptosis, affected gene expression related to apoptosis, and arrested the cell cycle.
  • Findings suggest that inhibiting BATF3 could be a promising targeted therapy strategy for CML, highlighting the importance of understanding molecular mechanisms in developing more effective cancer treatments.
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