Publications by authors named "Farah Kouzi"

Background/objectives: A specialized microenvironment in the bone marrow, composed of stromal cells including mesenchymal stem cells (MSCs), supports hematopoietic stem cell (HSC) self-renewal, and differentiation bands play an important role in leukemia development and progression. The reciprocal direct interaction between MSCs and CD34 HSCs under physiological and pathological conditions is yet to be fully characterized.

Methods: Here, we established a direct co-culture model between MSCs and CD34 HSCs or MSCs and acute myeloid leukemia cells (THP-1, Molm-13, and primary cells from patients) to study heterocellular communication.

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The RAS-MAPK-pathway is aberrantly regulated in cancer and developmental diseases called RASopathies. While typically the impact of Ras on the proliferation of various cancer cell lines is assessed, it is poorly established how Ras affects cellular differentiation. Here we implement the C2C12 myoblast cell line to systematically study the effect of Ras mutants and Ras-pathway drugs on differentiation.

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Acute myeloid leukemia (AML) is characterized by the accumulation of undifferentiated blast cells in the bone marrow and blood. In most cases of AML, relapse frequently occurs due to resistance to chemotherapy. Compelling research results indicate that drug resistance in cancer cells is highly dependent on the intracellular levels of reactive oxygen species (ROS).

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In acute myeloid leukemia (AML), a low level of reactive oxygen species (ROS) is associated with leukemic stem cell (LSC) quiescence, whereas a high level promotes blast proliferation. ROS homeostasis relies on a tightly-regulated balance between the antioxidant and oxidant systems. Among the oxidants, NADPH oxidases (NOX) generate ROS as a physiological function.

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The bone marrow (BM) microenvironment plays a crucial role in the development and progression of leukemia (AML). Intracellular reactive oxygen species (ROS) are involved in the regulation of the biology of leukemia-initiating cells, where the antioxidant enzyme GPx-3 could be involved as a determinant of cellular self-renewal. Little is known however about the role of the microenvironment in the control of the oxidative metabolism of AML cells.

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Article Synopsis
  • The original article left out some acknowledgments regarding funding.
  • The missing information stated that the research was supported by grants to KZ from UL and L-CNRS.
  • The correction has been made in both the PDF and HTML versions of the article.
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Article Synopsis
  • * Researchers found that blocking gap junctions, which facilitate communication between BM-MSCs and leukemic cells, could alter these interactions and potentially reduce chemoresistance in AML.
  • * The gap junction disruptor carbenoxolone (CBX) showed promise as a treatment, demonstrating an ability to induce cell death in AML cells without harming normal progenitor cells, and enhancing the effectiveness of the chemotherapy drug cytarabine.
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