Diallyl disulfide induces apoptosis and autophagy via mTOR pathway in myeloid leukemic cell line.

Leukemia is a hematological malignancy which is produced by uncontrolled proliferation of leukocyte precursors. Currently, alternative medicines, using herb extracts, have been developed for cancer treatment. In this study, the effect of diallyl disulfide (DADS) on the induction of apoptosis and autophagy was investigated in K562 and NB4 myeloid leukemia cells.

p53 and nitric oxide are involved in cytokine-induced apoptosis in Kasumi-1 and Molt-4 Leukemics cells.

Background: Immunotherapy has been developed to treat cancers. There are many signaling pathways involved in cytokine induced apoptosis of many cancers but their role remains unclear in some cancers such as leukemia.

Objective: To investigate the involvement of the nitric oxide (NO) and p53 tumor suppressor gene in apoptotic pathways induced by cytokines in leukemic cell lines.

Effect of Tumor Necrosis Factor-Alpha on Erythropoietin and Erythropoietin Receptor-Induced Erythroid Progenitor Cell Proliferation in β-Thalassemia/Hemoglobin E Patients.

Objective: Thalassemia is one of the genetic diseases that cause anemia and ineffective erythropoiesis. Increased levels of several inflammatory cytokines have been reported in β-thalassemia and might contribute to ineffective erythropoiesis. However, the mechanism by which tumor necrosis factor-alpha (TNF-α) is involved in ineffective erythropoiesis in thalassemic patients remains unclear.

Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in rheumatoid arthritis.

Proinflammatory cytokines play a role in the pathogenesis of anemia of chronic disease (ACD), which is a common cause of anemia in rheumatoid arthritis (RA). Anemia in RA is associated with increased apoptosis of erythroid cells. However, there is unclear information on the mechanism of ACD in the disease.

Cytokine-induced apoptosis of beta-thalassemia/hemoglobin E erythroid progenitor cells via nitric oxide-mediated process in vitro.

Background/aim: β-Thalassemia/hemoglobin E (β-thal/HbE) is a common hereditary anemia in Thailand. Ineffective erythropoiesis due to apoptosis and decreased lifespan of circulating thalassemic red blood cells are the major causes of anemia. Changes to bone marrow microenvironment could contribute to apoptotic events.

Nitric oxide and caspase 3 mediated cytokine induced apoptosis in acute leukemia.

Background: Leukemia is characterized by the uncontrolled accumulation of white blood cells. Recently, cytokines have been used in immunotherapy, which is a new strategy for leukemia treatment.

Objective: To investigate the effect of cytokines on induction of apoptosis in acute leukemic cell lines; HL-60, MV4-11, K-562 and Molt-4 and in addition, to study the involvement of nitric oxide (NO) in apoptotic pathways.

Role of interleukin-3 and signaling pathways on beta-thalassemia/HbE erythroid progenitor cell in culture.

In order to study the role of the cytokine interleukin-3 (IL-3) and its signaling pathways in erythropoiesis of beta-thalassemia/HbE erythroid progenitor cells, CD34 positive cells were isolated from peripheral blood of patients and healthy subjects. After culturing the cells in the presence or absence of IL-3, cell viability was measured by trypan blue staining and apoptotic cells were analyzed by flow cytometry. After 7 days of culture the highest percent erythroid progenitor cell viability was obtained with cells from healthy subjects, while the lowest percentage was found in those from splenectomized beta-thalassemia/HbE.