Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arsenic trioxide inhibits growth and promotes apoptosis in many different cancer cell lines. The National Cancer Institute is working cooperatively with research centers across the U.S. to evaluate its clinical activity in hematologic malignancies, such as acute promyelocytic leukemia, acute myeloid leukemia, acute lymphocytic leukemia, chronic myelogenous leukemia, non-Hodgkin's lymphoma, Hodgkin's disease, chronic lymphocytic leukemia, myelodysplastic syndrome, and multiple myeloma. It is also supporting research in solid tumors, such as advanced hormone-refractory prostate cancer and renal cell cancer and in cervical cancer and refractory transitional cell carcinoma of the bladder. The safety and pharmacokinetics of arsenic trioxide are also being evaluated in pediatric patients with refractory leukemia and lymphoma. The results of these ongoing studies should provide important insights into the clinical utility of arsenic trioxide in these diseases.
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PMID:Clinical trials of arsenic trioxide in hematologic and solid tumors: overview of the National Cancer Institute Cooperative Research and Development Studies. 1133 37

Burkitt lymphoma (BL) is an aggressive B-cell non-Hodgkin lymphoma (NHL) and it appears to be one of the most common childhood cancers in equatorial areas. Unprecedented gains have been made in the cure rates for BL during the past two decades and these reflect steady improvements in treatment protocols and a multidisciplinary approach to patient care. However, the life-threatening side effects associated with conventional treatment urge us to explore new strategies. Arsenic trioxide (ATO), a natural product that has improved the prognosis of acute promyelocytic leukemia (APL) from highly fatal to highly curable, has also been proven to be effective in treating BL cell lines through multiple pathways in our study. Our data indicates that ATO can inhibit the proliferation of BL cell lines through 1) arresting the cell cycle; 2) decreasing the respiratory function and transmembrane potential of mitochondrial; and 3) downregulating the expressions of Survivin, Bcl-2, MCL-1, and VEGF. We therefore suggest that dissecting the pharmaceutical mechanism of ATO at the molecular and cellular levels may be a good strategy to explore the value of traditional natural products in treating high malignant Burkitt lymphoma.
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PMID:Arsenic trioxide induces apoptosis of Burkitt lymphoma cell lines through multiple apoptotic pathways and triggers antiangiogenesis. 2147 91

Epstein-Barr virus (EBV) is associated with several malignancies, including carcinomas, such as nasopharyngeal carcinoma, and lymphomas, such as Burkitt's lymphoma and Hodgkin's lymphoma. The Latent Membrane Protein 1 (LMP1) is the major oncogene protein of EBV as its expression is responsible for the induction of cell transformation, immortalization and proliferation. Arsenic trioxide was shown to induce a cytotoxic effect on nasopharyngeal cancer cells associated with LMP1 down-regulation. However, the effect of arsenic on EBV-associated lymphoproliferative malignancies has been less studied. We investigated the effect of two different arsenical compounds, arsenic trioxide (As2O3) and sodium arsenite (NaAsO2) on the induction of cell death in P3HR1 cells, an Epstein-Barr virus-positive Burkitt lymphoma derived cell line. Both compounds inhibited cell growth and induced cell death. By flow-cytometry and Western blot analysis, we provide evidence that NaAsO2 induced caspase-dependent apoptosis whereas As2O3 triggered autophagic cell death. Furthermore, we show that NaAsO2 treatment led to a dramatic decrease of the expression level of LMP1 and the cellular protein PML. Importantly, this down-regulation was associated with a reactivation of EBV lytic cycle through the induction of immediate-early proteins Zta and Rta. These results are in agreement with a model in which LMP1 maintains EBV in a latent state by stabilizing PML expression. Altogether, our results suggest that NaAsO2 would represent a better therapeutic candidate than As2O3 in EBV-induced B lymphoma for its capacity to promote viral reactivation.
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PMID:Sodium arsenite induces apoptosis and Epstein-Barr virus reactivation in lymphoblastoid cells. 2524 Dec 56