ROS stress in cancer cells and therapeutic implications.

Use of Arsenic Trioxide (As2O3 ) in the Treatment of Acute Promyelocytic Leukemia (APL): II. Clinical Efficacy and Pharmacokinetics in Relapsed Patients

Background Two reports from China have suggested that arsenic trioxide can induce complete remissions in patients with acute promyelocytic leukemia (APL). We evaluated this drug in patients with APL in an attempt to elucidate its mechanism of action. Methods Twelve patients with APL who had relapsed after extensive prior therapy were treated with arsenic trioxide at doses ranging from 0.06 to 0.2 mg per kilogram of body weight per day until visible leukemic cells were eliminated from the bone marrow. Bone marrow mononuclear cells were serially monitored by flow cytometry for immunophenotype, fluorescence in situ hybridization, reverse-transcription–polymerase-chain-reaction (RT-PCR) assay for PML–RAR-α fusion transcripts, and Western blot analysis for expression of the apoptosis-associated proteins caspases 1, 2, and 3. Results Of the 12 patients studied, 11 had a complete remission after treatment that lasted from 12 to 39 days (range of cumulative doses, 160 to 515 mg). Adverse effects were relatively m...

https://www.nejm.org/doi/pdf/10.1056/NEJM199811053391901

Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide

Acute promyelocytic leukemia: from highly fatal to highly curable.

Apoptosis is deregulated in many cancers, making it difficult to kill tumours. Drugs that restore the normal apoptotic pathways have the potential for effectively treating cancers that depend on aberrations of the apoptotic pathway to stay alive. Apoptosis targets that are currently being explored for cancer drug discovery include the tumour-necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors, the BCL2 family of anti-apoptotic proteins, inhibitor of apoptosis (IAP) proteins and MDM2.

Promoting apoptosis as a strategy for cancer drug discovery

In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins

Establishment of a human acute promyelocytic leukemia-ascites model in SCID mice.

Group 3 innate lymphoid cells (ILC3) as a family member of innate lymphoid cells (ILCs), have been defined as novel innate immune cells in the past decade. ILC3 include a variety of heterogenous subsets with different phenotypes and functions, which are mainly distributed in barrier organs such as the intestine, lung and skin. They play an important role in immune regulation, tissue repair and lymphoid tissue formation. However, in various inflammatory diseases, ILC3 become dysregulated and participate in the pathogenesis through secreting a series of cytokines such as interleukin (IL)-17, IL-22, interferon-γ (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSF) to modulate other immune cells and induce the formation of ectopic lymphoid structures. Therefore, it is of great significance to explore the phenotype and function of ILC3 in order to advance the understanding of inflammatory diseases and find new therapeutic targets. In this article, the phenotypic characteristics, biological functions and research progress of ILC3 in inflammatory diseases were reviewed.

Hao-Jie Zhong

Papers

In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins

Establishment of a human acute promyelocytic leukemia-ascites model in SCID mice.

[Emerging pathogenic role of group 3 innate lymphoid cells in inflammatory diseases].

Studies on syntheses, crystal structures, dft calculation and anti-breast-cancer activities of arteminsin-purine hybrids