ArticleLeukemia2000
Arsenic trioxide (As2O3)-induced apoptosis and differentiation in retinoic acid-resistant acute promyelocytic leukemia model in hGM-CSF-producing transgenic SCID mice.
Article in Leukemia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 61 citations in OpenAlex.
- Comparative analysis of the efficacy and safety of antibody‑drug conjugates, radionuclide‑drug conjugates and their combination targeting claudin 18.2 in gastric cancer treatment.Oncology reports · 2026Article
- Arsenome, Arsenobolome, and Arsenobiolome.International journal of molecular sciences · 2025Review
- Arsenicum iodatum and arseicum album induces apoptosis and autophagy in glioblastoma multiforme.Bioinformation · 2025Article
- Pyroptosis and pyroptosis-inducing cancer drugs.Acta pharmacologica Sinica · 2022Review
- Fluorescent probes forChemical science · 2020Article
- Downregulation of Mcl-1 through GSK-3β activation contributes to arsenic trioxide-induced apoptosis in acute myeloid leukemia cells.Leukemia · 2013Article
- Arterial embolization hyperthermia using As2O3 nanoparticles in VX2 carcinoma-induced liver tumors.PloS one · 2011Article
- Arsenic trioxide inhibits human cancer cell growth and tumor development in mice by blocking Hedgehog/GLI pathway.The Journal of clinical investigation · 2011Article
- The NRF2-mediated oxidative stress response pathway is associated with tumor cell resistance to arsenic trioxide across the NCI-60 panel.BMC medical genomics · 2010Article
- Arsenic trioxide enhances the cytotoxic effect of thalidomide in a KG-1a human acute mylogenous leukemia cell line.Oncology letters · 2010Article
- Differentiation of SWO-38 glioma cells induced by CDA-2 is mediated by peroxisome proliferator-activated receptor gamma.Journal of neuro-oncology · 2009Article
- Cholera toxin induces malignant glioma cell differentiation via the PKA/CREB pathway.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- New therapeutic approach for myeloid leukemia: induction of apoptosis via modulation of reactive oxygen species production by natural compounds.International journal of hematology · 2006Review
- A novel therapeutic approach for hematological malignancies based on cellular differentiation and apoptosis.International journal of hematology · 2002Article
- The sensitivity of digestive tract tumor cells to As2O3 is associated with the inherent cellular level of reactive oxygen species.World journal of gastroenterology · 2002Article
- Arsenic trioxide, a therapeutic agent for APL.Oncogene · 2001Review
- Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission.Oncogene · 2001Review
- A novel differentiation-inducing therapy for acute promyelocytic leukemia with a combination of arsenic trioxide and GM-CSF.Leukemia · 2001Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent clinical studies in China and USA showed that arsenic trioxide (As2O3) is an effective treatment of acute promyelocytic leukemia (APL) patients refractory to all-trans retinoic acid (RA). We here investigate the effects of As2O3 on RA-resistant APL in vivo and in vitro using our RA-resistant APL model system. As2O3 can induce inhibition of cellular growth of both RA-sensitive NB4 and RA-resistant UF-1 APL cells via induction of apoptosis in vitro. The expression of BCL-2 protein decreased in a dose- and time-dependent manner in NB4 cells. Interestingly, the levels of BCL-2 protein were not modulated by As2O3, but it did upregulate BAX protein in UF-1 cells. UF-1 cells (1x10(7)) were transplanted into hGM-CSF-producing transgenic SCID mice and successfully formed subcutaneous tumors. After 40 days of implantation, mice were treated with As2O3, all-trans RA and PBS for 21 days. In all-trans RA- and PBS-treated mice, tumors grew rapidly, with a 4.5-fold increase in volume at day 21 compared to the initial size. In marked contrast, tumor size was decreased to half of the initial size by the treatment of As2O3, which resulted in cells with the typical appearance of apoptosis. Interestingly, one of the As2O3-treated mice showed mature granulocytes in the diminished tumor, suggesting that As2O3 had dual effects on RA-resistant APL cells in vivo: both inducing apoptosis and differentiation of the leukemic cells. We conclude that our RA-resistant APL model will be useful for evaluating novel therapeutic approaches to patients with RA-resistant APL, and for further investigation of the metabolism of As2O3 in vivo.
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