{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:42:01Z","timestamp":1791096121541,"version":"4.1.0"},"reference-count":61,"publisher":"American Society of Hematology","issue":"13","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Treatment of patients with adult T-cell leukemia\u2013lymphoma (ATLL) using conventional chemotherapy has limited benefit because human T-cell leukemia virus type 1 (HTLV-1) cells are resistant to most apoptosis-inducing agents. The recent report that arsenic trioxide induces apoptosis in HTLV-1\u2013transformed cells prompted investigation of the mechanism of action of this drug in HTLV-1 and HTLV-2 interleukin-2\u2013independent T cells and in HTLV-1\u2013immortalized cells or in ex vivo ATLL samples. Fluorescence-activated cell sorter analysis, fluorescence microscopy, and measures of mitochondrial membrane potential (\u0394\u03a8m) demonstrated that arsenic trioxide alone was sufficient to induce programmed cell death in all HTLV-1 and -2 cells tested and in ATLL patient samples. I\u03baB-\u03b1 phosphorylation strongly decreased, and NF-\u03baB translocation to the nucleus was abrogated. Expression of the antiapoptotic protein Bcl-XL, whose promoter is NF-\u03baB dependent, was down-regulated. The collapse of \u0394\u03a8m and the release of cytochrome c to the cytosol resulted in the activation of caspase-3, as demonstrated by the cleavage of PARP. A specific caspase-3 inhibitor (Ac-DEVD-CHO) could reverse this phenotype. The antiapoptotic factor Bcl-2 was then cleaved, converting it to a Bax-like death effector. These results demonstrated that arsenic trioxide induces apoptosis in HTLV-1\u2013 and -2\u2013infected cells through activation of the caspase pathway.<\/jats:p>","DOI":"10.1182\/blood.v98.13.3762","type":"journal-article","created":{"date-parts":[[2002,10,28]],"date-time":"2002-10-28T20:44:12Z","timestamp":1035837852000},"page":"3762-3769","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":89,"title":["Arsenic trioxide induces apoptosis in human T-cell leukemia virus type 1\u2013 and type 2\u2013infected cells by a caspase-3\u2013dependent mechanism involving Bcl-2 cleavage"],"prefix":"10.1182","volume":"98","author":[{"given":"Renaud","family":"Mahieux","sequence":"first","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cynthia","family":"Pise-Masison","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antoine","family":"Gessain","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John. N.","family":"Brady","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rene\u0301","family":"Olivier","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuelle","family":"Perret","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom","family":"Misteli","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, Institut Pasteur; and the Virus Tumor Biology Section and the Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christophe","family":"Nicot","sequence":"additional","affiliation":[{"name":"From Unite\u0301 d'Epide\u0301miologie et Physiopathologie des Virus Oncoge\u0300nes and Unite\u0301 d'Oncologie Virale, 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