{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:59:56Z","timestamp":1783990796746,"version":"3.55.0"},"reference-count":34,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T00:00:00Z","timestamp":1104537600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T00:00:00Z","timestamp":1104537600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Haematol"],"published-print":{"date-parts":[[2005]]},"abstract":"<jats:p>Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an interferon (IFN)-induced molecule with apoptotic activity. We examined gene mutations in the death domains of TRAIL receptor 1 &lt;i&gt;(TRAIL-R1)&lt;\/i&gt; and TRAIL receptor 2 &lt;i&gt;(TRAIL-R2)&lt;\/i&gt;, and in the &lt;i&gt;TRAIL&lt;\/i&gt; gene promoter in 46 chronic myelogenous leukemia (CML) patients. In 23 of the 46 patients, all the coding regions of &lt;i&gt;TRAIL-R2&lt;\/i&gt; were also examined. However, no mutation or loss of heterozygosity was found. Furthermore, no mutation in the death domains of &lt;i&gt;TRAIL-R1&lt;\/i&gt; and &lt;i&gt;TRAIL-R2&lt;\/i&gt; genes, which causes amino acid change, was found in 18 myelodysplastic syndrome (MDS) patients. Ribonuclease protection assay (RPA) and real-time quantitative polymerase chain reaction using polymorphonuclear neutrophils of five new CML patients showed that the TRAIL mRNA expression was very low before in vitro IFN-\u03b1 stimulation and markedly upregulated after IFN-\u03b1 stimulation. FAS mRNA was also upregulated with IFN-\u03b1 stimulation but the fold induction was far lower than that of TRAIL mRNA. In addition, RPA revealed that the ratio of (TRAIL-R1 plus TRAIL-R2) to TRAIL-R3 was also increased after IFN-\u03b1 stimulation. Taken together, gene mutations of &lt;i&gt;TRAIL-R1&lt;\/i&gt;, &lt;i&gt;TRAIL-R2&lt;\/i&gt; are infrequent in patients with CML and MDS. And&lt;i&gt;&lt;\/i&gt;so is the &lt;i&gt;TRAIL &lt;\/i&gt;promoter for CML. These mutations seem unrelated to tumorigenesis, disease progression, and response to IFN-\u03b1 therapy in CML. A markedly high induction of TRAIL mRNA by IFN-\u03b1 may have some relevance to IFN-\u03b1 action in CML patients.<\/jats:p>","DOI":"10.1159\/000083449","type":"journal-article","created":{"date-parts":[[2005,4,1]],"date-time":"2005-04-01T08:14:07Z","timestamp":1112343247000},"page":"113-123","source":"Crossref","is-referenced-by-count":10,"title":["Absence of Gene Mutation in TRAIL Receptor 1 &lt;i&gt;(TRAIL-R1)&lt;\/i&gt; and TRAIL Receptor 2 &lt;i&gt;(TRAIL-R2)&lt;\/i&gt; in Chronic Myelogenous Leukemia and Myelodysplastic Syndrome, and Analysis of mRNA Expressions of TRAIL and TRAIL-Related Genes in Chronic Myelogenous Leukemia"],"prefix":"10.1159","volume":"113","author":[{"given":"Li-Gen","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideo","family":"Tanaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kinro","family":"Ito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takuo","family":"Ito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanvira 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