{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T14:10:03Z","timestamp":1761919803372},"reference-count":18,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,3,26]],"date-time":"2014-03-26T00:00:00Z","timestamp":1395792000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Medicine"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Somatic mutations in cancer cell genes are classified according to their functional significance. Those that provide the malignant cells with significant advantage are collectively referred to as driver mutations and those that do not, are the passenger mutations. Accordingly, analytical criteria to distinguish driver mutations from passenger mutations have been recently suggested. Recent studies revealed mutations in interleukin\u20107 receptor\u2010<jats:italic>\u03b1<\/jats:italic> (IL7R) gene in 10% of pediatric T\u2010cell acute lymphoblastic leukemia (T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>) patients and in only a few cases of pediatric B\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>. <jats:italic>IL7R<\/jats:italic> mutations are also frequently found in patients with lung cancer, but whereas in pediatric T\u2010<jats:styled-content style=\"fixed-case\">ALL <\/jats:styled-content><jats:italic>IL7R<\/jats:italic> mutations are \u201cdrivers\u201d (consisting of gain\u2010of\u2010function mutations within a narrow 50\u2010base pair interval at exon 6 that confer cytokine\u2010independent cell growth and promote tumor transformation), in lung cancer, mutations are substitution mutations randomly distributed across the gene and are probably only \u201cpassenger\u201d events. Because the treatment response of adult T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content> is significantly poorer than that of childhood T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content> and because exon 6 <jats:italic>IL7R<\/jats:italic> mutations play a role in the pathogenesis of childhood T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>, we sought to determine how the pattern of <jats:italic>IL7R<\/jats:italic> mutations varies between adult and childhood T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>. To that end, we sequenced the 50\u2010base pair interval in exon 6 of the IL7R of DNA obtained from bone marrow samples of 35 randomly selected adult patients with T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>. Our analysis revealed that none of these 35 samples carried an <jats:italic>IL7R<\/jats:italic> mutation in exon 6. Whether differences in the genetic makeup of adult and childhood T\u2010<jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content> explain the differential response to therapy remains to be determined.<\/jats:p>","DOI":"10.1002\/cam4.194","type":"journal-article","created":{"date-parts":[[2014,3,26]],"date-time":"2014-03-26T17:21:02Z","timestamp":1395854462000},"page":"550-554","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Interleukin\u20107 receptor\u2010<i>\u03b1<\/i> gene mutations are not detected in adult T\u2010cell acute lymphoblastic leukemia"],"prefix":"10.1002","volume":"3","author":[{"given":"Uri","family":"Rozovski","sequence":"first","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ping","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maro","family":"Ohanian","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hagop","family":"Kantarjian","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zeev","family":"Estrov","sequence":"additional","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center Houston Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2014,3,26]]},"reference":[{"key":"e_1_2_6_2_1","volume-title":"WHO Classification of tumours of Haematopoietic and Lymphoid tissuesed","author":"Swerdlow S. 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