{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:23:48Z","timestamp":1788870228457,"version":"build-2803163510"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,8,16]],"date-time":"2013-08-16T00:00:00Z","timestamp":1376611200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["K12 HD043376"],"award-info":[{"award-number":["K12 HD043376"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R21 CA10262"],"award-info":[{"award-number":["R21 CA10262"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 CA114563"],"award-info":[{"award-number":["R01 CA114563"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"name":"COG Chair's","award":["U10 CA98543"],"award-info":[{"award-number":["U10 CA98543"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatric Blood &amp; Cancer"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>WT1<\/jats:italic>\n                      is aberrantly over\u2010expressed in most cases of AML. We recently demonstrated that\n                      <jats:italic>WT1 SNP<\/jats:italic>\n                      rs16754 correlates with favorable outcome and high diagnostic\n                      <jats:italic>WT1<\/jats:italic>\n                      expression in childhood AML. We examined the clinical correlates of diagnostic\n                      <jats:italic>WT1<\/jats:italic>\n                      expression within a contemporary COG trial and determined whether its prognostic impact differs between SNP+ and SNP\u2212 patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Procedure<\/jats:title>\n                    <jats:p>\n                      <jats:italic>WT1<\/jats:italic>\n                      mRNA expression was measured via qRT\u2010PCR in diagnostic specimens obtained from 225 patients enrolled on COG\u2010AAML03P1. Direct sequencing of\n                      <jats:italic>WT1<\/jats:italic>\n                      exon 7 was performed to determine SNP rs16754 genotype.\n                      <jats:italic>WT1<\/jats:italic>\n                      expression was correlated with disease characteristics, SNP status, and outcome.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Patients were categorized into four groups (quartiles: Q1 through Q4) based on diagnostic\n                      <jats:italic>WT1<\/jats:italic>\n                      expression for analysis.\n                      <jats:italic>FLT3\/ITD<\/jats:italic>\n                      (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.017) and\n                      <jats:italic>WT1<\/jats:italic>\n                      mutations (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.001) both occurred more frequently in patients with the highest\n                      <jats:italic>WT1<\/jats:italic>\n                      expression. SNP rs16754 frequency did not vary significantly among the quartiles. When all patients were considered, survival outcomes were similar between quartiles. However, when only SNP\u2212 patients (n\u2009=\u2009150) were analyzed, those with highest\n                      <jats:italic>WT1<\/jats:italic>\n                      expression (Q4) had the poorest OS (51% vs. 72% for Q1\u2013Q3,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.006) and EFS (35% vs. 54% for Q1\u2013Q3,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.031). Among SNP+ patients (n\u2009=\u200975), survival did not vary significantly between\n                      <jats:italic>WT1<\/jats:italic>\n                      expression quartiles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Although\n                      <jats:italic>WT1<\/jats:italic>\n                      expression was not prognostic when all patients were considered together, stratifying patients by SNP rs16754 genotype revealed significant differences in outcome. In SNP\u2212 patients, high\n                      <jats:italic>WT1<\/jats:italic>\n                      expression predicted decreased survival in univariate, but not multivariate, analysis, due to a preponderance of high\u2010risk cyto\/molecular abnormalities in the highest expression quartile. Pediatr Blood Cancer 2014;61:81\u201388. \u00a9 2013 Wiley Periodicals, Inc.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/pbc.24700","type":"journal-article","created":{"date-parts":[[2013,8,16]],"date-time":"2013-08-16T09:56:23Z","timestamp":1376646983000},"page":"81-88","source":"Crossref","is-referenced-by-count":19,"title":["The prognostic effect of high diagnostic\n                    <i>WT1<\/i>\n                    gene expression in pediatric AML depends on\n                    <i>WT1<\/i>\n                    SNP rs16754 status: Report from the Children's Oncology Group"],"prefix":"10.1002","volume":"61","author":[{"given":"Phoenix A.","family":"Ho","sequence":"first","affiliation":[{"name":"Clinical Research Division Fred Hutchinson Cancer Research Center Seattle Washington"},{"name":"Division of Pediatric Hematology\/Oncology Seattle Children's Hospital, University of Washington School of Medicine Seattle Washington"},{"name":"Children's Oncology Group Arcadia California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Todd A.","family":"Alonzo","sequence":"additional","affiliation":[{"name":"Children's Oncology Group Arcadia California"},{"name":"Department of Biostatistics University of Southern California Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert B.","family":"Gerbing","sequence":"additional","affiliation":[{"name":"Children's Oncology Group Arcadia California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Kuhn","sequence":"additional","affiliation":[{"name":"Clinical Research Division Fred Hutchinson Cancer Research Center Seattle Washington"},{"name":"School of Medicine University of Pittsburgh Pittsburgh Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica A.","family":"Pollard","sequence":"additional","affiliation":[{"name":"Clinical Research Division Fred Hutchinson Cancer 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