{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:00:09Z","timestamp":1790172009205,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T00:00:00Z","timestamp":1788998400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T00:00:00Z","timestamp":1788998400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pediatric Blood &amp;amp; Cancer"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>ETV6::RUNX1<\/jats:italic>\n                      is the most common genetic abnormality in pediatric B\u2010cell acute lymphoblastic leukemia (ALL; \u223c25%), yet the comprehensive genetic architecture and molecular predictors of intermediate\u2010risk (IR) stratification remain incompletely characterized.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed whole\u2010transcriptome sequencing (Illumina NovaSeq 6000, rRNA depletion, 41.70 Gb\/sample) on bone marrow samples from 93 pediatric\n                      <jats:italic>ETV6::RUNX1<\/jats:italic>\n                      \u2010positive B\u2010ALL patients. Bioinformatics analysis included STAR alignment, MuTect2 variant calling, FusionCatcher fusion detection, and VEP annotation. The Jaccard index with permutation testing assessed mutation co\u2010occurrence; logistic regression identified independent predictors of IR classification.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Beyond\n                      <jats:italic>ETV6::RUNX1<\/jats:italic>\n                      , we identified 51 distinct fusion genes across the cohort, including the reciprocal RUNX1\u2010ETV6 (73.1%), chr8::KLF1210 (38.7%), and KLF12\u2010chr8 (34.4%). Somatic mutations in 249 genes were detected; the most frequent were KIAA1715 (17.2%), KRAS (11.8%), and NSD2 (10.8%). Network analysis revealed significant chromatin modifier co\u2010occurrence (KIAA1715\u2010KMT2C:\n                      <jats:italic>J<\/jats:italic>\n                      = 0.136,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.015) and KRAS\u2010NRAS mutual exclusivity (\n                      <jats:italic>J<\/jats:italic>\n                      = 0.000,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.042). PTCH1 (OR = 3.50, 95% CI 0.21\u201358.49,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.41) and GNB1 (OR = 6.5, 95% CI 1.2\u201334.8,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.029) mutations independently predicted IR classification. chr8::KLF1210 fusion correlated with higher Day\u201019 MRD levels (\n                      <jats:italic>p<\/jats:italic>\n                      = 0.038).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      GNB1 mutation represents a novel independent predictor of IR stratification in\n                      <jats:italic>ETV6::RUNX1<\/jats:italic>\n                      \u2010positive B\u2010ALL. The chromatin modifier co\u2010occurrence module and extensive fusion architecture reveal biological heterogeneity within this favorable\u2010risk subtype, with potential implications for risk\u2010adapted therapeutic strategies.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/1545-5017.70636","type":"journal-article","created":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T14:00:39Z","timestamp":1789048839000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genomic Characterization of\n                    <i>ETV6::RUNX1<\/i>\n                    \u2010Positive Childhood B\u2010ALL in a Chinese Cohort: Novel Fusion Partners, Co\u2010Occurring Mutations, and Risk\u2010Stratifying Biomarkers"],"prefix":"10.1002","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5171-5474","authenticated-orcid":false,"given":"Hualei","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Laboratory Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-4854-1462","authenticated-orcid":false,"given":"Guichi","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0226-1574","authenticated-orcid":false,"given":"Qiang","family":"Yao","sequence":"additional","affiliation":[{"name":"Department of Laboratory Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunsheng","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Laboratory Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3983-979X","authenticated-orcid":false,"given":"Xue","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shilin","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huiying","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8970-9221","authenticated-orcid":false,"given":"Huirong","family":"Mai","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4210-3510","authenticated-orcid":false,"given":"Xiaoying","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Laboratory Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Hematology Shenzhen Children's Hospital  Shenzhen Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,10]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.20517\/jtgg.2024.88"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/s1470\u20102045(17)30186\u20109"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21219"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0900386"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/s2352\u20104642(18)30066\u2010x"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1400972"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/s0140\u20106736(12)62187\u20104"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41588\u2010022\u201001159\u2010z"},{"issue":"12","key":"e_1_2_11_10_1","first-page":"1985","article-title":"TEL\/AML1 Fusion Resulting From a Cryptic T(12;21) Is the Most Common Genetic Lesion in Pediatric ALL and Defines a Subgroup of Patients With an Excellent Prognosis","volume":"9","author":"Shurtleff S. 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