{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T18:11:55Z","timestamp":1789841515161,"version":"4.0.1"},"reference-count":60,"publisher":"BMJ","issue":"12","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Gut"],"accepted":{"date-parts":[[2015,8,15]]},"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>GI stromal tumours (GISTs) are clinically heterogenous exhibiting varying degrees of disease aggressiveness in individual patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We sought to identify genetic alterations associated with high-risk GIST, explore their molecular consequences, and test their utility as prognostic markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Designs<\/jats:title>\n                    <jats:p>\n                      Exome sequencing of 18 GISTs was performed (9 patients with high-risk\/metastatic and 5 patients with low\/intermediate-risk), corresponding to 11 primary and 7 metastatic tumours. Candidate alterations were validated by prevalence screening in an independent patient cohort (n=120). Functional consequences of\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutations were investigated in primary tissues and cell lines. Transcriptomic profiles for 8 GISTs (4\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutated, 4\n                      <jats:italic>SETD2<\/jats:italic>\n                      wild type) and DNA methylation profiles for 22 GISTs (10\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutated, 12\n                      <jats:italic>SETD2<\/jats:italic>\n                      wild type) were analysed. Statistical associations between molecular, clinicopathological factors, and relapse-free survival were determined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      High-risk GISTs harboured increased numbers of somatic mutations compared with low-risk GISTs (25.2 mutations\/high-risk cases vs 6.8 mutations\/low-risk cases; two sample t test p=3.1\u00d710\n                      <jats:sup>\u22125<\/jats:sup>\n                      ). Somatic alterations in the\n                      <jats:italic>SETD2<\/jats:italic>\n                      histone modifier gene occurred in 3 out of 9 high-risk\/metastatic cases but no low\/intermediate-risk cases. Prevalence screening identified additional\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutations in 7 out of 80 high-risk\/metastatic cases but no low\/intermediate-risk cases (n=29). Combined, the frequency of\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutations was 11.2% (10\/89) and 0% (0\/34) in high-risk and low-risk GISTs respectively.\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutant GISTs exhibited decreased H3K36me3 expression while\n                      <jats:italic>SETD2<\/jats:italic>\n                      silencing promoted DNA damage in GIST-T1 cells. In gastric GISTs,\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutations were associated with overexpression of\n                      <jats:italic>HOXC<\/jats:italic>\n                      cluster genes and a DNA methylation signature of hypomethylated heterochromatin. Gastric GISTs with\n                      <jats:italic>SETD2<\/jats:italic>\n                      mutations, or GISTs with hypomethylated heterochromatin, showed significantly shorter relapse-free survival on univariate analysis (log rank p=4.1\u00d710\n                      <jats:sup>\u22125<\/jats:sup>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our data suggest that\n                      <jats:italic>SETD2<\/jats:italic>\n                      is a novel GIST tumour suppressor gene associated with disease progression. Assessing\n                      <jats:italic>SETD2<\/jats:italic>\n                      genetic status and\n                      <jats:italic>SETD2<\/jats:italic>\n                      -associated epigenomic phenotypes may guide risk stratification and provide insights into mechanisms of GIST clinical aggressiveness.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gutjnl-2015-309482","type":"journal-article","created":{"date-parts":[[2015,9,3]],"date-time":"2015-09-03T22:50:37Z","timestamp":1441320637000},"page":"1960-1972","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":53,"title":["<i>SETD2<\/i>\n                    histone modifier loss in aggressive GI stromal tumours"],"prefix":"10.1136","volume":"65","author":[{"given":"Kie Kyon","family":"Huang","sequence":"first","affiliation":[{"name":"Cancer Science Institute of Singapore, National University of Singapore, Center for Translational 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