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Yet, the role of chromatin interactions and its regulation of gene expression in\n                      <jats:italic toggle=\"yes\">EGFR<\/jats:italic>\n                      -amplified glioblastoma remains unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In this study, we explored alterations in 3D chromatin organization of\n                      <jats:italic toggle=\"yes\">EGFR-<\/jats:italic>\n                      amplified glioblastoma and its subsequent impact by performing a comparative analysis of Hi-C, RNA-seq, and whole-genome sequencing (WGS) on\n                      <jats:italic toggle=\"yes\">EGFR<\/jats:italic>\n                      -amplified glioblastoma-derived A172 and normal astrocytes (HA1800 cell line).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A172 cells showed an elevated chromatin relaxation, and unexpected entanglement of chromosome regions. A genome-wide landscape of switched compartments and differentially expressed genes between HA1800 and A172 cell lines demonstrated that compartment activation reshaped chromatin accessibility and activated tumorigenesis-related genes. Topological associating domain (TAD) analysis revealed that altered TAD domains in A172 also contribute to oncogene activation and tumor repressor deactivation. Interestingly, glioblastoma-derived A172 cells showed a different chromatin loop contact propensity. Genes in tumorigenesis-associated signaling pathways were significantly enriched at the anchor loci of altered chromatin loops. Oncogene activation and tumor repressor deactivation were associated with chromatin loop alteration. Structure variations (SVs) had a dramatic impact on the chromatin conformation of\n                      <jats:italic toggle=\"yes\">EGFR-<\/jats:italic>\n                      amplified glioblastoma-derived tumor cells. Moreover, our results revealed that 7p11.2 duplication activated\n                      <jats:italic toggle=\"yes\">EGFR<\/jats:italic>\n                      expression in\n                      <jats:italic toggle=\"yes\">EGFR<\/jats:italic>\n                      -amplified glioblastoma via neo-TAD formation and novel enhancer-promoter interaction emergence between\n                      <jats:italic toggle=\"yes\">LINC01446<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">EGFR<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The disordered 3D genomic map and multi-omics data of\n                      <jats:italic toggle=\"yes\">EGFR-<\/jats:italic>\n                      amplified glioblastoma provide a resource for future interrogation of the relationship between chromatin interactions and transcriptome in tumorigenesis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.csbj.2022.04.007","type":"journal-article","created":{"date-parts":[[2022,4,8]],"date-time":"2022-04-08T21:30:34Z","timestamp":1649453434000},"page":"1967-1978","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":18,"title":["Alterations in 3D chromatin organization contribute to tumorigenesis of\n                    <i>EGFR<\/i>\n                    -amplified glioblastoma"],"prefix":"10.34133","volume":"20","author":[{"given":"Qi","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"},{"name":"Hunan International Scientific and Technological Cooperation Base of Brain Tumor Research, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nian","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"},{"name":"Hunan International Scientific and Technological Cooperation Base of Brain Tumor Research, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Han","family":"Zou","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"},{"name":"Hunan International Scientific and Technological Cooperation Base of Brain Tumor Research, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, Hunan 410008, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuning","family":"Fan","sequence":"additional","affiliation":[{"name":"Annoroad Gene Tech. 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