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In prostate cancer, there is evidence that large topologically associating domains in normal cells split and are accompanied by shifts in the epigenetic marks from inactive to active states. However, it is unclear whether changes in genome organization alone can account for the gene expression increase in cancer cells. By combining polymer physics concepts and data-driven modeling, we first calculated an ensemble of three-dimensional (3D) chromatin structures using only the 2D contact map as input. The enhancer-promoter (E\u2013P) distance distributions for the overexpressed Androgen Receptor (AR) and Forkhead Box Protein A1 (FOXA1) are broad, with mean values exceeding the threshold for direct E\u2013P contact. Importantly, the average E\u2013P distances decrease in the cancer cells, compared to normal cells in the\n                  <jats:italic>AR<\/jats:italic>\n                  locus, whereas in\n                  <jats:italic>FOXA1<\/jats:italic>\n                  they are roughly constant or increase modestly. Similarly, the number of multiway contacts increases as cancer progresses across cancer cell lines in the\n                  <jats:italic>AR<\/jats:italic>\n                  locus. In contrast, the number of multiway contacts in\n                  <jats:italic>FOXA1<\/jats:italic>\n                  is similar in normal and cancer cells. Because the 3D characteristics do not explain the enhanced gene expression in cancer cells, we developed Activity-by-Multiway-Contact (AMC) Model that integrates the multiway contacts with enhancer biochemical activity. The AMC model provides a plausible mechanism for the overexpression of both\n                  <jats:italic>AR<\/jats:italic>\n                  and\n                  <jats:italic>FOXA1<\/jats:italic>\n                  in prostate cancer. Moreover, using Micro-C data for breast cancer, we show that the number of multiway enhancer-promoter contacts increases in four of five genes studied. When multiway contacts are combined with biochemical activity, changes in gene expression found in the experiment, positively correlate with the AMC score. The predictions of the AMC model not only account for overexpression of genes in prostate and breast cancer but also provide a basis for understanding gene expression variations in other genes as well.\n                <\/jats:p>","DOI":"10.64898\/2026.04.25.720760","type":"posted-content","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T05:45:15Z","timestamp":1777441515000},"source":"Crossref","is-referenced-by-count":0,"title":["Connecting multiway enhancer-promoter interactions to changes in gene expression in cancer"],"prefix":"10.64898","author":[{"given":"Kiran","family":"Kumari","sequence":"first","affiliation":[{"name":"Department of Chemistry, The University of Texas at Austin, Austin, Texas 78712, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7589-1499","authenticated-orcid":false,"given":"Sucheol","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Chemistry, The University of Texas at Austin, Austin, Texas 78712, USA"},{"name":"School of Chemistry and Energy, Sungshin Women\u2019s University, Seoul, South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4377-7210","authenticated-orcid":false,"given":"Guang","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Chemistry, The University of Texas at Austin, Austin, Texas 78712, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1466-8258","authenticated-orcid":false,"given":"Kathleen S.","family":"Metz Reed","sequence":"additional","affiliation":[{"name":"Center for Cancer Research, National Cancer Institute, NIH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3530-3020","authenticated-orcid":false,"given":"Tom","family":"Misteli","sequence":"additional","affiliation":[{"name":"Center for Cancer Research, National Cancer Institute, NIH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Thirumalai","sequence":"additional","affiliation":[{"name":"Department of Chemistry, The University of Texas at Austin, Austin, Texas 78712, USA"},{"name":"Department of Physics, The University of Texas at Austin, Austin, Texas 78712, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026043013151042000_2026.04.25.720760v1.1","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-022-05365-x"},{"issue":"1","key":"2026043013151042000_2026.04.25.720760v1.2","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1146\/annurev-cancerbio-030617-050134","article-title":"Regulation and dysregulation of chromosome structure in cancer","volume":"2","year":"2018","journal-title":"Annual Review of Cancer Biology"},{"key":"2026043013151042000_2026.04.25.720760v1.3","doi-asserted-by":"crossref","first-page":"1069","DOI":"10.1016\/j.trecan.2023.07.017","article-title":"Spatial promoter\u2013enhancer hubs in cancer: Organization, regulation, and function","volume":"9","year":"2023","journal-title":"Trends in Cancer"},{"issue":"1","key":"2026043013151042000_2026.04.25.720760v1.4","first-page":"1","article-title":"A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome","volume":"10","year":"2019","journal-title":"Nature communications"},{"issue":"2","key":"2026043013151042000_2026.04.25.720760v1.5","first-page":"e202104108","article-title":"Chromosome compartmentalization alterations in prostate cancer cell lines model disease progression","volume":"221","year":"2021","journal-title":"Journal of Cell Biology"},{"issue":"1","key":"2026043013151042000_2026.04.25.720760v1.6","doi-asserted-by":"crossref","first-page":"7111","DOI":"10.1038\/s41467-023-42651-2","article-title":"Tracing cancer evolution and heterogeneity using Hi-C","volume":"14","year":"2023","journal-title":"Nature Communications"},{"key":"2026043013151042000_2026.04.25.720760v1.7","doi-asserted-by":"crossref","unstructured":"Lavanya Choppavarapu , Kun Fang , Tianxiang Liu , Aigbe G Ohihoin , and Victor X Jin . 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