Rowley, M. J. & Corces, V. G. Organizational ideas of 3D genome structure. Nat. Rev. Genet. 19, 789–800 (2018).
Krijger, P. H. L. & De Laat, W. Regulation of disease-associated gene expression within the 3D genome. Nat. Rev. Mol. Cell Biol. 17, 771–782 (2016).
Deng, S., Feng, Y. & Pauklin, S. 3D chromatin structure and transcription regulation in most cancers. J. Hematol. Oncol. Pharm. 15, 1–23 (2022).
Wang, M., Sunkel, B. D., Ray, W. C. & Stanton, B. Z. Chromatin construction in most cancers. BMC Mol. Cell Biol. 23, 1–10 (2022).
Dekker, J., Rippe, Okay., Dekker, M. & Kleckner, N. Capturing chromosome conformation. Science 295, 1306–1311 (2002).
Lieberman-Aiden, E. et al. Complete mapping of long-range interactions reveals folding ideas of the human genome. Science 326, 289–293 (2009).
Huang, H. et al. CTCF mediates dosage-and sequence-context-dependent transcriptional insulation by forming native chromatin domains. Nat. Genet. 53, 1064–1074 (2021).
Wutz, G. et al. Topologically associating domains and chromatin loops rely upon cohesin and are regulated by CTCF, WAPL, and PDS5 proteins. EMBO J. 36, 3573–3599 (2017).
Merkenschlager, M. & Nora, E. P. CTCF and cohesin in genome folding and transcriptional gene regulation. Annu. Rev. Genom. Hum. 17, 17–43 (2016).
Dixon, J. R. et al. Integrative detection and evaluation of structural variation in most cancers genomes. Nat. Genet. 50, 1388–1398 (2018).
Li, Y. et al. Patterns of somatic structural variation in human most cancers genomes. Nature 578, 112–121 (2020).
Kronenberg, Z. N. et al. Prolonged haplotype-phasing of long-read de novo genome assemblies utilizing Hello-C. Nat. Commun. 12, 1935 (2021).
Wu, S. et al. Round ecDNA promotes accessible chromatin and excessive oncogene expression. Nature 575, 699–703 (2019).
Zhang, Y. et al. Enhancing Hello-C information decision with deep convolutional neural community HiCPlus. Nat. Commun. 9, 750 (2018).
Liu, T. & Wang, Z. HiCNN: a really deep convolutional neural community to raised improve the decision of Hello-C information. Bioinformatics 35, 4222–4228 (2019).
Li, Z. & Dai, Z. SRHiC: a deep studying mannequin to boost the decision of Hello-C information. Entrance. Genet. 11, 353 (2020).
Erdmann-Pham, D. D. et al. Tracing most cancers evolution and heterogeneity utilizing Hello-C. Nat. Commun. 14, 7111 (2023).
Fullwood, M. J. & Ruan, Y. ChIP‐based mostly strategies for the identification of lengthy‐vary chromatin interactions. J. Cell. Biochem. 107, 30–39 (2009).
Fullwood, M. J., Wei, C.-L., Liu, E. T. & Ruan, Y. Subsequent-generation DNA sequencing of paired-end tags (PET) for transcriptome and genome analyses. Genome Res. 19, 521–532 (2009).
Li, G. et al. ChIA-PET device for complete chromatin interplay evaluation with paired-end tag sequencing. Genome Biol. 11, 1–13 (2010).
Fang, R. et al. Mapping of long-range chromatin interactions by proximity ligation-assisted ChIP-seq. Cell Res. 26, 1345–1348 (2016).
Mumbach, M. R. et al. HiChIP: environment friendly and delicate evaluation of protein-directed genome structure. Nat. Strategies 13, 919–922 (2016).
Zheng, M. et al. Multiplex chromatin interactions with single-molecule precision. Nature 566, 558–562 (2019).
Nagano, T. et al. Single-cell Hello-C reveals cell-to-cell variability in chromosome construction. Nature 502, 59–64 (2013).
Nagano, T. et al. Cell-cycle dynamics of chromosomal group at single-cell decision. Nature 547, 61–67 (2017).
Flyamer, I. M. et al. Single-nucleus Hello-C reveals distinctive chromatin reorganization at oocyte-to-zygote transition. Nature 544, 110–114 (2017).
Tan, L., Xing, D., Chang, C.-H., Li, H. & Xie, X. S. Three-dimensional genome buildings of single diploid human cells. Science 361, 924–928 (2018).
Li, G. et al. Joint profiling of DNA methylation and chromatin structure in single cells. Nat. Strategies 16, 991–993 (2019).
Lee, D.-S. et al. Simultaneous profiling of 3D genome construction and DNA methylation in single human cells. Nat. Strategies 16, 999–1006 (2019).
Liu, Z. et al. Linking genome buildings to capabilities by simultaneous single-cell Hello-C and RNA-seq. Science 380, 1070–1076 (2023).
Qu, J. et al. Simultaneous profiling of chromatin structure and transcription in single cells. Nat. Struct. Mol. Biol. 30, 1393–1402 (2023).
Xie, X. et al. Simultaneous single-cell three-dimensional genome and gene expression profiling uncovers dynamic enhancer connectivity underlying olfactory receptor selection. Preprint at https://doi.org/10.21203/rs.3.rs-3210240/v1 (2023).
Rao, S. S. et al. Cohesin loss eliminates all loop domains. Cell 171, 305–320. e324 (2017).
Canela, A. et al. Genome group drives chromosome fragility. Cell 170, 507–521.e518 (2017).
Gryder, B. E., Khan, J. & Stanton, B. Z. Measurement of differential chromatin interactions with absolute quantification of structure (AQuA-HiChIP). Nat. Protoc. 15, 1209–1236 (2020).
Lai, B. et al. Trac-looping measures genome construction and chromatin accessibility. Nat. Strategies 15, 741–747 (2018).
Hughes, J. R. et al. Evaluation of tons of of cis-regulatory landscapes at excessive decision in a single, high-throughput experiment. Nat. Genet. 46, 205–212 (2014).
Hsieh, T.-H. S. et al. Mapping nucleosome decision chromosome folding in yeast by micro-C. Cell 162, 108–119 (2015).
Hua, P. et al. Defining genome structure at base-pair decision. Nature 595, 125–129 (2021).
Sunkel, B. D. et al. Proof of pioneer issue exercise of an oncogenic fusion transcription issue. iScience 24, 102867 (2021).
Boone, M. A. et al. The FLI portion of EWS/FLI contributes a transcriptional regulatory perform that’s distinct and separable from its DNA-binding perform in Ewing sarcoma. Oncogene 40, 4759–4769 (2021).
Gryder, B. E. et al. Histone hyperacetylation disrupts core gene regulatory structure in rhabdomyosarcoma. Nat. Genet. 51, 1714–1722 (2019).
Laubscher, D. et al. BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma. Nat. Commun. 12, 6924 (2021).
Pomella, S. et al. Interplay between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in fusion unfavorable rhabdomyosarcoma. Nat. Commun. 12, 192 (2021).
Yohe, M. E. et al. MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma. Sci. Transl. Med. 10, eaan4470 (2018).
Yan, J. et al. Systematic evaluation of binding of transcription elements to noncoding variants. Nature 591, 147–151 (2021).
Baxter, J. S. et al. Seize Hello-C identifies putative goal genes at 33 breast most cancers danger loci. Nat. Commun. 9, 1028 (2018).
Zaret, Okay. S. Pioneer transcription elements initiating gene community adjustments. Annu. Rev. Genet. 54, 367–385 (2020).
Iyyanki, T. et al. Subtype-associated epigenomic panorama and 3D genome construction in bladder most cancers. Genome Biol. 22, 1–20 (2021).
Hnisz, D. et al. Activation of proto-oncogenes by disruption of chromosome neighborhoods. Science 351, 1454–1458 (2016).
Wang, X., Luan, Y. & Yue, F. EagleC: a deep-learning framework for detecting a full vary of structural variations from bulk and single-cell contact maps. Sci. Adv. 8, eabn9215 (2022).
Spielmann, M., Lupiáñez, D. G. & Mundlos, S. Structural variation within the 3D genome. Nat. Rev. Genet. 19, 453–467 (2018).
Wang, J. et al. Epigenomic panorama and 3D genome construction in pediatric high-grade glioma. Sci. Adv. 7, eabg4126 (2021).
Montefiori, L. E. et al. Enhancer hijacking drives oncogenic BCL11B expression in lineage-ambiguous stem cell leukemia. Most cancers Discov. 11, 2846–2867 (2021).
Mallard, C. et al. Hello-C detects genomic structural variants in peripheral blood of pediatric leukemia sufferers. Mol. Case Stud. 8, a006157 (2022).
Voronina, N. et al. The panorama of chromothripsis throughout grownup most cancers sorts. Nat. Commun. 11, 2320 (2020).
Sungalee, S. et al. Histone acetylation dynamics modulates chromatin conformation and allele-specific interactions at oncogenic loci. Nat. Genet. 53, 650–662 (2021).
Music, T. et al. Integrative identification by Hello-C revealed distinct superior structural variations in Lung Adenocarcinoma tissue. Phenomics 3, 390–407 (2023).
Du, Y. et al. Dynamic Interaction between structural variations and 3D genome group in pancreatic most cancers. Adv. Sci. 9, 2200818 (2022).
Akdemir, Okay. C. et al. Disruption of chromatin folding domains by somatic genomic rearrangements in human most cancers. Nat. Genet. 52, 294–305 (2020).
Dixon, J. R. et al. Topological domains in mammalian genomes recognized by evaluation of chromatin interactions. Nature 485, 376–380 (2012).
Nora, E. P. et al. Spatial partitioning of the regulatory panorama of the X-inactivation centre. Nature 485, 381–385 (2012).
Ke, Y. et al. 3D chromatin buildings of mature gametes and structural reprogramming throughout mammalian embryogenesis. Cell 170, 367–381. e320 (2017).
Du, Z. et al. Allelic reprogramming of 3D chromatin structure throughout early mammalian improvement. Nature 547, 232–235 (2017).
Sima, J. et al. Figuring out cis parts for spatiotemporal management of mammalian DNA replication. Cell 176, 816–830. e818 (2019).
Tanizawa, H., Kim, Okay.-D., Iwasaki, O. & Noma, Okay.-I. Architectural alterations of the fission yeast genome throughout the cell cycle. Nat. Struct. Mol. Biol. 24, 965–976 (2017).
Li, Y. et al. Transcription-coupled structural dynamics of topologically associating domains regulate replication origin effectivity. Genome Biol. 22, 1–29 (2021).
Wang, X. et al. Genome-wide detection of enhancer-hijacking occasions from chromatin interplay information in rearranged genomes. Nat. Strategies 18, 661–668 (2021).
Yang, M. et al. Proteogenomics and Hello-C reveal transcriptional dysregulation in excessive hyperdiploid childhood acute lymphoblastic leukemia. Nat. Commun. 10, 1519 (2019).
Ooi, W. F. et al. Built-in paired-end enhancer profiling and whole-genome sequencing reveals recurrent CCNE1 and IGF2 enhancer hijacking in main gastric adenocarcinoma. Intestine 69, 1039–1052 (2020).
Abdalla, M. O. A. et al. The Eleanor ncRNAs activate the topological area of the ESR1 locus to stability towards apoptosis. Nat. Commun. 10, 3778 (2019).
Wu, P. et al. 3D genome of a number of myeloma reveals spatial genome disorganization related to copy quantity variations. Nat. Commun. 8, 1937 (2017).
Szabo, Q. et al. Regulation of single-cell genome group into TADs and chromatin nanodomains. Nat. Genet. 52, 1151–1157 (2020).
Bintu, B. et al. Tremendous-resolution chromatin tracing reveals domains and cooperative interactions in single cells. Science 362, eaau1783 (2018).
Rao, S. S. et al. A 3D map of the human genome at kilobase decision reveals ideas of chromatin looping. Cell 159, 1665–1680 (2014).
Liu, F., Wu, D. & Wang, X. Roles of CTCF in conformationand capabilities of chromosome. Semin. Cell Dev. Biol. 90, 168–173 (2019).
Tanwar, V. S., Jose, C. C. & Cuddapah, S. Function of CTCF in DNA harm response. Mutat. Res. 780, 61–68 (2019).
Alharbi, A. B., Schmitz, U., Bailey, C. G. & Rasko, J. E. CTCF as a regulator of other splicing: new methods for an outdated participant. Nucleic Acids Res. 49, 7825–7838 (2021).
Nakamura, R. et al. CTCF looping is established throughout gastrulation in medaka embryos. Genome Res. 31, 968–980 (2021).
Agrawal, P. & Rao, S. Tremendous-enhancers and CTCF in early embryonic cell destiny selections. Entrance. Cell Dev. Biol. 9, 653669 (2021).
Lyu, X., Rowley, M. J. & Corces, V. G. Architectural proteins and pluripotency elements cooperate to orchestrate the transcriptional response of hESCs to temperature stress. Mol. Cell 71, 940–955. e947 (2018).
Flavahan, W. A. et al. Insulator dysfunction and oncogene activation in IDH mutant gliomas. Nature 529, 110–114 (2016).
Alpsoy, A. et al. BRD9 is a essential regulator of androgen receptor signaling and prostate most cancers development. Most cancers Res. 81, 820–833 (2021).
Wong, Okay. M., Music, J. & Wong, Y. H. CTCF and EGR1 suppress breast most cancers cell migration by means of transcriptional management of Nm23-H1. Sci. Rep. 11, 491 (2021).
Sivapragasam, S. et al. CTCF binding modulates UV harm formation to advertise mutation scorching spots in melanoma. EMBO J. 40, e107795 (2021).
Hou, Y. et al. CTCF mediates replicative senescence by means of POLD1. Entrance. Cell Dev. Biol. 9, 618586 (2021).
Miyata, Okay. et al. Pericentromeric noncoding RNA adjustments DNA binding of CTCF and inflammatory gene expression in senescence and most cancers. Proc. Natl Acad. Sci. 118, e2025647118 (2021).
Michaelis, C., Ciosk, R. & Nasmyth, Okay. Cohesins: chromosomal proteins that forestall untimely separation of sister chromatids. Cell 91, 35–45 (1997).
Gassler, J. et al. A mechanism of cohesin‐dependent loop extrusion organizes zygotic genome structure. EMBO J. 36, 3600–3618 (2017).
Brackley, C. A. et al. Nonequilibrium chromosome looping by way of molecular slip hyperlinks. Phys. Rev. Lett. 119, 138101 (2017).
Terakawa, T. et al. The condensin complicated is a mechanochemical motor that translocates alongside DNA. Science 358, 672–676 (2017).
Ocampo-Hafalla, M., Muñoz, S., Samora, C. P. & Uhlmann, F. Proof for cohesin sliding alongside budding yeast chromosomes. Open Biol. 6, 150178 (2016).
De Koninck, M. & Losada, A. Cohesin mutations in most cancers. Chilly Spring Harb. Perspect. Med. 6, a026476 (2016).
Waldman, T. Rising themes in cohesin most cancers biology. Nat. Rev. Most cancers 20, 504–515 (2020).
Fisher, J. B., McNulty, M., Burke, M. J., Crispino, J. D. & Rao, S. Cohesin mutations in myeloid malignancies. Developments Most cancers 3, 282–293 (2017).
Bailey, M. L. et al. Paralogous artificial lethality underlies genetic dependencies of the cancer-mutated gene STAG2. Life Sci. Alliance 4, e202101083 (2021).
Surdez, D. et al. STAG2 mutations alter CTCF-anchored loop extrusion, scale back cis-regulatory interactions and EWSR1-FLI1 exercise in Ewing sarcoma. Most cancers Cell 39, 810–826. e819 (2021).
Carico, Z. M., Stefan, H. C., Justice, M., Yimit, A. & Dowen, J. M. A cohesin most cancers mutation reveals a job for the hinge area in genome group and gene expression. PLoS Genet. 17, e1009435 (2021).
Ma, J. et al. miR-223 regulates cell proliferation and invasion by way of concentrating on PDS5B in pancreatic most cancers cells. Mol. Ther. Nucleic Acids 14, 583–592 (2019).
Tothova, Z. et al. Cohesin mutations alter DNA harm restore and chromatin construction and create therapeutic vulnerabilities in MDS/AML. JCI Perception 6, e142149 (2021).
Atkin, N. D., Raimer, H. M., Wang, Z., Zang, C. & Wang, Y. H. Assessing acute myeloid leukemia susceptibility in rearrangement‐pushed sufferers by DNA breakage at topoisomerase II and CCCTC‐binding issue/cohesin binding websites. Genes Chromosomes Most cancers 60, 808–821 (2021).
Kriz, A. J., Colognori, D., Sunwoo, H., Nabet, B. & Lee, J. T. Balancing cohesin eviction and retention prevents aberrant chromosomal interactions, Polycomb-mediated repression, and X-inactivation. Mol. Cell 81, 1970–1987. e1979 (2021).
Gröschel, S. et al. A single oncogenic enhancer rearrangement causes concomitant EVI1 and GATA2 deregulation in leukemia. Cell 157, 369–381 (2014).
Valentijn, L. J. et al. TERT rearrangements are frequent in neuroblastoma and establish aggressive tumors. Nat. Genet. 47, 1411–1414 (2015).
Northcott, P. A. et al. Enhancer hijacking prompts GFI1 household oncogenes in medulloblastoma. Nature 511, 428–434 (2014).
Weischenfeldt, J. et al. Pan-cancer evaluation of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking. Nat. Genet. 49, 65–74 (2017).
Jia, Q., Chen, S., Tan, Y., Li, Y. & Tang, F. Oncogenic super-enhancer formation in tumorigenesis and its molecular mechanisms. Exp. Mol. Med. 52, 713–723 (2020).
Zhuang, H.-H., Qu, Q., Teng, X.-Q., Dai, Y.-H. & Qu, J. Superenhancers as grasp gene regulators and novel therapeutic targets in mind tumors. Exp. Mol. Med. 55, 290–303 (2023).
Xu, Z. et al. Structural variants drive context-dependent oncogene activation in most cancers. Nature 612, 564–572 (2022).
Kim, Okay. et al. Spatial and clonality-resolved 3D most cancers genome alterations reveal enhancer-hijacking as a possible prognostic marker for colorectal most cancers. Cell Rep. 42, 112778 (2023).
Wakita, S. et al. Experimental technique for haplotype phasing throughout your complete size of chromosome 21 in trisomy 21 cells utilizing a chromosome elimination approach. J. Hum. Genet. 67, 565–572 (2022).
Edge, P., Bafna, V. & Bansal, V. HapCUT2: strong and correct haplotype meeting for various sequencing applied sciences. Genome Res. 27, 801–812 (2017).
Ijaz, J. et al. Haplotype-specific meeting of shattered chromosomes in esophageal adenocarcinomas. Cell Genom. 4, 100484 (2024).
Sakamoto, Y. et al. Phasing evaluation of lung most cancers genomes utilizing an extended learn sequencer. Nat. Commun. 13, 3464 (2022).
Garg, S. In direction of routine chromosome-scale haplotype-resolved reconstruction in most cancers genomics. Nat. Commun. 14, 1358 (2023).
Snuderl, M. et al. Mosaic amplification of a number of receptor tyrosine kinase genes in glioblastoma. Most cancers Cell 20, 810–817 (2011).
Szerlip, N. J. et al. Intratumoral heterogeneity of receptor tyrosine kinases EGFR and PDGFRA amplification in glioblastoma defines subpopulations with distinct development issue response. Proc. Natl. Acad. Sci. 109, 3041–3046 (2012).
Kumar, P. et al. ATAC-seq identifies 1000’s of extrachromosomal round DNA in most cancers and cell traces. Sci. Adv. 6, eaba2489 (2020).
Morton, A. R. et al. Purposeful enhancers form extrachromosomal oncogene amplifications. Cell 179, 1330–1341. e1313 (2019).
Helmsauer, Okay. et al. Enhancer hijacking determines extrachromosomal round MYCN amplicon structure in neuroblastoma. Nat. Commun. 11, 5823 (2020).
Misteli, T. The self-organizing genome: ideas of genome structure and performance. Cell 183, 28–45 (2020).
Kim, T. et al. Comparative characterization of 3D chromatin group in triple-negative breast cancers. Exp. Mol. Med. 54, 585–600 (2022).
Li, P. et al. Alteration of chromatin high-order conformation related to oxaliplatin resistance acquisition in colorectal most cancers cells. Exploration 3, 20220136 (2023).
Achinger-Kawecka, J. et al. The potential of epigenetic remedy to focus on the 3D epigenome in endocrine-resistant breast most cancers. Nat. Struct. Mol. Biol. 31, 498–512 (2024).

