Chromatin structure in cancer
Abstract In the past decade, we have seen the emergence of sequence-based methods to understand chromosome organization. With the confluence of in situ approaches to capture information on looping, topological domains, and larger chromatin compartments, understanding chromatin-driven disease is beco...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-07-01
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| Series: | BMC Molecular and Cell Biology |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12860-022-00433-6 |
| _version_ | 1818502560613400576 |
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| author | Meng Wang Benjamin D. Sunkel William C. Ray Benjamin Z. Stanton |
| author_facet | Meng Wang Benjamin D. Sunkel William C. Ray Benjamin Z. Stanton |
| author_sort | Meng Wang |
| collection | DOAJ |
| description | Abstract In the past decade, we have seen the emergence of sequence-based methods to understand chromosome organization. With the confluence of in situ approaches to capture information on looping, topological domains, and larger chromatin compartments, understanding chromatin-driven disease is becoming feasible. Excitingly, recent advances in single molecule imaging with capacity to reconstruct “bulk-cell” features of chromosome conformation have revealed cell-to-cell chromatin structural variation. The fundamental question motivating our analysis of the literature is, can altered chromatin structure drive tumorigenesis? As our community learns more about rare disease, including low mutational frequency cancers, understanding “chromatin-driven” pathology will illuminate the regulatory structures of the genome. We describe recent insights into altered genome architecture in human cancer, highlighting multiple pathways toward disruptions of chromatin structure, including structural variation, noncoding mutations, metabolism, and de novo mutations to architectural regulators themselves. Our analysis of the literature reveals that deregulation of genome structure is characteristic in distinct classes of chromatin-driven tumors. As we begin to integrate the findings from single cell imaging studies and chromatin structural sequencing, we will be able to understand the diversity of cells within a common diagnosis, and begin to define structure–function relationships of the misfolded genome. |
| first_indexed | 2024-12-10T21:11:54Z |
| format | Article |
| id | doaj.art-b03cffda469f4fb282386959c3719889 |
| institution | Directory Open Access Journal |
| issn | 2661-8850 |
| language | English |
| last_indexed | 2024-12-10T21:11:54Z |
| publishDate | 2022-07-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Molecular and Cell Biology |
| spelling | doaj.art-b03cffda469f4fb282386959c37198892022-12-22T01:33:25ZengBMCBMC Molecular and Cell Biology2661-88502022-07-0123111010.1186/s12860-022-00433-6Chromatin structure in cancerMeng Wang0Benjamin D. Sunkel1William C. Ray2Benjamin Z. Stanton3Center for Childhood Cancer and Blood Diseases, Abigail Wexner Research Institute at Nationwide Children’s HospitalCenter for Childhood Cancer and Blood Diseases, Abigail Wexner Research Institute at Nationwide Children’s HospitalBattelle Center for Mathematical Medicine, Abigail Wexner Research Institute at Nationwide Children’s HospitalCenter for Childhood Cancer and Blood Diseases, Abigail Wexner Research Institute at Nationwide Children’s HospitalAbstract In the past decade, we have seen the emergence of sequence-based methods to understand chromosome organization. With the confluence of in situ approaches to capture information on looping, topological domains, and larger chromatin compartments, understanding chromatin-driven disease is becoming feasible. Excitingly, recent advances in single molecule imaging with capacity to reconstruct “bulk-cell” features of chromosome conformation have revealed cell-to-cell chromatin structural variation. The fundamental question motivating our analysis of the literature is, can altered chromatin structure drive tumorigenesis? As our community learns more about rare disease, including low mutational frequency cancers, understanding “chromatin-driven” pathology will illuminate the regulatory structures of the genome. We describe recent insights into altered genome architecture in human cancer, highlighting multiple pathways toward disruptions of chromatin structure, including structural variation, noncoding mutations, metabolism, and de novo mutations to architectural regulators themselves. Our analysis of the literature reveals that deregulation of genome structure is characteristic in distinct classes of chromatin-driven tumors. As we begin to integrate the findings from single cell imaging studies and chromatin structural sequencing, we will be able to understand the diversity of cells within a common diagnosis, and begin to define structure–function relationships of the misfolded genome.https://doi.org/10.1186/s12860-022-00433-6Chromatin structureGenome sequencingCancer epigeneticsSarcomaStructural variationChromatin imaging |
| spellingShingle | Meng Wang Benjamin D. Sunkel William C. Ray Benjamin Z. Stanton Chromatin structure in cancer BMC Molecular and Cell Biology Chromatin structure Genome sequencing Cancer epigenetics Sarcoma Structural variation Chromatin imaging |
| title | Chromatin structure in cancer |
| title_full | Chromatin structure in cancer |
| title_fullStr | Chromatin structure in cancer |
| title_full_unstemmed | Chromatin structure in cancer |
| title_short | Chromatin structure in cancer |
| title_sort | chromatin structure in cancer |
| topic | Chromatin structure Genome sequencing Cancer epigenetics Sarcoma Structural variation Chromatin imaging |
| url | https://doi.org/10.1186/s12860-022-00433-6 |
| work_keys_str_mv | AT mengwang chromatinstructureincancer AT benjamindsunkel chromatinstructureincancer AT williamcray chromatinstructureincancer AT benjaminzstanton chromatinstructureincancer |