Current advances in the role of classical non‐homologous end joining in hematologic malignancies
Abstract Background Double‐strand breaks (DSBs) are universally acknowledged as the most detrimental type of DNA damage, and their effective repair primarily depends on the non‐homologous end joining (NHEJ) pathway. Such DSBs, which require NHEJ for resolution, can arise from intrinsic and extrinsic...
Saved in:
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2025-06-01
|
| Series: | Clinical and Translational Discovery |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/ctd2.70053 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850168862544232448 |
|---|---|
| author | Pengcheng Liu Zizhen Xu |
| author_facet | Pengcheng Liu Zizhen Xu |
| author_sort | Pengcheng Liu |
| collection | DOAJ |
| description | Abstract Background Double‐strand breaks (DSBs) are universally acknowledged as the most detrimental type of DNA damage, and their effective repair primarily depends on the non‐homologous end joining (NHEJ) pathway. Such DSBs, which require NHEJ for resolution, can arise from intrinsic and extrinsic DNA‐damaging factors or emerge naturally during essential biological processes like V(D)J recombination and antibody class switch recombination. Main Body Failure to properly repair DSBs may lead to genomic instability, disruption of cellular functions, and immunodeficiency, thereby promoting the development of hematologic malignancies. Conversely, overexpression of NHEJ‐related genes can enhance resistance to DNA‐damaging therapies in these cancers. Analyzing mutations in key classical NHEJ (cNHEJ) components and understanding their mechanisms could provide valuable biomarkers for predicting therapeutic outcomes and guiding treatment decisions. Consequently, defects in cNHEJ may offer insights into the development of novel drugs targeting DNA repair pathways. Conclusion We focus on genetic changes and alterations in gene regulation, while also providing an overview of cNHEJ. |
| format | Article |
| id | doaj-art-42970b3866f946df845aecfd5bc53905 |
| institution | OA Journals |
| issn | 2768-0622 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical and Translational Discovery |
| spelling | doaj-art-42970b3866f946df845aecfd5bc539052025-08-20T02:20:52ZengWileyClinical and Translational Discovery2768-06222025-06-0153n/an/a10.1002/ctd2.70053Current advances in the role of classical non‐homologous end joining in hematologic malignanciesPengcheng Liu0Zizhen Xu1Department of Laboratory Medicine College of Health Science and Technology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai ChinaDepartment of Laboratory Medicine College of Health Science and Technology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai ChinaAbstract Background Double‐strand breaks (DSBs) are universally acknowledged as the most detrimental type of DNA damage, and their effective repair primarily depends on the non‐homologous end joining (NHEJ) pathway. Such DSBs, which require NHEJ for resolution, can arise from intrinsic and extrinsic DNA‐damaging factors or emerge naturally during essential biological processes like V(D)J recombination and antibody class switch recombination. Main Body Failure to properly repair DSBs may lead to genomic instability, disruption of cellular functions, and immunodeficiency, thereby promoting the development of hematologic malignancies. Conversely, overexpression of NHEJ‐related genes can enhance resistance to DNA‐damaging therapies in these cancers. Analyzing mutations in key classical NHEJ (cNHEJ) components and understanding their mechanisms could provide valuable biomarkers for predicting therapeutic outcomes and guiding treatment decisions. Consequently, defects in cNHEJ may offer insights into the development of novel drugs targeting DNA repair pathways. Conclusion We focus on genetic changes and alterations in gene regulation, while also providing an overview of cNHEJ.https://doi.org/10.1002/ctd2.70053DNA damage repairhematologic malignanciesleukaemialymphomamyelomanon‐homologous end joining |
| spellingShingle | Pengcheng Liu Zizhen Xu Current advances in the role of classical non‐homologous end joining in hematologic malignancies Clinical and Translational Discovery DNA damage repair hematologic malignancies leukaemia lymphoma myeloma non‐homologous end joining |
| title | Current advances in the role of classical non‐homologous end joining in hematologic malignancies |
| title_full | Current advances in the role of classical non‐homologous end joining in hematologic malignancies |
| title_fullStr | Current advances in the role of classical non‐homologous end joining in hematologic malignancies |
| title_full_unstemmed | Current advances in the role of classical non‐homologous end joining in hematologic malignancies |
| title_short | Current advances in the role of classical non‐homologous end joining in hematologic malignancies |
| title_sort | current advances in the role of classical non homologous end joining in hematologic malignancies |
| topic | DNA damage repair hematologic malignancies leukaemia lymphoma myeloma non‐homologous end joining |
| url | https://doi.org/10.1002/ctd2.70053 |
| work_keys_str_mv | AT pengchengliu currentadvancesintheroleofclassicalnonhomologousendjoininginhematologicmalignancies AT zizhenxu currentadvancesintheroleofclassicalnonhomologousendjoininginhematologicmalignancies |