Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment

Abstract Chromosomal translocations are the main etiological factor of hematologic malignancies. These translocations are generally the consequence of aberrant DNA double-strand break (DSB) repair. DSBs arise either exogenously or endogenously in cells and are repaired by major pathways, including n...

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Autores principales:	Mohsen Valikhani, Elahe Rahimian, Seyed Esmaeil Ahmadi, Rouzbeh Chegeni, Majid Safa
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Double-strand break Double-strand break repair Non-homologous end-joining Alternative end-joining pathways Hematologic malignancies Targeted therapy Diseases of the blood and blood-forming organs RC633-647.5 Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/f65821dddac94eee87c69283e2a72504
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spelling	oai:doaj.org-article:f65821dddac94eee87c69283e2a725042021-11-07T12:18:16ZInvolvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment10.1186/s40164-021-00242-12162-3619https://doaj.org/article/f65821dddac94eee87c69283e2a725042021-11-01T00:00:00Zhttps://doi.org/10.1186/s40164-021-00242-1https://doaj.org/toc/2162-3619Abstract Chromosomal translocations are the main etiological factor of hematologic malignancies. These translocations are generally the consequence of aberrant DNA double-strand break (DSB) repair. DSBs arise either exogenously or endogenously in cells and are repaired by major pathways, including non-homologous end-joining (NHEJ), homologous recombination (HR), and other minor pathways such as alternative end-joining (A-EJ). Therefore, defective NHEJ, HR, or A-EJ pathways force hematopoietic cells toward tumorigenesis. As some components of these repair pathways are overactivated in various tumor entities, targeting these pathways in cancer cells can sensitize them, especially resistant clones, to radiation or chemotherapy agents. However, targeted therapy-based studies are currently underway in this area, and furtherly there are some biological pitfalls, clinical issues, and limitations related to these targeted therapies, which need to be considered. This review aimed to investigate the alteration of DNA repair elements of C-NHEJ and A-EJ in hematologic malignancies and evaluate the potential targeted therapies against these pathways.Mohsen ValikhaniElahe RahimianSeyed Esmaeil AhmadiRouzbeh ChegeniMajid SafaBMCarticleDouble-strand breakDouble-strand break repairNon-homologous end-joiningAlternative end-joining pathwaysHematologic malignanciesTargeted therapyDiseases of the blood and blood-forming organsRC633-647.5Neoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENExperimental Hematology & Oncology, Vol 10, Iss 1, Pp 1-26 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Double-strand break Double-strand break repair Non-homologous end-joining Alternative end-joining pathways Hematologic malignancies Targeted therapy Diseases of the blood and blood-forming organs RC633-647.5 Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Double-strand break Double-strand break repair Non-homologous end-joining Alternative end-joining pathways Hematologic malignancies Targeted therapy Diseases of the blood and blood-forming organs RC633-647.5 Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Mohsen Valikhani Elahe Rahimian Seyed Esmaeil Ahmadi Rouzbeh Chegeni Majid Safa Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
description	Abstract Chromosomal translocations are the main etiological factor of hematologic malignancies. These translocations are generally the consequence of aberrant DNA double-strand break (DSB) repair. DSBs arise either exogenously or endogenously in cells and are repaired by major pathways, including non-homologous end-joining (NHEJ), homologous recombination (HR), and other minor pathways such as alternative end-joining (A-EJ). Therefore, defective NHEJ, HR, or A-EJ pathways force hematopoietic cells toward tumorigenesis. As some components of these repair pathways are overactivated in various tumor entities, targeting these pathways in cancer cells can sensitize them, especially resistant clones, to radiation or chemotherapy agents. However, targeted therapy-based studies are currently underway in this area, and furtherly there are some biological pitfalls, clinical issues, and limitations related to these targeted therapies, which need to be considered. This review aimed to investigate the alteration of DNA repair elements of C-NHEJ and A-EJ in hematologic malignancies and evaluate the potential targeted therapies against these pathways.
format	article
author	Mohsen Valikhani Elahe Rahimian Seyed Esmaeil Ahmadi Rouzbeh Chegeni Majid Safa
author_facet	Mohsen Valikhani Elahe Rahimian Seyed Esmaeil Ahmadi Rouzbeh Chegeni Majid Safa
author_sort	Mohsen Valikhani
title	Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
title_short	Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
title_full	Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
title_fullStr	Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
title_full_unstemmed	Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
title_sort	involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment
publisher	BMC
publishDate	2021
url	https://doaj.org/article/f65821dddac94eee87c69283e2a72504
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Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment

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