Author: Haolu Sun1, Guijuan Chen2, Baochang Guo3, Shushu Lv4, Guojun Yuan2
1 Department of Pathophysiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230011, China.
2 School of Environment and Chemical Engineering, Anhui Vocational and Technical College, Hefei, 230011, China.
3 Rehabilitation Department of Traditional Chinese Medicine, 969 Hospital of the Joint Support Force of the Chinese People's Liberation Army, Hohhot, 010000, China.
4 Department of Pathology, The First Affiliated Hospital of Huzhou University, Huzhou 313000, China.
Conference/Journal: J Cancer
Date published: 2023 Jan 31
Other: Volume ID: 14 , Issue ID: 3 , Pages: 417-433 , Special Notes: doi: 10.7150/jca.80097. , Word Count: 214
Normal somatic cells inevitably experience replicative stress and senescence during proliferation. Somatic cell carcinogenesis can be prevented in part by limiting the reproduction of damaged or old cells and removing them from the cell cycle [1, 2]. However, Cancer cells must overcome the issues of replication pressure and senescence as well as preserve telomere length in order to achieve immortality, in contrast to normal somatic cells [1, 2]. Although telomerase accounts for the bulk of telomere lengthening methods in human cancer cells, there is a non-negligible portion of telomere lengthening pathways that depend on alternative lengthening of telomeres (ALT) . For the selection of novel possible therapeutic targets for ALT-related disorders, a thorough understanding of the molecular biology of these diseases is crucial . The roles of ALT, typical ALT tumor cell traits, the pathophysiology and molecular mechanisms of ALT tumor disorders, such as adrenocortical carcinoma (ACC), are all summarized in this work. Additionally, this research compiles as many of its hypothetically viable but unproven treatment targets as it can (ALT-associated PML bodies (APB), etc.). This review is intended to contribute as much as possible to the development of research, while also trying to provide a partial information for prospective investigations on ALT pathways and associated diseases.
Keywords: ALT; Telomerase; diseases; molecular mechanism; therapeutic targets.
PMID: 36860927 PMCID: PMC9969575 DOI: 10.7150/jca.80097