ALTercations at telomeres: stress, recombination and extrachromosomal affairs.
Taylor K LoeEros Lazzerini DenchiGianna M TricolaBenura AzerogluPublished in: Biochemical Society transactions (2023)
Approximately 15% of human cancers depend on the alternative lengthening of telomeres (ALT) pathway to maintain telomeres and proliferate. Telomeres that are elongated using ALT display unique features raising the exciting prospect of tailored cancer therapies. ALT-mediated telomere elongation shares several features with recombination-based DNA repair. Strikingly, cells that use the ALT pathway display abnormal levels of replication stress at telomeres and accumulate abundant extrachromosomal telomeric DNA. In this review, we examine recent findings that shed light on the ALT mechanisms and the strategies currently available to suppress this telomere elongation mechanism.
Keyphrases
- dna repair
- dna damage
- dna damage response
- induced apoptosis
- endothelial cells
- squamous cell carcinoma
- stress induced
- oxidative stress
- cell proliferation
- squamous cell
- lymph node metastasis
- childhood cancer
- young adults
- endoplasmic reticulum stress
- smoking cessation
- heat stress
- children with cerebral palsy
- current status