One of the hallmarks of cancer cells is their indefinite replicative potential, made possible by the activation of a telomere maintenance mechanism (TMM). The majority of cancers reactivate the reverse transcriptase, telomerase, to maintain their telomere length but a minority (10% to 15%) utilize an alternative lengthening of telomeres (ALT) pathway. Here, we review the phenotypes and molecular markers specific to ALT, and investigate the significance of telomere mutations and sequence variation in ALT cell lines. We also look at the recent advancements in understanding the different mechanisms behind ALT telomere elongation and finally, the progress made in identifying potential ALT-targeted therapies, including those already in use for t...
Maintaining replicative immortality is a crucial step in the development of cancers and is achieved ...
Abstract The vast majority of adult cancer cells achieve cellular immortality by activating a telome...
Telomere shortening necessitates that tumor cells activate a telomere maintenance mechanism (TMM) to...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
To escape from the normal limits on proliferative potential, cancer cells must employ a means to cou...
<div><p>The Alternative Lengthening of Telomeres (ALT) pathway is a telomerase-independent pathway f...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Abstract Telomeres are specialized nucleoprotein structures responsible for protecting chromosome en...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Overcoming cellular senescence that is induced by telomere shortening is critical in tumorigenesis. ...
Immortalisation is a hallmark of cancer and requires activation of a telomere lengthening mechanism ...
Telomeres are biological constructs that protect the genomic information from DNA damage repair path...
Maintaining replicative immortality is a crucial step in the development of cancers and is achieved ...
Abstract The vast majority of adult cancer cells achieve cellular immortality by activating a telome...
Telomere shortening necessitates that tumor cells activate a telomere maintenance mechanism (TMM) to...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of repli...
To escape from the normal limits on proliferative potential, cancer cells must employ a means to cou...
<div><p>The Alternative Lengthening of Telomeres (ALT) pathway is a telomerase-independent pathway f...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Abstract Telomeres are specialized nucleoprotein structures responsible for protecting chromosome en...
Tumour cells can adopt telomere maintenance mechanisms (TMMs) to avoid telomere shortening, an inevi...
Overcoming cellular senescence that is induced by telomere shortening is critical in tumorigenesis. ...
Immortalisation is a hallmark of cancer and requires activation of a telomere lengthening mechanism ...
Telomeres are biological constructs that protect the genomic information from DNA damage repair path...
Maintaining replicative immortality is a crucial step in the development of cancers and is achieved ...
Abstract The vast majority of adult cancer cells achieve cellular immortality by activating a telome...
Telomere shortening necessitates that tumor cells activate a telomere maintenance mechanism (TMM) to...