Dimitri Conomos, Hilda A. Pickett, Roger R. Reddel
Abstract
To escape from the normal limits on proliferative potential, cancer cells must employ a means to counteract the gradual telomere attrition that accompanies semi-conservative DNA replication. While the majority of human cancers do this by up-regulating telomerase enzyme activity, most of the remainder use a homologous recombination-mediated mechanism of telomere elongation known as alternative lengthening of telomeres (ALT). Many molecular details of the ALT pathway are unknown, and even less is known regarding the mechanisms by which this pathway is activated. Here, we review current findings about telomere structure in ALT cells, including DNA sequence, shelterin content, and heterochromatic state. We speculate that remodeling of the telomere architecture may contribute to the emergence and maintenance of the ALT phenotype.
This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 February 2017.
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#7,778,510
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#78,031
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Outputs of similar age from Frontiers in oncology
#46
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Altmetric has tracked 25,373,627 research outputs across all sources so far. This one has received more attention than most of these and is in the 69th percentile.
So far Altmetric has tracked 22,416 research outputs from this source. They receive a mean Attention Score of 3.0. This one has done well, scoring higher than 87% of its peers.
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We're also able to compare this research output to 328 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.
