Cancer cells establish replicative immortality by activating a telomere-maintenance
mechanism (TMM), be it telomerase or the alternative lengthening of telomeres (ALT) …

Ubiquitination is an essential regulator of most, if not all, signalling pathways, and defects in
cellular signalling are central to cancer initiation, progression and, eventually, metastasis …

Telomeres, the end fragments of chromosomes, play key roles in cellular proliferation and
senescence. Here we characterize the genetic architecture of naturally occurring variation in …

Eukaryotic cells compartmentalize their internal milieu in order to achieve specific reactions
in time and space. This organization in distinct compartments is essential to allow …

To escape replicative senescence, cancer cells have to overcome telomere attrition during
DNA replication. Most of cancers rely on telomerase to extend and maintain telomeres, but 4 …

Genetic alterations, including DNA mutations and chromosomal abnormalities, are primary
drivers of tumor formation and cancer progression. These alterations can endow cells with a …

Over the course of three decades of study, the deubiquitinase Herpesvirus associated
Ubiquitin-Specific Protease/Ubiquitin-Specific Protease 7 (HAUSP/USP7) has gradually …

Alternative lengthening of telomeres (ALT) is a mechanism of telomere maintenance that is
observed in many of the most recalcitrant cancer subtypes. Telomeres in ALT cancer cells …

Telomeres are DNA repeats at the ends of linear chromosomes and are replicated by
telomerase, a ribonucleoprotein reverse transcriptase. Telomere length regulation and …

Cancer cells acquire replicative immortality by activating a telomere maintenance
mechanism (TMM), either the telomerase or the Alternative Lengthening of Telomeres (ALT) …