Telomeres and telomerase in cancer.

By S. Artandi, R. DePinho. Carcinogenesis, 2010

844 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Hallmarks of cancer: the next generation. (2011, positive): “In contrast, experiments in mice engineered to lack telomerase indicate that the consequently shortened telomeres can shunt premalignant cells into a senescent state that contributes (along with apoptosis) to attenuated tumorigenesis in mice genetically destined to develop particular forms of cancer”
The DNA damage response and cancer therapy (2012, background): “Although sometimes considered distinct from the DDR, the mechanisms that control the integrity of telomeric DNA at the end of each human chromosome also act as a barrier against genomic instability and mutatio”
Human papillomavirus oncoproteins: pathways to transformation (2010, background): “For cells to become immortal they must induce the expression of telomerase, an enzyme often activated in cancers that is important for replicating the DNA sequences at the ends of chromosomes called telomeres”
Chromothripsis and kataegis induced by telomere crisis (2015, neutral): “Dicentric chromosomes can be formed during the early stages of human tumorigenesis when telomere shortening has led to dysfunctional telomeres (reviewed in Artandi and DePinho, 2010).”