Senescence and immortalization: role of telomeres and telomerase.

By J. Shay, W. Wright. Carcinogenesis, 2005

751 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.

Mitochondrial Energetics and Therapeutics (2010, neutral): “Therefore, the replicative life span of human diploid fibroblasts, the Hayflick limit (219, 220), is presumably due to mitochondrial ROS production and not the end-replication problem.”
Cellular senescence: when bad things happen to good cells (2007, background): “Rare mutational or epigenetic events can activate TERT expression or recombination mechanisms to elongate telomere”
Cancer stem cells: models and concepts. (2007, background): “To become immortal, cancer cells must be endowed with a system for the maintenance of telomere length, in most cases based on telomerase, a ribonucleoproteic enzymatic complex that counteracts the progressive shortening of telomere repeat sequences during in vitro proliferation of normal somatic cel”
Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “Indeed, several lines of evidence have recently implicated oncogene-induced cellular senescence (OIS), which is induced prematurely (that is, before telomeric shortening can account for it [Shay and Wright, 2005]), as a vital cause of arrest of benign neoplasms.”