Articles tagged with Cellular Senescence
Manuel Serrano proposes a new vision of cellular senescence as a mechanism to eliminate unwanted cells and promote tissue regeneration. Recent research reveals that senescence is not intrinsically negative for the organism, but rather a protective mechanism against cell damage.
A new study found that adjuvant chemotherapy increases markers of molecular aging in the blood of BC survivors, including p16INK4a and ARF expression. These age-promoting effects may last for several years after treatment and even be permanent.
A team of investigators has identified a previously unknown mechanism regulating oncogene-induced senescence (OIS), a natural response to tumor development. Down-regulation of deoxyribonucleoside pools causes DNA damage, leading to cell cycle arrest and senescence. Restoration of depleted dNTP pools can suppress DNA damage and OIS.
Disabling the Skp2 gene after oncogenic stress induces cellular senescence in cancer cells, restricting tumor growth. Researchers believe this could lead to novel agents that suppress tumor development in common types of cancer.
Researchers enhanced a type of cellular senescence to suppress prostate tumor development and growth in mice. This novel approach uses Pten-loss-induced cellular senescence to prevent cancer progression.
A new study reveals that cellular senescence, a natural process for fighting cancer in younger persons, can actually promote cancer in older individuals by triggering the secretion of proteins that cause inflammation. This process is linked to almost every major disease associated with aging, including many cancers.
A new study identifies CUL7 E3 ubiquitin ligase as a key regulator of protein degradation linked to cellular senescence. The researchers found that the enzyme targets insulin receptor substrate 1 (IRS-1) for degradation, leading to oncogene-induced senescence.
Dr. Smith, editor of GSA's Journal of Gerontology: Biological Sciences, receives the Robert W. Kleemeier Award for his decades-long research on cellular senescence. His work focuses on chromatin structure alterations in this process.
Researchers found that MYC binds to the WRN gene promoter, activating WRN expression and promoting cellular senescence in tumor cells. This discovery suggests a potential therapeutic target for cancer treatment by inhibiting WRN in MYC-induced tumor cells.