Cellular Senescence Controlled by p53 is a Barrier to Environmental

@inproceedings{Vergel2015CellularSC,
  title={Cellular Senescence Controlled by p53 is a Barrier to Environmental},
  author={Carcinogenesisdel Mar Vergel and Sandra Mu{\~n}oz-Galv{\'a}n and Daniel Otero-Albiol and Amancio Carnero},
  year={2015}
}
Cancer development in humans and animals may be caused by environmental factors. It has been estimated that approximately 80% of human tumors are generated by exposure to environmental carcinogens. The carcinogens may initiate or induce progression of tumors in several ways. Cellular senescence is a natural barrier used by cells to respond to stress. The molecular analysis of immortal clones shows alterations, either structural or epigenetic, in the genes involved in cellular senescence. It is… Expand

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References

SHOWING 1-10 OF 55 REFERENCES
Tumor cell senescence in cancer treatment.
TLDR
Clinical and preclinical studies indicate that expression of different biological classes of senescence-associated growth-regulatory genes in tumor cells has significant prognostic implications, which makes it possible to design new therapeutic approaches to improving the efficacy and to decreasing the side effects of cancer therapy. Expand
Carcinogen-specific mutational and epigenetic alterations in INK4A, INK4B and p53 tumour-suppressor genes drive induced senescence bypass in normal diploid mammalian cells
TLDR
As SIPS/OIS bypass is a prerequisite for the immortalization of normal diploid human epithelial cells, the results with the Syrian hamster model will provide a basis for delineating combinations of key molecular changes underpinning this important event in human carcinogenesis. Expand
Cellular Senescence as a Target in Cancer Control
TLDR
The potential of cellular senescence to be used as target for anticancer therapy is reviewed, suggesting that it is a natural mechanism to prevent undesired oncogenic stress in somatic cells that has been lost in malignant tumors. Expand
Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TLDR
It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus. Expand
Characterization of the p53 Response to Oncogene-Induced Senescence
TLDR
PPP1CA (the catalytic subunit of PP1α), recently identified as contributing to Ras-induced senescence, might be this second signal contributing to the irreversibility of the senescent phenotype, which is suggested to be a Ras-dependent, p53-independent, second signal. Expand
Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis
TLDR
It is shown that conditional inactivation of Trp53 in the mouse prostate fails to produce a tumour phenotype, whereas complete Pten inactivation in the prostate triggers non-lethal invasive prostate cancer after long latency, and support a model for cooperative tumour suppression in which p53 is an essential failsafe protein of Pten-deficient tumours. Expand
Cellular senescence and cancer
TLDR
To escape mortality a developing tumour must overcome multiple ‘proliferative lifespan barriers’ (PLBs) by successive genetic events, each conferring a new wave of clonal expansion. Expand
Hallmarks of senescence in carcinogenesis and cancer therapy
TLDR
The emerging knowledge about the pathways that lead to senescence and determine the pattern of gene expression in senescent cells may lead to more effective treatments for cancer. Expand
BRAFE600-associated senescence-like cell cycle arrest of human naevi
TLDR
It is shown that sustained BRAFV600E expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity, a commonly usedsenescence marker. Expand
MAP17 enhances the malignant behavior of tumor cells through ROS increase.
TLDR
This work shows the tumorigenic capability of MAP17 through a connection between Na+-coupled co-transporters and ROS, and shows that MAP17-dependent ROS increase and tumorigenesis are dependent on its PDZ-binding domain, since disruption of its sequence by point mutations abolishes its ability to enhance ROS production and tumorsigenesis. Expand
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