Senescence

Helen Rizos; Lyndee L. Scurr

doi:10.1007/978-3-7091-0371-5_11

Senescence

Helen Rizos^*, Lyndee L. Scurr

^*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and can potently prevent tumour formation in vivo. The precise mechanisms driving senescence are still not completely defined, although the pRb and p53 tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal ageing and age-related diseases, including cancer. It is not yet clear whether the pro-ageing actions of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced program may depend on establishing a new equilibrium that favours tumour suppressor activity.

Original language	English
Title of host publication	Melanoma Development
Subtitle of host publication	Molecular Biology, Genetics and Clinical Application
Editors	A Bosserhoff
Place of Publication	Wien
Publisher	Springer, Springer Nature
Pages	235-254
Number of pages	20
ISBN (Electronic)	9783709103715
ISBN (Print)	9783709103708
DOIs	https://doi.org/10.1007/978-3-7091-0371-5_11
Publication status	Published - 18 May 2011
Externally published	Yes

Keywords

ONCOGENE-INDUCED SENESCENCE
CELL-CYCLE ARREST
MELANOMA SUSCEPTIBILITY GENES
HUMAN-DIPLOID FIBROBLASTS
HEMATOPOIETIC STEM-CELLS
DNA-DAMAGE RESPONSE
IN-VIVO
TUMOR SUPPRESSION
BETA-GALACTOSIDASE
C-MYC

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10.1007/978-3-7091-0371-5_11

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title = "Senescence",

abstract = "Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and can potently prevent tumour formation in vivo. The precise mechanisms driving senescence are still not completely defined, although the pRb and p53 tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal ageing and age-related diseases, including cancer. It is not yet clear whether the pro-ageing actions of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced program may depend on establishing a new equilibrium that favours tumour suppressor activity.",

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author = "Helen Rizos and Scurr, {Lyndee L.}",

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doi = "10.1007/978-3-7091-0371-5_11",

language = "English",

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T1 - Senescence

AU - Rizos, Helen

AU - Scurr, Lyndee L.

PY - 2011/5/18

Y1 - 2011/5/18

N2 - Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and can potently prevent tumour formation in vivo. The precise mechanisms driving senescence are still not completely defined, although the pRb and p53 tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal ageing and age-related diseases, including cancer. It is not yet clear whether the pro-ageing actions of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced program may depend on establishing a new equilibrium that favours tumour suppressor activity.

AB - Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and can potently prevent tumour formation in vivo. The precise mechanisms driving senescence are still not completely defined, although the pRb and p53 tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal ageing and age-related diseases, including cancer. It is not yet clear whether the pro-ageing actions of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced program may depend on establishing a new equilibrium that favours tumour suppressor activity.

KW - ONCOGENE-INDUCED SENESCENCE

KW - CELL-CYCLE ARREST

KW - MELANOMA SUSCEPTIBILITY GENES

KW - HUMAN-DIPLOID FIBROBLASTS

KW - HEMATOPOIETIC STEM-CELLS

KW - DNA-DAMAGE RESPONSE

KW - IN-VIVO

KW - TUMOR SUPPRESSION

KW - BETA-GALACTOSIDASE

KW - C-MYC

U2 - 10.1007/978-3-7091-0371-5_11

DO - 10.1007/978-3-7091-0371-5_11

M3 - Chapter

SN - 9783709103708

SP - 235

EP - 254

BT - Melanoma Development

A2 - Bosserhoff, A

PB - Springer, Springer Nature

CY - Wien

ER -

Senescence

Abstract

Keywords

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