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Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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A Sensitive Method to Quantify Senescent Cancer Cells
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Modeling of senescent cell dynamics predicts a late-life decrease in cancer incidence.

Margaux Bieuville1, Tazzio Tissot2, Alexandre Robert3

  • 1Eco-Anthropologie (EA UMR 7206), MNHN, CNRS Université Paris-Diderot Paris France.

Evolutionary Applications
|March 27, 2023
PubMed
Summary
This summary is machine-generated.

Cellular senescence, a trade-off between cancer and aging mortality, explains cancer incidence patterns. This process can optimize reproductive success and is influenced by life-history traits.

Keywords:
Peto's paradoxageingcancerdemographyevolutionlife‐history traitssenescent cells

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Techniques to Induce and Quantify Cellular Senescence
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Area of Science:

  • Evolutionary biology
  • Gerontology
  • Cancer research

Background:

  • Current cancer theories struggle to predict age-specific incidence and interspecies prevalence.
  • Observed decelerating cancer rates in old age and lack of correlation with species size contradict existing models.
  • A trade-off between cancer mortality and other aging-related causes is hypothesized.

Purpose of the Study:

  • To explore the hypothesis that cellular senescence explains incongruent cancer epidemiological patterns.
  • To investigate the trade-off between cancer and aging mortality mediated by senescent cells.
  • To model the adaptive role of cellular senescence and its impact on species-specific cancer risk.

Main Methods:

  • Developed a deterministic model of cellular damage, apoptosis, and senescence.
  • Translated cellular dynamics into an organismal survival metric incorporating life-history traits.
  • Analyzed the adaptive significance of senescence, species size effects, and senescent cell removal.

Main Results:

  • Cellular senescence can be adaptive, optimizing lifetime reproductive success.
  • Life-history traits significantly influence cellular trade-offs.
  • Model predictions align with observed epidemiological patterns across mammal species.

Conclusions:

  • Cellular senescence offers a framework to resolve inconsistencies in cancer incidence and prevalence.
  • Integrating cellular biology with eco-evolutionary principles is key to understanding cancer.
  • Senescence plays a crucial role in balancing cancer risk and aging-related mortality across species.