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Related Experiment Video

Updated: May 17, 2026

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

Aging, cellular senescence, and cancer.

Judith Campisi¹

¹Buck Institute for Research on Aging, Novato, California 94945, USA. jcampisi@buckinstitute.org

Annual Review of Physiology

|November 13, 2012

Summary

This summary is machine-generated.

Aging causes tissue damage and cancer, linked by cellular senescence. This cellular stress response, while tumor-suppressive, may also drive age-related diseases through chronic inflammation.

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Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

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SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

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Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Area of Science:

Gerontology
Cell Biology
Pathology

Background:

Aging is associated with degenerative pathologies (loss of function) and hyperplastic pathologies (e.g., cancer).
Malignant cells gain aberrant functions to form lethal tumors, contrasting with cellular degeneration.

Purpose of the Study:

To explore the link between aging pathologies and cellular senescence.
To discuss cellular senescence as a potential common mechanism underlying both degenerative and hyperplastic aging pathologies.

Main Methods:

Review of existing scientific literature on aging, cellular senescence, and pathology.
Analysis of evidence connecting cellular senescence to inflammation and age-related diseases.

Main Results:

Cellular senescence, a stress response, is a known tumor suppressor.
Emerging evidence suggests senescence also drives degenerative and hyperplastic pathologies, potentially via chronic inflammation.

Conclusions:

Cellular senescence may be an antagonistically pleiotropic mechanism in aging.
The senescence response could be a unifying factor in diverse aging-related pathologies, linking tissue degeneration and cancer development.