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Molecular damage in cancer: an argument for mTOR-driven aging

Mikhail V Blagosklonny1

  • 1Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. blagosklonny@oncotarget.com

Aging
|January 17, 2012
PubMed

Insights

Molecular damage is not a key driver of aging, contrary to popular belief. Instead, it initiates cancer, distinguishing it from aging despite shared pathways like TOR.

Area of Science:

  • Gerontology and Cancer Biology
  • Molecular Biology and Genetics

Background:

  • Aging is often associated with accumulated molecular damage, but this link is debated.
  • Cancer, a disease of aging, is known to be initiated by molecular damage.
  • The TOR pathway is activated in both aging and cancer, suggesting shared mechanisms.

Purpose of the Study:

  • To challenge the notion that molecular damage accumulation is the primary cause of aging.
  • To differentiate the roles of molecular damage in aging versus cancer.
  • To explore how molecular damage contributes to the development of cancer hallmarks.

Main Methods:

  • Comparative analysis of aging and cancer biology.
  • Review of molecular damage accumulation in aging.
  • Examination of cancer initiation and progression mechanisms.
  • Exploration of the TOR pathway in aging and cancer.

Main Results:

  • Accumulation of molecular damage is not a key factor in the aging process.
  • Molecular damage plays a crucial role in cancer initiation, distinguishing it from aging.
  • The TOR pathway's activation is common to both aging and cancer.
  • Random molecular damage, through selection and multiplication, leads to non-random cancer hallmarks.

Conclusions:

  • The established link between molecular damage and aging requires re-evaluation.
  • Molecular damage is a critical differentiator between aging and cancer.
  • Understanding these distinctions is vital for developing targeted therapies for age-related diseases and cancer.

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