Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Aging Sci. 2009 Dec;2(3):174-86.

Aging and inflammation: etiological culprits of cancer.

Author information

1
Department of Pathology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.

Abstract

The biochemical phenomenon of aging, as universal as it is, still remains poorly understood. A number of diseases are associated with aging either as a cause or consequence of the aging process. The incidence of human cancers increases exponentially with age and therefore cancer stands out as a disease that is intricately connected to the process of aging. Emerging evidence clearly suggests that there is a symbiotic relationship between aging, inflammation and chronic diseases such as cancer; however, it is not clear whether aging leads to the induction of inflammatory processes thereby resulting in the development and maintenance of chronic diseases or whether inflammation is the causative factor for inducing both aging and chronic diseases such as cancer. Moreover, the development of chronic diseases especially cancer could also lead to the induction of inflammatory processes and may cause premature aging, suggesting that longitudinal research strategies must be employed for dissecting the interrelationships between aging, inflammation and cancer. Here, we have described our current understanding on the importance of inflammation, activation of NF-kappaB and various cytokines and chemokines in the processes of aging and in the development of chronic diseases especially cancer. We have also reviewed the prevailing theories of aging and provided succinct evidence in support of novel theories such as those involving cancer stem cells, the molecular understanding of which would likely hold a great promise towards unraveling the complex relationships between aging, inflammation and cancer.

KEYWORDS:

Aging; NF-κB; cancer; immunity; inflammation

PMID:
19997527
PMCID:
PMC2789465
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Bentham Science Publishers Ltd. Icon for PubMed Central
    Loading ...
    Support Center