About this Research Topic
The overall incidence of cancer increases exponentially with age. However, the relationship between cellular, tissue or organ senescence and cancer is poorly understood. In particular, there is no clear understanding of the mechanisms by which ageing promotes both a progressive decline in the function of multiple cells and tissues, as well as hyperplastic pathologies, the most deadly of which is cancer. Some researchers claim that there is no evidence of any effect of ageing itself on the molecular and cellular processes leading to cancer. Having said that, it is intriguing that some animals don’t seem to exhibit signs of senescence, and cancer is therefore rarely produced. The elucidation of such underlying mechanisms relating ageing with cancer might help to design strategies aimed at both preventing cancer and prolonging life.
Different and not yet well-integrated hypotheses of ageing and cancer have been proposed. At a cellular level, the senescence response is widely recognized as a potent tumor suppressor mechanism through the activation of p53 and pRb pathways, leading to a drastic arrest of cell proliferation. In contrast, some researchers claim that the accumulation of senescent cells in organs or tissues may stimulate chronic inflammation, the outcome of which would be degenerative and hyperplastic pathologies such as cancer. Others highlight the fact that, during the processes of ageing, the stromal-epithelial interactions decline within different organs, leading to anomalous epithelial changes and, ultimately, cancer.
This Research Topic aims to discuss the correlation between ageing and carcinogenesis. We welcome Original Research and Review articles discussing the following themes:
- Ageing, chronic inflammation and cancer
- Age-related loss of regenerative ability and cancer
- Changes in stroma-epithelium interactions during ageing and carcinogenesis
- Cancer and immortality
- Molecular mechanisms underlying ageing-related and cancer onset
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Dr. Carlos M Galmarini is the owner of Topazium Artificial Intelligence. The Topics Editors report no further commercial or financial relationships that could be construed as a potential conflict of interest.
Different and not yet well-integrated hypotheses of ageing and cancer have been proposed. At a cellular level, the senescence response is widely recognized as a potent tumor suppressor mechanism through the activation of p53 and pRb pathways, leading to a drastic arrest of cell proliferation. In contrast, some researchers claim that the accumulation of senescent cells in organs or tissues may stimulate chronic inflammation, the outcome of which would be degenerative and hyperplastic pathologies such as cancer. Others highlight the fact that, during the processes of ageing, the stromal-epithelial interactions decline within different organs, leading to anomalous epithelial changes and, ultimately, cancer.
This Research Topic aims to discuss the correlation between ageing and carcinogenesis. We welcome Original Research and Review articles discussing the following themes:
- Ageing, chronic inflammation and cancer
- Age-related loss of regenerative ability and cancer
- Changes in stroma-epithelium interactions during ageing and carcinogenesis
- Cancer and immortality
- Molecular mechanisms underlying ageing-related and cancer onset
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Dr. Carlos M Galmarini is the owner of Topazium Artificial Intelligence. The Topics Editors report no further commercial or financial relationships that could be construed as a potential conflict of interest.
Keywords: ageing, carcinogenesis, cellular senescence, chronic inflammation, stromal-epithelial interactions
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
