Influence of Age on Colorectal Cancer’s 5-Year Survival

The post-mitotic cell reached by normal cell populations after serial divisions has been regarded as the hallmark of cell senescence. It was proposed that this non-dividing cell is a mechanism of protection against malignant transformation and different approaches have been used to induce the post-mitotic state. There are contradictions and paradoxes between the concepts and the data, which are described herein. There are also contradictions between data from different laboratories that attempted to identify the mechanisms leading to the post-mitotic cell. The contradictions are bypassed with the claim that there are different pathways to cell senescence. The contradictions and the differences between the data should be explained before these phenomena can be understood.

Section: Cancers Through Aging and Senescence Of The Human Organism: mentioning

confidence: 99%

Cancers and the concept of cell senescence

Macieira‐Coelho

2009

Putative mechanisms responsible for the decline in cancer prevalence during organism senescence

Macieira‐Coelho

2015

Most scientific literature reports that aging favors the development of cancers. Each type of cancer, however, initiates and evolves differently, and their natural history can start much earlier in life before their clinical manifestations. The incidence of cancers is spread throughout human life span, and is the result of pre- and post-natal aggressions, individual susceptibility, developmental changes that evolve continuously throughout an individual's life, and time of exposure to carcinogens. Finally, during human senescence, the incidence declines for all cancers. Frequently, the progression of cancers is also slower in aged individuals. There are several possible explanations for this decline at the tissue, cell, and molecular levels, which are described here in. It is time to ask why some tumors are characteristic of either the young, the aged, or during the time of a decline in the reproductive period, and finally, why the incidence of cancers declines late during senescence of human beings. These questions need to be addressed before the origin of cancers can be understood.

Untitled

Macieira‐Coelho¹

2001

Cancers are different diseases that start and evolve each in its own manner, and trigger variable responses from the organism depending upon the neoplastic process under way and upon the physiopathology of the organism. The clinical incidence of the different cancers is spread through the human life span, with regional differences for each cancer: for many cancers the incidence is increasing at younger ages. More than half of the cancers become clinically manifest during the second half of the human life span and their frequency increases with age, but their natural history starts way back at earlier ages. The data suggest that the late manifestation is the result of the accumulation of events through time rather than of aging. Interestingly, late in the human life span the incidence of neoplastic disease declines. Is this due to the cohort of late survivals naturally resistant to the development of neoplastic processes, or to the characteristics of the last 'window' of the human life span? The evolution of neoplastic disease is the result of pre- and postnatal aggressions suffered by the organism, individual susceptibility, and developmental changes that evolve continuously from the beginning to the end of the human life span. The identification of the causes of the incidences of the different cancers through the human life span will help to understand both neoplastic disease and aging of the organism.