Peto's paradox states: "There appears to be no correlation between body size, longevity and cancer across species and the absence of such a relationship is referred to as Peto’s Paradox".
Example: whales and elephants are massive cell conglomerates with long lifespans. Why don't they have high cancer rates, higher than humans? Why do humans not have higher cancer rates than smaller mammals? Is there a paradox? If so, what does it mean for the use of small, short-lived mammals such as mice as cancer models?
Maybe you should try the lifetime of a single cell? the number of mitoses per unit of time (in which acts the carcinogen; as an example); the duration of the G1 and S phases, during which it has the DNA repair. I imagine that the G1 and S phases may be very different in small and large animals; instead G2 and M should not be very different. I still believe that the selective pressure acting differently in very large populations (small animals) and very small populations (large mammals). I can not look at these assumptions because I do not have the cultural tools needed.
Thanks for the response! Unfortunately, we as a scientific community don't seem to know the average cell division number of a cancer-susceptiple cell in different species nor different tissue types, do we?
It would be interesting to know whether certain tissues have exuberant cancer incidence rates. The ectocervix appears to be such a region, probably related to carcinogen exposure? Even compared to Caucasian skin in sun-exposed USA, the ectocervix has a very high cancer rate when compared based on surface area and taking into account only half of the population has an ectocervix.
I do not know if what I wrote in another thread may interest you.
Staying within the carcinomas ( epithelial malignancies ), these are very rare in some anatomical sites (and when present, they are in the context of some syndromic complex), epididymis , seminal vesicles , uterine tubes , the small intestine etc. Conversely locations where cancers arise most frequently are the transition areas where active chronic inflammatory processes result in a high cells turnover (sometimes with metaplastic processes ) . In these circumstances carcinogens ( chemical and biological ) have more effect ( the bronchial mucosa, the cervix where there is a transition between squamous and columnar epithelium , the gastric mucosa which changes and becomes absorbent type ( intestinal metaplasia ), etc. . Other areas of transition are particularly subject to turnover following the sequence of hormonal secretory and proliferative stimuli ( ductulus in the breast , at the junction between the duct and lobule where the majority of breast cancers occurs , the endometrium etc). Probably this is not the sole cause of the difference in the incidence of cancer in various epithelia, but it can be one of the main switchboards. Seems to me that, for example, the seminal vesicles have been studied to find some intrinsic characteristic to justify their inability to develop cancer , but I think with few results.
In other circumstances specific genes are likely involved. The keratoacanthoma of the skin that arises from structures of the hair. It shares many morphological and molecular characters with squamous cell carcinoma of the epidermis, however, are probably still active genes that regulate hair growth (anagen and catagen). Thus, this tumor grows and regresses on schedule by the hair cycle.
https://www.researchgate.net/post/Can_cancer_come_from_any_type_of_cell_or_are_there_some_cell_types_that_never_produce_cancer?_tpcectx=profile_answers
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