3 ms·

Not in equal amounts - cancer is highly correlated with senescence.

Retric 6y ago
The requiring multiple mutations bit is correlated with senescence. For the simplest model assume you need 2 mutations each at 1 in 1 billion odds from 1 of 30,000,000,000,000 cells in the human body. After 1 year, there are 60,000 cells 1 mutation away from cancer. Year N there are N * 60,000 cells. Such a simple model results in linear increases in cancer risks over time without any other effects from age. More complex models can get very close to the observed annual risk of cancer adjusted for age etc. The question is how much this is just over fitting the data.
- inglor_cz 6y ago
  In a healthy organism, damaged cells may be forced to kill themselves (apoptosis) before they do any harm, or killed outright by NK cells during their surveillance patrols. There are corrective mechanisms that animals including humans use to control cancer; even if a cell mutates into something dangerous, it does not mean that a malignant tumor follows. Mice, who have much fewer cells than humans, get cancer much earlier than we do. Elephants and whales, whose cell count exceeds that of humans by several orders of magnitude, seem to be actually less prone to cancer than humans are. This is all about the ability of the body to squash individual cancerous cells or smallish tumors into nonexistence before they have a chance to take hold. As long as this self-defensive mechanism works, everything is fine.
  - Retric 6y ago
    Detecting errors requires cellular machinery to detect them, which are themselves susceptible to mutation. Conceptually, disabling the checksum doesn’t directly cause cancer, you need more mutations after that point. Thus the multiple mutation model. That said, it’s not like these risks are identical in all species, just that their related. A nematode can spend less energy lowering cancer risks than a blue whale.

The requiring multiple mutations bit is correlated with senescence. For the simplest model assume you need 2 mutations each at 1 in 1 billion odds from 1 of 30,000,000,000,000 cells in the human body. After 1 year, there are 60,000 cells 1 mutation away from cancer. Year N there are N * 60,000 cells. Such a simple model results in linear increases in cancer risks over time without any other effects from age. More complex models can get very close to the observed annual risk of cancer adjusted for age etc. The question is how much this is just over fitting the data.

inglor_cz 6y ago
In a healthy organism, damaged cells may be forced to kill themselves (apoptosis) before they do any harm, or killed outright by NK cells during their surveillance patrols. There are corrective mechanisms that animals including humans use to control cancer; even if a cell mutates into something dangerous, it does not mean that a malignant tumor follows. Mice, who have much fewer cells than humans, get cancer much earlier than we do. Elephants and whales, whose cell count exceeds that of humans by several orders of magnitude, seem to be actually less prone to cancer than humans are. This is all about the ability of the body to squash individual cancerous cells or smallish tumors into nonexistence before they have a chance to take hold. As long as this self-defensive mechanism works, everything is fine.
- Retric 6y ago
  Detecting errors requires cellular machinery to detect them, which are themselves susceptible to mutation. Conceptually, disabling the checksum doesn’t directly cause cancer, you need more mutations after that point. Thus the multiple mutation model. That said, it’s not like these risks are identical in all species, just that their related. A nematode can spend less energy lowering cancer risks than a blue whale.