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Discovery of "Cancer-Proof" Rodent Cells
anglico sends news of research out of the University of Rochester that has identified a gene that "cancer-proofs" cells in rodents. "Despite a 30-year lifespan that gives ample time for cells to grow cancerous, a small rodent species called a naked mole rat has never been found with tumors of any kind — and now biologists at the University of Rochester think they know why. The findings, presented in the Proceedings of the National Academy of Sciences, show that the mole rat's cells express a gene called p16 that makes the cells 'claustrophobic,' stopping the cells' proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells' growth barely changed, whereas regular mouse cells became fully cancerous."
I'm not worried. I always use poison or traps anyway. You see, its just to difficult to reliably give them cancer.
Judging by the story, and in the context of my almost complete lack of formal training in cell biology, it sounds like the cells might not be resistant to cancer-causing virii, but rather it just means the infected cells can't multiply past a certain point. Sort of like carrying a disease but not showing any symptoms.
For those of you who aren't familiar with them, naked mole rats are pretty weird in a bunch of other ways
They lack the neurotransmitter that lets them feel pain, which is evolutionarily unique as far as I know. Their respiratory systems are adapted to handle the high concentrations of CO2 that build up in their burrows. Their metabolic rate is 2/3 of other similarly sized rodents, and they can slow it even further in times of need.
Their behavior is even weirder. The colonies (200-300 in population) are organized eusocialy, ie in the same manner as a bee or ant colony. There in one queen, with a harem of 3-4 males that produce all the offspring for the entire colony. Like ants, naked mole rats form separate castes for diggers, soldiers, etc. Oh, and to top it all off their front teeth are on the outside of their mouths to help them dig.
Facts do not cease to exist because they are ignored. -Aldous Huxley
The thing is, that's one of the things that defines cancer, so this is an important step towards defeating it. Cancer isn't one disease; it's pretty much any mutation (or, more commonly, series of mutations) that make a cell or group of cells override the checks that the body usually puts on division. Cancer cells don't exhibit density-dependent inhibition like normal cells; it sounds like this p16 gene can help enforce this despite mutations in what are normally oncogenes.
Now you know how I feel when there's an article about API's, Ubuntu, or codecs.
Human cells have and express p16-INK4A normally - it's part of the CDKN2A gene locus. It is a cell cycle control gene whose main function is to put the brakes on replication. p16 is expressed in human cells and is often mutated or outright deleted in many human cancers of all cell types.
COSMIC (new window)
The difference described in naked mole rats is that their cells induce p16 expression after minimal contact with neighboring cells while human and rat cells need more prodding to turn on cell cycle control genes.
This is a cool finding, but does not have a direct application in human cancers anytime soon. It's very hard to turn on a gene that has been mutated or deleted in cancer cells. You have to do it in practically every cell, otherwise, they grow back. Even then it may be too late. Loss of contact inhibition may be necessary in early oncogenesis, but restoration of p16 expression in a cancer cell that already has multiple genetic mutations, may not do much at that point. So, it's an interesting finding and I hope it leads to a better understanding of cancer and cancer prevention. But honestly, we have cool findings like this once a week. It just requires the right spin to sell it to the media - like calling something a "cancer-proof" gene - and it finds its way here.