Cancer Resistant Mouse Provides Possible Cure 364
Evoluder writes to tell us that scientists at Wake Forest University have found a "cancer resistant mouse" and bred it to make a small army of cancer resistant mice. When transplanting blood from one of these mice to a normal non-resistant mouse they are able to provide "lifetime cancer protection". From the article: "The cancer-resistant mice all stem from a single mouse discovered in 1999. "The cancer resistance trait so far has been passed to more than 2,000 descendants in 14 generations," said Cui, associate professor of pathology. It also has been bred into three additional mouse strains. About 40 percent of each generation inherits the protection from cancer."
Reference (Score:5, Informative)
Another cure??? (Score:5, Informative)
Some angiogenesis inhibitors have proven to be very helpful in treating cancer, but they are not a cure. They aren't nearly as effective in humans as they were in mice, it appears.
I'm always skeptical (and you should be too), when you hear about something that isn't even in clinical trials, as a possible cure for some disease people get. People simply don't respond the same as mice.
That said, this does look promising as an avenue, but I wouldn't go out and take up smoking just yet.
Good Idea/Bad Idea (Score:4, Informative)
A cancerous cell is one that doesn't know when to quit. It is outside the normal cell cycle, and not listening to every cell's built in death trigger. Forvige my lack of specific biology terminalogy.
So these mice are "cancer-resistant"? When exposed to carcenigous, do they ignore them? When exposed to massive ammounts of UV light, do they tan but not burn? Do they burn but not get skin cancer? If you clogged thier lungs with cig smoke, would they develop a cough but not cancer?
How the frak does this work? Are the little mice cells just really tuned into thier death trigger? When a cell mutates enough that it doesn't listen to it's death trigger, it is a cancer. Are these mice just impervious to cell mutation?
If so, wouldn't that make them an evolutionary dead end? Cancer, while bad, is a by-product of evolution. If cells weren't allowed to ever mutate again, would that spell the end of mice evolution? And if we impart that "cancer-immunity" to we humans, would that spell the end of evolution?
By all means, someone correct what I have wrong. Biology was never my strong suit. (Nor is spelling)
BBC article . Structure of important enzyme . (Score:4, Informative)
http://news.bbc.co.uk/2/hi/health/4698264.stm [bbc.co.uk]
Re:Beware. (Score:4, Informative)
Assuming that this article [latimes.com] isn't completely incorrect, I'd say it's pretty safe to say that we'll have trouble fucking it up. It exists in every mammal [including mice] and has existed for well over 600 Million years. Fun read on a fascinating topic.
Re:Good Idea/Bad Idea (Score:5, Informative)
Re:Cancer resistant... (Score:4, Informative)
Re:Good Idea/Bad Idea (Score:4, Informative)
Mutations during meiosis are not cancer, so no cancer doesn't mean no evolution.
Re:*squeak* *squeak* (Score:2, Informative)
Yes, Pinky and The Brain
One is a genius
The other's insane.
They're laboratory mice
Their genes have been spliced
They're dinky
They're Pinky and The Brain, Brain, Brain, Brain
Brain, Brain, Brain, Brain
Brain.
Re:BBC article . Structure of important enzyme . (Score:3, Informative)
1) Transformation, in which the cell begins to replicate outside of normal controls. You can get a tumour this way, but without step 2, the tumour doesn't get very far before the cells start to grow quiescent - they lose vitality and stop dividing.
The reason they slow down is that their telomeres have degraded. Telomeres are long stretches of "junk" DNA at the end of each chromosome. Every cycle of DNA replication erodes the end of each chromosome (due to the way replication works at the molecular level). Telomeres absorb this loss without causing erosion of active genes.
A human zygote cell is only capable of ~80-90 cell divisions before these telomeres have fully eroded and active genes are affected. Fortunately, 2^90 is plenty of cells for an adult with a typical lifespan.
2) Activation of telomerase. The purpose of telomerase seems to be to refresh telomeres in the genes of sperm/egg cells to start the cycle fresh for a new human. In "successful" cancer, telomerase permits the cancerous cells to reproduce indefinitely by maintaining telomeres.
*wistful sigh* Ah, the PhD I never did. Then again, I can afford to feed my family in my current career...
Re:Another cure??? (Score:5, Informative)
Part of the problem may be the difference in lifetimes between mice and humans, as well as problems in detecting small tumors.
Anti-angiogenic therapy leads to a hypoxic tumor microenvironment (the tissue surrounding the tumor), which can, in turn, lead a tumor to fragment into smaller tumors. (This has been predicted in mathematical/computer models and verified in some experiments and clinical evidence.)
In a mouse, those small tumors may not have time to grow large enough to detect, whereas in a human, those fragments have more time to do so, leading to recurrence. Or the small tumors may preferentially grow away from the low-O2/low-glucose region to invade nearby tissues.
Other, slow time-scale interactions may also not come into play for short mouse lifespans but may be important on human lifespans.
Of course, the genetic differences are there, too. The problems with the mouse model have always been interesting. -- Paul
Yes, you can... (Score:5, Informative)
The first is by expression profiling- looking at difference in gene expression. See http://en.wikipedia.org/wiki/Gene_chip [wikipedia.org] This will actually give you a readout of how the two cells are different in terms of how they use different genes to express their differences.
The other is positional cloning. You basically breed a resistant mouse with a non-resistant mouse to get an F1 intercross. If you are dealing with inbred mice, these are genetically identical but each chromosome is different- one from mom and one from dad. You breed this generation with eachother to get an F2 intercross and then phenotype the offspring (are they resistant to cancer?) and then genotype them (what are their genetic differences?). Genes undergo semi-random reassortment through cross-over events and all offspring in the F2 incross have a random sprinkling of genes from mom and dad. You then do linkage analysis to find out which genetic differences are most closely linked to the phenotype you are looking for.
Well, Almost.... (Score:3, Informative)
Read around the higlighted area of this page:
http://72.14.207.104/search?q=cache:9GiRpofmvSgJ: