Skip to comments.Virus kills breast cancer cells in laboratory
Posted on 09/25/2011 10:09:20 PM PDT by hiho hiho
HERSHEY, Pa. -- A nondisease-causing virus kills human breast cancer cells in the laboratory, creating opportunities for potential new cancer therapies, according to Penn State College of Medicine researchers who tested the virus on three different breast cancer types that represent the multiple stages of breast cancer development.
Adeno-associated virus type 2 (AAV2) is a virus that regularly infects humans but causes no disease. Past studies by the same researchers show that it promotes tumor cell death in cervical cancer cells infected with human papillomavirus. Researchers used an unaltered, naturally occurring version of AAV2 on human breast cancer cells.
"Breast cancer is the most prevalent cancer in the world and is the leading cause of cancer-related death in women," said Samina Alam, research associate in microbiology and immunology. "It is also complex to treat."
Craig Meyers, professor of microbiology and immunology, said breast cancer is problematic to treat because of its multiple stages. "Because it has multiple stages, you can't treat all the women the same. Currently, treatment of breast cancer is dependent on multiple factors such as hormone-dependency, invasiveness and metastases, drug resistance and potential toxicities. Our study shows that AAV2, as a single entity, targets all different grades of breast cancer."
Cells have multiple ways of dying. If damage occurs in a healthy cell, the cell turns on production and activation of specific proteins that allow the cell to commit suicide. However, in cancer cells these death pathways often are turned off, while the proteins that allow the cell to divide and multiply are stuck in the "on" position.
One way to fight cancer is to find ways to turn on these death pathways, which is what researchers believe is happening with the AAV2 virus.
In tissue culture dishes in the laboratory, 100 percent of the cancer cells are destroyed by the virus within seven days, with the majority of the cell death proteins activated on the fifth day. In another study, a fourth breast cancer derived cell line, which is the most aggressive, required three weeks to undergo cell death.
"We can see the virus is killing the cancer cells, but how is it doing it?" Alam said. "If we can determine which viral genes are being used, we may be able to introduce those genes into a therapeutic. If we can determine which pathways the virus is triggering, we can then screen new drugs that target those pathways. Or we may simply be able to use the virus itself."
Research needs to be completed to learn how AAV2 is killing cancer cells and which of its proteins are activating the death pathways. According to Meyers, the cellular myc gene seems to be involved. While usually associated with cell proliferation, myc is a protein also known to promote cell death. The scientists have observed increased expression of myc close to the time of death of the breast cancer cells in the study. They report their results in a recent issue of Molecular Cancer.
AAV2 does not affect healthy cells. However, if AAV2 were used in humans, the potential exists that the body's immune system would fight to remove it from the body. Therefore, by learning how AAV2 targets the death pathways, researchers potentially can find ways to treat the cancer without using the actual virus.
In ongoing studies, the Penn State researchers also have shown AAV2 can kill cells derived from prostate cancer, methoselioma, squamous cell carcinoma, and melanoma. A fourth line of breast cancer cells -- representing the most aggressive form of the disease -- also was studied in a mouse breast tumor model, followed by treatment with AAV2. Preliminary results show the destruction of the tumors in the mice, and researchers will report the findings of those mouse studies soon.
Other researchers on this project are Brian S. Bowser and Mohd Israr, Department of Microbiology and Immunology; Michael J. Conway, Section of Infection Diseases, Yale School of Medicine; and Apurva Tandon, Department of Microbiology, Immunology and Pathology, Colorado State University.
The Pennsylvania Department of Health, Breast and Cervical Cancer Initiative supported this research. The researchers have filed for a U.S. patent on this work.
Dah! That should be the first approach as it seems quite obvious and probably not difficult at all as the virus doesn't do any harm to the individual. Of course it may also be the one that causes the drug companies to make the least money be far. Is there anything we all can do to not let this get deep sixed by the drug companies and their henchmen?
Mad scientist ping.
Remember that nutria were imported to eat all the water lillies which were thought to be harmless until they clogged up rivers and lakes. Now the nutrias take their rest in burrowed levees shaded by kudzu vines with their only enemy the infestation of fire ants.
Not to worry, however, it was reported that a Texas Aggie biologist is experimenting with bringing in the only known natural enemy of fire ants—a rare Brazilian gnat that kills them by biting the back of their neck and sucking their brains out. (I’m not making this up}
A virus that kills cells shouldn’t be a problem. Bring it on.
If it regularly infects humans why are there not more spontaneous remissions of at least a small kind. The quest it seems would be to grow it independently and fuse it ongoingly into the body at a rate that the body cannot overcome it until the cancer is gone and according to the article that should not take too much time.
Maybe it will turn out that to get the virus to kill a large percentage of the cancers, or to do so with fewer unwanted side effects, it will have to be genetically modified, which is something the pharmaceutical companies can happily slap a patent on.
How regular is regular, they don’t say. It might be passed around through every hundredth person or something like that. Also what does it take, intimate contact or the kind of casual contagion that spreads colds? Getting the virus earlier and having it overcome and learned by the immune system might also interfere with it being available when it would do good to a cancer patient.
They probably would like us to believe so but to simply grow it and transfuse it into the body in larger numbers than the body can get rid of quickly just like any other virus, i.e. the common cold etc., probably would work but at much less expense.
Always a danger with things like this. Almost all viruses end up killing cells once they have managed to hijack the cells’ replication machinery in order to crank out more copies of the virus. For people having normally competent immune systems this virus probably won’t be any threat. But if it gets out to, say, the HIV ward, there could be trouble.
Don't you think that that is where inundating the body with a large enough quantity of it would work as the immune system can only handle just so much at a time?
So there would be a standard and a deluxe version of the treatment. Those who can pay for the deluxe version and think it’s worth it, can do so.
Only empirical studies could tell us whether this approach would allow the virus to hang around long enough to slay the cancer cells. If worse comes to worst, there are also immunosuppressant drugs that would allow the virus to stick around longer.
Then they will send in Chinese Needle Snakes to eat the gnats, then snake-eating gorillas, and then when wintertime rolls around, the gorillas will simply freeze to death.
Sounds like a plan. :)
Oh, no that wouldn't happen. The eviro-weenies would get a judge to appoint a guardian ad litem for the gorillas that would make sure they received adequate Section 8 housing.
It seems what you are talking about is only a differences between the delivery mechanisms. One is done through the [number of] pills, other is through a procedure, most likely within a clinical environment.
It’s not obvious that the pharma would be more costly, especially if there are several companies with tweaked formula capsules (after all, the virus would be the known main “ingredient”) possibly binding it to certain proteins which could also make them “targeted” to specific types of cancer or specific environments, such as genetic or regional.
Also, pharma gets cheaper with the passing of time (going off patent, volume manufacturing etc.) and competition, while the clinical procedures get more expensive with time - I assume here that the cost of virus production is negligible relative to other costs.
How can this be? If it infects your cells then your cells are not functioning properly. What am I missing here?
I believe that what is meant is that the virus is able to get inside the cell and live there despite the cell or bodies’ defense against such intrusion. So, you’d find this virus inside cells but no disease or pathogenic indications - the cell tolerates the presence of the virus. As another FReeper noted - this doesn’t always remain static and the virus can mutate or adapt to cause problems not previously experienced. But it’s possible we would be willing to swap that risk and or problem in place of cancer.
The dreaded ampersand has come back to haunt me. Yeah, you got me ace...
CLEANUP ON AISLE 5!!!!!!!!!!! STAT!!!
Just avert your eyes.....the mess will be cleaned up and not one amper&and will be visible! I SWEAR!
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