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Protein Converts Pancreatic Cancer Cells Back Into Healthy Cells
An anonymous reader writes: Scientists working in the area of pancreatic cancer research have uncovered a technique that sees cancerous cells transform back into normal healthy cells. The method relies in the introduction of a protein called E47, which bonds with particular DNA sequences and reverts the cells back to their original state. The study (abstract) was a collaboration between researchers at the Sanford-Burnham Medical Research Institute, University of California San Diego and Purdue University. The scientists are hopeful that it could help combat the deadly disease in humans.
The problem is that neither cancer nor cold are of "common" types: there are quite a few types of each.
One man's cancer could be quite different from another man's, even if they are both found at the same place in the body. The pancreatic cancer mentioned in the article is only one type of pancreatic cancer, although it is the most common form that would originally form there. Cancer in the pancreas could also be another type of cancer that was formed elsewhere and metastasized.
Similarly, there are many different viruses that can cause "cold".
"We mustn't be caught by surprise by our own advancing technology" -- Aldous Huxley
I should hope we do.
Pissing about curing someone's sniffle that'll be gone tomorrow when we could have spent that time/money pushing cancer research - no matter how slow and small a contribution - seems a bloody bad trade-off.
The cure for a cold is to wait 2 weeks.
Who knows we may use the common cold to actually cure cancer.
But my memory of what's special about Pancreatic Cancer - is that you are f*cked to a high degree of certainty if you get it.
Not the most common type of cancer, and there are many types of it - but for those with this cancer, in this place, it's pretty damn important as there weren't a surfeit of alternatives.
Yes, but they also have certain commonalities. Just like almost all gas engines have a fuel pump, if you want to kill a gas engine, you might want to consider cutting power to the fuel pump. They have have different types of ignition systems, they might have forced air induction, they might be 4, 6, 8 cylinders, etc... but most cancer cells do share a lot of common pathways.
That's a good point. Mind if I forward your post to my doctor?
"I like to lick butts!" by MobileTatsu-NJG (#32700246) (Score:5, Informative)
The way this was done was really clever: it uses a virus that causes cancer to treat cancer. Specifically, the retroviral vector is an engineered strain of Moloney Murine Leukemia Virus (MoMuLV), which can cause leukemia in mice (it is not known to cause disease in humans, though retroviral infection does carry at least a small risk of mutagenesis). The viral vector inserts a gene that expresses the protein E47, which acts in a variety of ways to make cancer cells revert to acting like healthy cells.
This is an exciting idea, though as the press release notes, "we are screening for molecules—potential drugs—that can induce overexpression of E47." That's a way of noting that retroviral vector gene therapy is in its infancy, and that it would be much better if we could find a small molecule instead.
And also the above- established tumors notoriously mutate and become genetically heterogeneous over time, greatly increasing the chances that at least some of the cancer cells are resistant to whatever line of attack you throw at them. Cancer cells that have mutant forms of E47's targets wouldn't be reprogrammed. Still, any advance against pancreatic cancer is highly welcome.
"FDA staff reviewers expressed concern about the number of patients who were left out of the study because they died."
The commonality amongst cancers is that they are aneuploid. This has been known for quite some time but is ignored in studies like this. The cells will not be "normal" after this treatment unless it somehow corrected the aneuploidy (this was not measured, but there is no reason to think it did). Since both point mutation rate and chromosomal instability are increased in most aneuploid cells they easily adapt to treatments targeting specific proteins/DNA sequences over time, leading to drug resistance. This study only observed mice for 5 weeks which is not very long. It may not have been long enough for the cells to adapt. Also, the tumorigenic cells were already expressing the "growth-suppressive" protein when transplanted into mice, the treatment was not applied in vivo.
Even if some way of activating this protein or mimicking it's effects in vivo can be devised, it is unlikely be translated into a cure until there is a method allowing sustained targeting of aneuploid cells. If we had such a method, we would want to get rid of the cells rather than only suppress their growth since a subset is likely to become resistant to any treatment we can apply eventually.
That isn't to say the information reported by Kim et al. is not useful (assuming it is accurate). Rather my point is that the hyping of scientific findings really needs to stop. It is out of control and leading to the spread and sustenance of misinformation. In the researcher's favor, I do note they only talk about "combating" the disease rather than curing it.