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Senescence & Cancer

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Postby MrMistery » Fri Aug 12, 2005 9:00 pm

Not even if we ask them nicely?
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Postby Chris4 » Fri Aug 12, 2005 11:01 pm

Well you could do that by giving them drugs which induce apoptosis. But thats not really asking, thats forcing them :D
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Postby MrMistery » Sat Aug 13, 2005 8:28 pm

So can we force them? Is there such a drug?
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Postby Dr.Stein » Sun Aug 14, 2005 8:13 am

Yes, we can ask healthy cells to commit suicide, die before the time :wink: We change their fate :lol:
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Postby Poison » Sun Aug 14, 2005 5:35 pm

MrMistery wrote:Not even if we ask them nicely?

Would you like to try? ;) :lol:
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Postby MrMistery » Sun Aug 14, 2005 7:43 pm

I meant is there a drug that will induce apoptosis in cancer cells?
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Postby Dr.Stein » Mon Aug 15, 2005 1:43 am

Irradiation can do that well, but it is not a drug though :)
Or hybridoma, it will help cancer to end their own life for sure :wink:
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Postby Poison » Mon Aug 15, 2005 6:16 pm

I haven't came across to one yet (but of course this doesn't mean there isn't). The researchers are trying to find such kind of method.
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Postby Chris4 » Mon Aug 15, 2005 8:12 pm

Velcade and Genasence appear to be two apoptosis-inducing drugs.
http://plan2004.cancer.gov/discovery/apoptosis.htm
http://cis.nci.nih.gov/fact/7_49.htm

The drug company websites:
http://www.mlnm.com/products/velcade/index.asp
http://www.genta.com/genta/Products/genasense.html

Although Velcade is really a proteasome inhibitor, i guess you could say it induces apoptosis as it causes Bax to build up and this induces apoptosis. But i would have thought it would cause a lot of other proteins to build up and this could create all kinds of problems in the cell. You can see why these kind of drugs have severe side effects :cry:
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Postby Poison » Fri Aug 19, 2005 2:59 pm

Side effects are the negative part of cancer curing. Unfortunately... :(
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Postby weesper » Tue Sep 06, 2005 8:12 am

Some things were said here about senescence but I think the most important issue has been missed still; YES normal cells go into senescence after a certain number of divisions and cancer cells presumably overcome this by expressing telomerase (although the exact role and fucntion of telomerase and how 'cancer-specific' still hasnt become clear after years of research) but more importantly why senescence is so impt is also because normal cells go into senescence as a protective mechanism against tumor formation after mutation in growth promoting oncogenes such as K-ras; the cell probably senses this above normal stimulation of growth and then decides to stop dividing terminally and thereby it is protected from becoming malignant. Now of course the big question is how do tumours overcome this innate protective barrier against tumor formation, resolving that question will give us a much better insight into the early steps of tumor formation (transformation assays or screens or based on the idea of retrieving the brakes that function in senescence and that are mutated in cancer).

Secondly leaky blood vessels arise in angiogenesis because the microenvironment lacks the right mixture of cytokines required for proper balanced angiogenesis (involving VEGF, angiopoietins, PDGF etc etc).

And thirdly using bacteria to eat cancer is something that's actively researched at the moment since tumours are hypoxic and certain bacteria grow better in hypoxic conditions providing the researcher with a natural targeting mechanism.

I think this clarifies some issues that have been discussed here. Further discussion always welcome. gr weesper
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cancer cell lines

Postby crazycells » Wed Sep 14, 2005 4:44 am

In an earlier conversation it was stated "if cancer cells can change back into regular cells."

The issue...

Cancer cells compared to regular cells:

Regular cells have proteins on the surface that categorize that cell type. These proteins are involved in recognizing the cell as it's self; or recognizing Self. Cancer cells have changes in their DNA that change the proteins on the surface of the cell. Ultimately, changing Self. One reason the cancer cells don't respond to drug treatment sometimes is because the protein receptor on the surface of the cell may no longer be there. T

The cancer cell DNA may have changed in a way that the drug cannot respond to drugs that bind to ligands on the surface of the cell. The proteins on the surface are changing in cancer cells. Finding the protein that was changed or impaired can help some cancers. An example of this is the PPAR-gamma, this is a receptor that when impaired can cause type II diabetes in some patients. Recent studies imply that this receptor in fatty tissues (when impaired) can lead to the development of fatty-tissue cancer. Treatment with Type II Diabetic drugs makes these cells go back to normal function (in the lab).

Cancer cells are much like other cells; they have cell lines. A cancer stem cell line gives rise to various cancer cells. The cancer stem cell is also believed to be the agent causing cancer to metastasize.

In closing, development of drugs against one protein or one change in the cell may not totally fix the problem. There are different cancer cell lines that develop from various changes in the cell lines. Finding the various cancer stem lines and how to treat with drugs and kill those cells will be great prevention of spreading of cancer. There are several drugs that can "shrink" tumors. But, there are no drugs that can not keep it from eventually spreading and becoming malignant. Out of all the cells in a tumor only one or a few of these cells actually move to other locations. Find these cells and how to kill them and utilize current drug treatment to shrink the tumor.
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