How cancer cells differ from normal cells in terms of mortality?
The big difference between cancer cells and normal cells is that cancer cells can divide forever and live forever. We call this immortality. Normal cells share a number of departments and then stop growing. They are old and they either die or they are sitting there doing nothing. They are deadly.
Cancer cells have a way to maintain their telomeres. Their telomeres do not shorten. Every time normal cells divide, they lose some DNA sequences of telomeres. Finally, when DNA telomeres become too short, you stop growing. There are other factors contributing to the mortality of normal cells.
It is the immortality of cancer cells that makes them so dangerous?
Cancer cells divide uncontrollably. Then there are cancer cells growing in a single position of your body that may invade surrounding tissues and interfere with the activity in normal tissues. They form a tumor. Cancer cells can also circulate the body and to other places, and form tumors to new sites. This is due in part to the immortality of cancer cells. They are not dead. Normal cells grow in a place and at some point be exhausted.
Talk to your cancer cells, making it "more deadly."
The majority of cancer cells, about 90 percent, activating a molecule called telomerase. Telomerase is normally used in normal cells except for stem cells. Cancer cells, telomerase is active. Telomerase is to increase the role of telomere DNA: a shorter telomeres. This is why cancer cells do not lose their telomeres. In normal cells, telomerase is turned off, so there is no way to maintain telomere length. [This suggests that] if you kill telomerase in cancer cells, telomere [progressively shortened], and tumor cells die.
But recently, we found that telomerase extends just a string of DNA. The other track must be synthesized from other molecules, other proteins. We found the molecule that is responsible for the synthesis of the vision of others. If you block the function of this molecule, if telomeres can not be properly maintained so that the cell simply stops growing.
We are just at that stage now. We do not know how to work together. We're working on it and I hope that in future we can find a way to guide this process, do not directly affect telomerase, but the goal is the synthesis of the other strand. This is another way to stop cancer cell growth.
What is the next step to move forward in this research?
The next step is to know how it is regulated. We wonder whether in normal cells the synthesis of another chain is also because you want to specifically target cancer cells. If there, [know] if the same process is governed by different pathways in normal cells versus cancer cells. Our ultimate goal is to see if there are specific objectives, we can prevent cancer cells.
