Cancer cells can treat tumors

Cancer cells can treat tumors.
New investigating suggests that many cancer cells are equipped with a cordial of suicide pill: a protein on their surfaces that gives them the ability to send an "eat me" wink to immune cells. The challenge now, the researchers say, is to acknowledge out how to coax cancer cells into emitting the signal rather than a dangerous "don't eat me" signal england. A scrutiny published online Dec 22 2010 in Science Translational Medicine reports that the cells throw out the enticing "eat me" signal by displaying the protein calreticulin.

But another molecule, called CD47, allows most cancer cells to sidestep destruction by sending the antithesis signal: "Don't eat me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the whistle - could alleviate fight cancer, but mysteries remained hgh normal range. "Many normal cells in the body have CD47, and yet those cells are not attacked by the anti-CD47 antibody," Mark Chao, a Stanford graduate student and the study's lead author, said in a university dispatch release.

And "At that time, we knew that anti-CD47 antibody therapy selectively killed only cancer cells without being toxic to most normal cells, although we didn't know why". Now, the immature research has shown that calreticulin exists in a variety of cancers, including some types of leukemia, non-Hodgkin's lymphoma and bladder, understanding and ovarian cancers.

So "This research demonstrates that the object that blocking the CD47 'don't eat me' signal works to kill cancer is that leukemias, lymphomas and many blank tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, guide of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The analysis also shows that most normal cell populations don't publicize calreticulin and are, therefore, not depleted when we expose them to a blocking anti-CD47 antibody".

The next procedure is to understand how calreticulin works. "We want to know how it contributes to the disease process and what is phenomenon in the cell that causes the protein to move to the cell surface," Dr Ravindra Majeti, an aide-de-camp professor of hematology and study co-principal investigator, said in the release as example. "Any of these mechanisms come forward potential new ways to treat the disease by interfering with those processes".