Cancer cells can treat tumors

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

But another molecule, called CD47, allows most cancer cells to keep off rubbing out by sending the opposite signal: "Don't eat me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the unique - could balm tussle cancer, but mysteries remained pharmacy. "Many orthodox cells in the body have CD47, and yet those cells are not distressed by the anti-CD47 antibody," Mark Chao, a Stanford graduate schoolgirl and the study's lead author, said in a university news release.

And "At that time, we knew that anti-CD47 antibody care selectively killed only cancer cells without being toxic to most healthy cells, although we didn't have knowledge of why". Now, the new research has shown that calreticulin exists in a category of cancers, including some types of leukemia, non-Hodgkin's lymphoma and bladder, cognition and ovarian cancers.

So "This scrutinization demonstrates that the reason that blocking the CD47 'don't break bread me' signal works to kill cancer is that leukemias, lymphomas and many packed tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, leader of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The into or also shows that most universal stall populations don't display calreticulin and are, therefore, not depleted when we betray them to a blocking anti-CD47 antibody".

The next imprint is to understand how calreticulin works. "We want to know how it contributes to the contagion process and what is happening in the cell that causes the protein to get going to the cell surface," Dr Ravindra Majeti, an subsidiary professor of hematology and study co-principal investigator, said in the release vigrx delay spray in delaware. "Any of these mechanisms put up potential new ways to review the disease by interfering with those processes".