Cancer cells can treat tumors

Cancer cells can treat tumors.
New analysis suggests that many cancer cells are equipped with a friendly of suicide pill: a protein on their surfaces that gives them the genius to send an "eat me" significant to immune cells. The challenge now, the researchers say, is to suppose out how to coax cancer cells into emitting the special rather than a dangerous "don't eat me" signal mymensinh noti para cuda cudi. A inspect published online Dec 22 2010 in Science Translational Medicine reports that the cells turn out the enticing "eat me" blink by displaying the protein calreticulin.

But another molecule, called CD47, allows most cancer cells to evade end 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 gesticulate - could aid contend cancer, but mysteries remained. "Many orthodox cells in the body have CD47, and yet those cells are not upset by the anti-CD47 antibody," Mark Chao, a Stanford graduate swat 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 rational cells, although we didn't be familiar with why". Now, the new research has shown that calreticulin exists in a order of cancers, including some types of leukemia, non-Hodgkin's lymphoma and bladder, perception and ovarian cancers.

So "This experimentation demonstrates that the reason that blocking the CD47 'don't pack away me' signal works to kill cancer is that leukemias, lymphomas and many unrelieved tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, numero uno of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The inquire into also shows that most run-of-the-mill stall populations don't display calreticulin and are, therefore, not depleted when we unveil them to a blocking anti-CD47 antibody".

The next vestige is to understand how calreticulin works. "We want to know how it contributes to the virus process and what is happening in the cell that causes the protein to opportunity to the cell surface," Dr Ravindra Majeti, an deputy professor of hematology and study co-principal investigator, said in the release banane. "Any of these mechanisms suggest potential new ways to bonus the disease by interfering with those processes".