Cancer cells can treat tumors

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

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

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

So "This research demonstrates that the reasoning that blocking the CD47 'don't eat me' signal works to kill cancer is that leukemias, lymphomas and many unshakeable tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, number one of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The scrutinization 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 mark is to understand how calreticulin works. "We want to know how it contributes to the disease process and what is occasion in the cell that causes the protein to move to the cell surface," Dr Ravindra Majeti, an helper professor of hematology and study co-principal investigator, said in the release breast actives use korle kotodin a breast boro hoy?. "Any of these mechanisms furnish potential new ways to treat the disease by interfering with those processes".