Cancer cells can treat tumors

Cancer cells can treat tumors.
New examine suggests that many cancer cells are equipped with a cordial of suicide pill: a protein on their surfaces that gives them the cleverness to project an "eat me" sign to immune cells. The problem now, the researchers say, is to assume out how to coax cancer cells into emitting the striking rather than a dangerous "don't eat me" signal pulsatile secretion growth hormone. A review published online Dec 22 2010 in Science Translational Medicine reports that the cells let fly out the enticing "eat me" weighty by displaying the protein calreticulin.

But another molecule, called CD47, allows most cancer cells to circumvent extinction by sending the conflicting signal: "Don't breakfast me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the special - could advise hostilities cancer, but mysteries remained i found it. "Many routine cells in the body have CD47, and yet those cells are not phoney by the anti-CD47 antibody," Mark Chao, a Stanford bachelor disciple and the study's lead author, said in a university news broadcast release.

And "At that time, we knew that anti-CD47 antibody curing selectively killed only cancer cells without being toxic to most conformist cells, although we didn't be acquainted with why" our website. Now, the untrodden research has shown that calreticulin exists in a brand of cancers, including some types of leukemia, non-Hodgkin's lymphoma and bladder, thought and ovarian cancers.

So "This investigate demonstrates that the motive that blocking the CD47 'don't eat me' significant works to kill cancer is that leukemias, lymphomas and many worthy tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, foreman of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The examination also shows that most universal apartment populations don't manifest calreticulin and are, therefore, not depleted when we imperil them to a blocking anti-CD47 antibody".

The next track is to tolerate how calreticulin works. "We want to have knowledge of how it contributes to the disease process and what is episode in the cell that causes the protein to move to the stall surface," Dr Ravindra Majeti, an aide professor of hematology and study co-principal investigator, said in the release acaiberry. "Any of these mechanisms offering covert new ways to treat the sickness by interfering with those processes".