Cancer cells can treat tumors.
New enquire suggests that many cancer cells are equipped with a persuasion of suicide pill: a protein on their surfaces that gives them the faculty to project an "eat me" unusual to immune cells. The problem now, the researchers say, is to sculpture out how to coax cancer cells into emitting the significant rather than a dangerous "don't eat me" signal creating a press page . A swot published online Dec 22 2010 in Science Translational Medicine reports that the cells enrapture out the enticing "eat me" notify by displaying the protein calreticulin.
But another molecule, called CD47, allows most cancer cells to keep genocide by sending the opposing signal: "Don't devour me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the consequential - could assist rise up cancer, but mysteries remained furosemide. "Many run-of-the-mill cells in the body have CD47, and yet those cells are not moved by the anti-CD47 antibody," Mark Chao, a Stanford mark critic and the study's lead author, said in a university dope release.
And "At that time, we knew that anti-CD47 antibody healing selectively killed only cancer cells without being toxic to most routine cells, although we didn't conscious why". Now, the revitalized research has shown that calreticulin exists in a class of cancers, including some types of leukemia, non-Hodgkin's lymphoma and bladder, intellect and ovarian cancers.
So "This examine demonstrates that the insight that blocking the CD47 'don't eat me' special works to kill cancer is that leukemias, lymphomas and many -carat tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, chief honcho of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The enquiry also shows that most reasonable cubicle populations don't reveal calreticulin and are, therefore, not depleted when we leak them to a blocking anti-CD47 antibody".
The next bow out is to cotton on how calreticulin works. "We want to positive how it contributes to the disease process and what is occasion in the cell that causes the protein to move to the stall surface," Dr Ravindra Majeti, an subsidiary professor of hematology and study co-principal investigator, said in the release butea gel is available. "Any of these mechanisms proposal potency new ways to treat the affliction by interfering with those processes," Majeti said.