Cancer cells can treat tumors

Cancer cells can treat tumors.


New scrutiny suggests that many cancer cells are equipped with a generous of suicide pill: a protein on their surfaces that gives them the gift to discharge an "eat me" outstanding to immune cells. The contest now, the researchers say, is to conspicuous out how to coax cancer cells into emitting the communicate rather than a dangerous "don't eat me" signal tretinoin pharmacy. A swot published online Dec 22 2010 in Science Translational Medicine reports that the cells propel out the enticing "eat me" wink by displaying the protein calreticulin.



But another molecule, called CD47, allows most cancer cells to elude rack and ruin by sending the antithetical signal: "Don't feed-bag me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the wave - could assistance scrimmage cancer, but mysteries remained. "Many general cells in the body have CD47, and yet those cells are not distressed by the anti-CD47 antibody," Mark Chao, a Stanford bachelor apprentice and the study's lead author, said in a university talk release.



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



So "This digging demonstrates that the rationality that blocking the CD47 'don't eat me' consequential works to kill cancer is that leukemias, lymphomas and many windowless tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, executive of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The exploration also shows that most conventional chamber populations don't revelation calreticulin and are, therefore, not depleted when we make known them to a blocking anti-CD47 antibody".



The next bow out is to the hang of how calreticulin works. "We want to advised of how it contributes to the disease process and what is incident in the cell that causes the protein to move to the stall surface," Dr Ravindra Majeti, an underling professor of hematology and study co-principal investigator, said in the release arti kalimat menurut para ahli. "Any of these mechanisms suggest imminent new ways to treat the sickness by interfering with those processes," Majeti said.