понедельник, 18 ноября 2013 г.

Cancer cells can treat tumors.

Cancer cells can treat tumors.
New scrutiny suggests that many cancer cells are equipped with a variety of suicide pill: a protein on their surfaces that gives them the genius to throw an "eat me" indicate to immune cells. The take exception to now, the researchers say, is to bust out how to coax cancer cells into emitting the momentous rather than a dangerous "don't eat me" signal scriptovore.com. A observe published online Dec 22 2010 in Science Translational Medicine reports that the cells enrapture out the enticing "eat me" singular by displaying the protein calreticulin.

But another molecule, called CD47, allows most cancer cells to sidestep knocking down by sending the antagonistic signal: "Don't sup me". In earlier research, Stanford University School of Medicine scientists found that an antibody that blocks CD47 - turning off the outstanding - could aide bicker cancer, but mysteries remained pictures. "Many typical cells in the body have CD47, and yet those cells are not upset by the anti-CD47 antibody," Mark Chao, a Stanford calibrate swotter and the study's lead author, said in a university front-page news release.

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

So "This study demonstrates that the insight that blocking the CD47 'don't eat me' conspicuous works to kill cancer is that leukemias, lymphomas and many compressed tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, big cheese of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The fact-finding also shows that most standard cubicle populations don't presentation calreticulin and are, therefore, not depleted when we reveal them to a blocking anti-CD47 antibody".

The next footfall is to appreciate how calreticulin works. "We want to understand how it contributes to the disease process and what is event in the cell that causes the protein to move to the room surface," Dr Ravindra Majeti, an aide-de-camp professor of hematology and study co-principal investigator, said in the release check this out. "Any of these mechanisms present the new ways to treat the cancer by interfering with those processes," Majeti said.

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