Saturday, 4 March 2017

Cancer Cells Can Treat Tumors

Cancer Cells Can Treat Tumors.
New on suggests that many cancer cells are equipped with a sympathetic of suicide pill: a protein on their surfaces that gives them the ability to send an "eat me" notify to immune cells. The challenge now, the researchers say, is to judge out how to coax cancer cells into emitting the signal rather than a dangerous "don't eat me" signal. A lucubrate published online Dec 22 2010 in Science Translational Medicine reports that the cells cast out the enticing "eat me" signal by displaying the protein calreticulin.

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

And "At that time, we knew that anti-CD47 antibody therapy selectively killed only cancer cells without being toxic to most normal cells, although we didn't know why". Now, the supplemental 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 aim that blocking the CD47 'don't eat me' signal works to kill cancer is that leukemias, lymphomas and many durable tumors also display a calreticulin 'eat me' signal," Dr Irving Weissman, top banana of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and a co-principal investigator of the study, said in the release. "The inquire into also shows that most normal cell populations don't unfurl calreticulin and are, therefore, not depleted when we expose them to a blocking anti-CD47 antibody".

The next gradation is to understand how calreticulin works. "We want to know how it contributes to the disease process and what is taking place in the cell that causes the protein to move to the cell surface," Dr Ravindra Majeti, an aide professor of hematology and study co-principal investigator, said in the release penis ko strong karne ka tarika. "Any of these mechanisms propose potential new ways to treat the disease by interfering with those processes".

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