myeloma mouse. inhibition common cell signaling molecule slows the growth of tumors (colored areas) in mice.
a surprising target for cancer drugs was discovered - a cell signaling molecule used by cancer cells and healthy cells as well. Blocking the molecule thwarts a wide variety of tumors - including some that are resistant to most available drugs - without harming healthy cells, two teams report in the March issue of Cancer Cell
researchers research. for cancer drugs have traditionally focused on the molecular signaling pathways that go awry in cancer cells. That's why they often ignored the growth factor receptor similar to insulin (IGF-1R), even if they knew that tumors need to grow and the receiver spread. Unlike many potential drug targets, IGF-1R appears normal in most cancers. And because the IGF-1R is used by healthy cells too, the researchers reasoned that blocking it would destroy the good cells with the bad.
But a team from the Dana-Farber Cancer Institute in Boston and colleagues of the Novartis Institutes for Biomedical Research in Basel, Switzerland, decided to take another look because so much evidence has accumulated over the years showed that IGF-R1 plays a crucial role in the development of cancer. When they treated mice that had been injected with cells from human multiple myeloma - a type of blood cancer - with a molecule that inhibits IGF-1R, the tumor growth is slowed and the animals survived more long time. In addition, the inhibitor of IGF-1R has managed to bring down several myeloma cells resistant to standard treatments. The mechanism is apparently complex. A series of experiments to test tubes revealed that the inhibitor not only alters the activity of the protein directly controlled by the IGF-1R, but also affected proteins considered in completely separate signaling pathways
Some scientists are not surprised by the unconventional success. It is possible that the tumors can become "addicted" to molecules of ordinary cell signaling, ubiquitous, says Lance Liotta, who leads the proteomics program at the National Cancer Institute in Bethesda, Maryland. Without a solution, cancer cells wither and die, whereas healthy cells can apparently get without it. "Just because we do not see the differential expression [of the protein] in cancer cells does not mean it is not a good target," says Liotta.
Related Sites
Kenneth Anderson website
Novartis Institute for biomedical research, Basel
An article on proteomics cancer Liotta efforts
more on IGF-1R
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