17 March 2008

New target of anti-cancer therapy: pyruvate kinase PKM2

American scientists have determined which substance is responsible for the rapid growth of cancer cells, which actually makes them deadly to the body, the BBC reports. The researchers hope that now doctors will find a way to disrupt the natural process of tumor development and stop the disease at an early stage.

Scientists from Harvard University have isolated an enzyme that gives cancer cells the ability to consume huge amounts of glucose needed to fuel uncontrolled growth.

The enzyme pyruvate kinase has two varieties, but the research team found that only one of them – PKM2 – provides rapid glucose consumption by cancer cells. When, during an experiment in the laboratory, scientists forced tumor cells to "switch" to another type of enzyme, blocking the production of PKM2, their growth slowed down. When these cells were transplanted into mice, the rate of tumor formation was already much lower.

The ability of cancer cells to consume glucose in much larger quantities compared to ordinary cells was discovered by German scientist, Nobel Prize winner in Physiology or Medicine Otto Warburg more than 75 years ago. However, until now, the chemical aspect of this mechanism has not been fully studied.

Scientists do not exclude that the substance responsible for glucose metabolism may vary depending on the type of cancer. However, they are confident that the results obtained will help doctors in the fight against a dangerous disease.

"Because PKM2 was found in all the cancer cells we studied, because it was not found in most normal tissues and because it plays a crucial role in tumor formation, this form of pyruvate kinase is a possible target in anti–cancer therapy," said Lewis Cantley, head of the research group.

At the same time, scientists emphasize that it is difficult to judge how effective the results of the study will be in clinical settings. For this, they say, additional research is needed.

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Portal "Eternal youth" www.vechnayamolodost.ru 17.03.2008

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