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Natural self-destruction mechanism may be the key to treating blood cancer

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Posted July 18, 2016

Treating blood cancer is difficult because of its fundamental mechanism. It is characterized by pathological alterations of marrow cells, which are producing blood. Usually these cells die when they are damaged, but in the case of cancer this self-destruction mechanism does not work as it should. Now scientists from the Technical University of Munich identified the mechanism behind this self-destruction, which is turned off by leukaemia.

Self-destruction mechanism allows replacing damaged cells with new ones, but blood cancer disrupts this process. Image credit: Linda Bartlett, NIH via Wikimedia, Public Domain

Self-destruction mechanism allows replacing damaged cells with new ones, but blood cancer disrupts this process. Image credit: Linda Bartlett, NIH via Wikimedia, Public Domain

Acute myeloid leukaemia, which is a frequent kind of blood cancer, affects bone marrows that participate in blood production. Different blood cells are produced from stem cells, called progenitor cells, in the bone marrow, but this process is disturbed in the case of cancer and progenitor cells are turned into leukaemia-initiating cells, usually referred to as LICs. They cannot develop to fully become blood cells, which eventually causes leukaemia symptoms. Now scientists discovered that FLT3 gene, mutations of which are associated with myeloid leukaemia, is permanently active when the person has cancer. This causes inflammation-like stimuli in the cell, subjecting it to permanent stress.

In a healthy body this stimuli would trigger a self-destruction process. And eventually this cell would be replaced with a new healthy one. But LICs do not self-destruct, which brings it to the spotlight of attention of many scientists. There are several different ways cells are destroyed. Ones of them is apoptosis, when cell shrinks in a controlled manner, and one of them is necroptosis, during which cell dies quickly, releasing its contents to its surroundings and causing a strong inflammatory stimulus. Scientists conducted a research and found that a protein called RIPK3 triggers necroptosis.

Study also showed that RIPK3 protein is blocked when cells are affected by cancer, which leads to LICs surviving way longer than they normally would. Ulrike Höckendorf, lead author of the study, said: “We conclude from our findings that particularly aggressive cancer cells have the capacity to block RIPK3. Exactly how they accomplish this, however, remains to be investigated”. Scientists found that apoptosis is also neutralized in many cancer cells. This knowledge allows scientists to start thinking of new therapies.

Scientists are thinking that artificially reproducing the effect of RIPK3 using medication would be a new and very effective approach to target cancer cells. However, until it is possible more research has to be done.

Source: tum.de

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