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Researchers comes up with drug to cure blood cancer

Scientists have developed a new drug that strips cancer cells of their “immortality” and may treat patients suffering from one of the most aggressive forms of leukaemia.

The drug, called HXR9, prevents cancer cells from sidestepping apoptosis – the process that causes unhealthy and damaged cells to die.

Researchers from the University of Bradford in the UK found that it could be used to treat acute myeloid leukaemia (AML).

The drug targets a particular family of genes, called HOX genes, which are involved in controlling the rapid growth of cells. In adults, these are switched off but in cancer cells, they can be turned back on.

This helps to give the cancer cells the ability to continuously grow and divide by circumventing the normal mechanisms that trigger apoptosis – effectively making them immortal, researchers said.

“Acute myeloid leukaemia is a pretty intractable disease and does not respond to many treatments. This is a novel therapeutic target that has not been shown before to be effective against this form of leukaemia,” said Richard Morgan, from the University of Bradford.

Researchers analysed gene expression data from 269 AML patients and found an association between the activity of a group of HOX genes and the patient survival rate.

They then tested HXR9 on cancerous cells taken from patients suffering from AML and found it caused the cancer cells to undergo a process known as necroptosis.

Necroptosis causes the cells to explode and spew their contents into the bloodstream rather than simply digesting themselves as normally occurs in apoptosis.

This increases the likelihood that there will be a subsequent immune reaction against the cancer cells, according to Morgan.

The researchers found that when they combined HXR9 with another drug, a protein kinase C inhibitor called Ro31, it enhanced the reduction in cancer growth even further.

“It could well be used in combination treatments but the initial trials will be as a single therapy,” Morgan said.


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