New drug may provide hopes for blood cancer patients

Scientists have developed a new drug that has the potential to strip cancer cells of their “immortality”, a finding that could help in treating patients suffering from one of the most aggressive forms of leukaemia. Acute myeloid leukemia (AML) is a type of cancer of the blood and bone marrow with excess immature white blood cells and is responsible for 265,000 worldwide cases each year. The drug candidate, called HXR9, works by preventing the cancer cells from sidestepping the natural process that causes unhealthy and damaged cells to die — known as apoptosis.

“Acute myeloid leukaemia is a pretty intractable disease and doesn’t respond to many treatments. This is a novel therapeutic target that hasn’t been shown before to be effective against this form of leukaemia,” said a Professor. The drug targets a particular family of genes, called HOX genes, which helps to give cancer cells the ability to continuously grow and divide.  HXR9 was found to strip the cancer cells of this ability by turning off the HOX genes,the Prof. said.

In the study, the team 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. When HXR9 was tested on cancerous cells, they underwent 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, Morgan noted. In addition, HXR9 “could well be used in combination treatments but the initial trials will be as a single therapy”, the Prof. said.

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Researchers discover rescue protein that delays cell death

A team of researchers has discovered a rescue protein that delays the cell death and can offer a treatment for cancer, neurodegeneration and infection.

The study was published in journal Cell.The team has discovered how a set of proteins delays the "executioner" machinery that kills damaged or infected cells in a process called necroptosis.

The scientists believe these finding may have wide clinical implications if researchers can develop drugs to control the cellular rescue machinery.

Rescue treatments that prevent necroptosis in transplanted organs could reduce injury to the transplant caused by lack of oxygen, researchers said.

Drugs to rescue cells from necroptosis could also help prevent injuries to tissue deprived of blood by heart attack and stroke. In such cases, restoring blood flow and oxygenation triggers inflammation that kills tissue.

The scientists said cell-rescuing drugs could also thwart cancer spread by protecting blood vessel cells from being killed by tumor cells.

Tumor cells escape the bloodstream to spread in the body by killing blood vessels. Blocking the rescue machinery might also prove useful in treating cancers, by enhancing death of cancer cells by necroptosis.

In treating neurodegenerative disorders such as ALS--also known as Lou Gehrig`s Disease--activating the rescue machinery could help prevent death of brain cells.

In treating viral infections such as influenza, rescue treatment could extend the life of cells infected by the virus, so that the body`s immune system would be more strongly alerted to fight the infection.

Scientists knew that the "executioner" in necroptosis was a protein called MLKL.When MLKL is activated by the necroptosis machinery, it triggers a piercing of the plasma membrane surrounding the cell, ultimately killing it.

However, the scientists discovered how cells could survive necroptosis.Researchers showed the plasma membrane could repair itself by forming "bubbles" of broken plasma membrane that would shed from the cell to repair the holes.

Experiments showed the set of proteins called ESCRT-III was responsible for forming the repair bubbles. The research also revealed that ESCRT-III delayed or prevented necroptosis by repairing breaks in the plasma membrane.

The delay gave the dying cells time to release signals to alert surrounding cells to the presence of a viral infection.The investigators also discovered that activating MLKL is not a point of no return for cell survival, and that ESCRT-III could resuscitate damaged cells.In experiments relevant to transplantation, the researchers measured levels of activated MLKL protein in tissue samples from kidneys used in transplants.

Such cells experience stress during the transplantations, and researchers suspected the cells would show signs of necroptosis.The scientists found that although MLKL was activated in the kidney cells after transplantation, the cells did not die, and this protection correlated with an increase in the levels of the ESCRT-III machinery necessary for rescue of cells with active MLKL.

Douglas Green, Ph.D., chair of the St. Jude Department of Immunology emphasized that the current findings are only "suggestive" at this point, because the experiments were done in cell cultures and tissue samples. Further studies are needed to establish that the rescue machinery functions in whole organs.

The research by Green and his colleagues will also aim at discovering the biological signals regulating ESCRT-III, to enable more precise control of the rescue machinery."Those studies could yield drugs to regulate the rescue process," Green said.

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