Super drug' for pediatric blood cancer may soon be reality

A "super drug" that helps slow down the progression of blood cancer in children could soon become a reality, say researchers.

Patients with leukemia have a very low percentage of red blood cells, making them anemic, and have approximately 80 times more white blood cells than people without cancer.

However, the survival rate is only 30 per cent for children diagnosed with MLL-translocation leukemia, a cancer that affects the blood and bone marrow.

"These white blood cells infiltrate many of the tissues and organs of the affected individuals and is a major cause of death in leukemia patients," said a scientist.

 "This is a monster cancer that we've been dealing with for many years in children.

"We're finally at a point where in five to 10 years, we can get a drug in kids that can be effective. If we can bring that survival rate up to 85 per cent, that's a major accomplishment," he said.

In the study, the team demonstrated that when a key protein responsible for leukemia, MLL, is stabilised, it slows the progression of the leukemia.

This MLL stabilisation process could potentially work in cancers with solid tumours, such as breast or prostate cancer.

The next step will be to combine the treatments from the past two years of research into a pediatric leukemia "super drug" to test on humans in a clinical trial, the researchers said.

"This opens up a new therapeutic approach not only for leukemia, which is so important for the many children who are diagnosed with this terrible cancer, but also for other types of cancers that plague the population," the study showed.

The team also identified compounds that could slow cancer growth by interrupting a gene transcription process known as "Super Elongation Complex " (SEC). 

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New drug may reduce skin cancer spread by 90 per cent

Scientists have developed a new compound that reduces the spread of melanoma cells by up to 90 per cent, an advance that may pave the way for a potential new drug to fight the deadly skin cancer.
The man-made, small-molecule drug compound goes after a genes ability to produce RNA molecules and certain proteins in melanoma tumors. 

This gene activity, or transcription process, causes the disease to spread but the compound can shut it down. Up until now, few other compounds of this kind have been able to accomplish this. 

"Its been a challenge developing small-molecule drugs that can block this gene activity that works as a signaling mechanism known to be important in melanoma progression," said Richard Neubig, professor at Michigan State University (MSU) in the US.
"Our chemical compound is actually the same one that weve been working on to potentially treat the disease scleroderma, which now we've found works effectively on this type of cancer," said Neubig.
Scleroderma is a rare and often fatal autoimmune disease that causes the hardening of skin tissue, as well as organs such as the lungs, heart and kidneys. 

The same mechanisms that produce fibrosis, or skin thickening, in scleroderma also contribute to the spread of cancer.
The findings are an early discovery that could be highly effective in battling the deadly skin cancer. It is estimated about 10,000 people die each year from the disease. 

"Melanoma is the most dangerous form of skin cancer with around 76,000 new cases a year in the US," said Kate Appleton, a postdoctoral student at MSU. 

"One reason the disease is so fatal is that it can spread throughout the body very quickly and attack distant organs such as the brain and lungs," said Appleton. 

Researchers found that the compounds were able to stop proteins, known as Myocardin-related transcription factors, or MRTFs, from initiating the gene transcription process in melanoma cells.
These triggering proteins are initially turned on by another protein called RhoC (Ras homology C) which is found in a signaling pathway that can cause the disease to aggressively spread in the body. 

The compound reduced the migration of melanoma cells by 85 to 90 per cent. The team also discovered that the potential drug greatly reduced tumors specifically in the lungs of mice that had been injected with human melanoma cells. 

"We used intact melanoma cells to screen for our chemical inhibitors. This allowed us to find compounds that could block anywhere along this RhoC pathway," Neubig said. 

Being able to block along this entire path allowed the researchers to find the MRTF signaling protein as a new target. 

Appleton said figuring out which patients have this pathway turned on is an important next step in the development of their compound because it would help them determine which patients would benefit the most.

 

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Human blood created from human stem cells in lab

Scientists have discovered two genetic programs that are responsible for taking blank-slate stem cells to turn them into both red and white cells that make up human blood.

Igor Slukvin, the lead researcher from University of Wisconsin-Madison explained that this was the first demonstration of the production of different kinds of cells from human pluripotent stem cells, using transcription factors.

Slukvin said that by over-expressing just two transcription factors, they could reproduce the sequence of events they see in the "embryo" where blood was made, in the laboratory dish.

The method developed by Slukvin's group was shown to produce blood cells in abundance. For every million stem cells, the researchers were able to produce 30 million blood cells.

According to Slukvin, an unfulfilled aspiration is to produce hematopoietic stem cells, multipotent stem cells found in bone marrow that are used to treat some cancers, including leukemia and multiple myeloma, in the lab.

The study is published in the journal Nature Communications.
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Genetic cause of childhood leukemia discovered

Scientists have for the first time identified an inherited genetic mutation linked to increased risk of developing the most common type of childhood leukemia.

"At the very least this discovery gives us a new window into inherited causes of childhood leukemia. More immediately, testing for this mutation may allow affected families to prevent leukemia in future generations," said study author.

The mutation was first observed in a family treated at a hospital, of which several family members of different generations had been diagnosed with childhood acute lymphoblastic leukemia (ALL).

A second, non-related, leukemia-prone family cared for at a different hospital was later found to have the same mutation. A series of experiments were conducted confirming that the observed mutation compromised the normal function of the gene, which may increase the risk of developing ALL. The inherited genetic mutation is located in a gene called PAX5, which is known to play a role in the development of some B cell cancers, including ALL.PAX5, a transcription factor or "master gene," regulates the activity of several other genes and is essential for maintaining the identity and function of B cells.

In all study participants, one of the two copies of the PAX5 gene was missing, leaving only the mutated version. The newly discovered gene mutation may someday help scientists determine how to target transcription factors to treat other non-inherited forms of leukemia where the PAX5 mutation is present.

"With a better understanding of the genetic elements that induce cancer susceptibility, or drive cancer to grow, we can more precisely target therapy as well as potentially prevent cancer from occurring in the first place," added a researcher.

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