The world-first procedure has been successfully used to regrow muscles in a mouse model, but it could be applied to all tissue-based illnesses in humans such as in the liver, pancreas or brain, the researchers say.

The research team, which is based at UNSW and formerly from Sydney's Westmead Children's Hospital, adapted a technique currently being trialled in bone marrow transplantation. Adult stem cells are given a gene that makes them resistant to chemotherapy, which is used to clean out damaged cells and allow the new stem cells to take hold.

A paper detailing the breakthrough appears in the prestigious journal Stem Cells this week.

The ability of adult stem cells to regenerate whole tissues opens up a world of new possibilities for many human diseases, according to the lead authors of the paper, Professor Peter Gunning, Professor Edna Hardeman and Dr Antonio Lee, from UNSW's School of Medical Sciences.

"The beauty of this technique is that chemotherapy makes space for stem cells coming into muscle and also gives the stem cells an advantage over the locals. It's the first strategy that gives the good guys the edge in the battle to cure sick tissues," Professor Gunning said.

"What has been the realm of science fiction is looking more and more like the medicine of the future," he said.

The procedure solves one of the major hurdles involving stem cell therapy “ getting the cells to survive for more than an hour or so after inserting them into damaged tissue.

"In muscle, most stem cells die in the first hour or are present in such low numbers that they are not much help," Professor Gunning said. "Until now, the new healthy cells had no advantage over the existing damaged tissue and were getting out-competed.

While trials of the procedure are at the pre-clinical stage, researchers are looking to launch human trials treating specific forms of muscular dystrophy such as oculopharyngeal dystrophy within the next three to five years.

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In the new study, the researchers wanted to further explore the genes that distinguish the Lgr5 stem cells from other intestinal cells. After examining 200 or so genes, they landed on a handful that differed between stem cells and all other cells. Of those, Clevers said Ascl2 was the only transcription factor, a class of genes that are generally important to setting the fates of cells.

When they induced the activity of the Ascl2 transcription factor throughout the intestinal lining of mice, it caused the overgrowth of crypts and the development of additional crypts on surfaces of the villi, they report. In intestines of adult mice lacking Ascl2, the Lgr5 stem cells disappeared within days. All together, those findings led the researchers to conclude that Ascl2 is the key to intestinal stem cell fate.

While he said the findings may not have any immediate practical implications, they could yet yield some insight into the cancer stem cells that give rise to other colon cancer cells.

"In colon cancer tumors, there are a very limited number of cells that express this transcription factor," Clevers said. "It's likely that the same gene turns cancer cells into cancer stem cells."

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