Ann: FDA Regulatory Progress Update - Conference Call Details, page-4

ABC promoting this story from SA today. got funding months ago. http://www.unisa.edu.au/Media-Centre/Releases/NHMRC-funding-for-vital-health-research/
Always amazes me how really early breakthrough science gets publicity and then commercialisation and follow up gets so little so the general public remain so uneducated about the whole trial process , cost and time it takes.
   Well TIS could teach them a thing or 2 about choosing the correct pathway and trial structures or could they?
Full paper as published - pdf
http://www.cell.com/developmental-cell/pdf/S1534-5807(15)00761-3.pdf


Dr Michael Samuel  -Adelaide-  accidental discovery while researching cancer
Head, Tumour Microenvironment Laboratory
Qualifications: B.Sc.(Hons.) ANU, Ph.D. Melb

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From ABC
http://www.abc.net.au/am/content/2015/s4376886.htm


KIM LANDERS: Australian researchers have made an accidental discovery which has the potential to heal a lot of wounds and save a lot of money.

The treatment of chronic wounds costs the Australian health system billions of dollars a year.

There's now hope that a simple treatment will halve the amount of time it takes for those wounds to heal.

Simon Lauder reports.

SIMON LAUDER: Wounds can't heal without a layer of cells called the extracellular matrix.

Dr Michael Samuel was studying the matrix to find out more about cancer instead he stumbled on a discovery which could make wounds heal much faster.

MICHAEL SAMUEL: Certainly unexpected and quite the opposite of what I expected to find yes.

SIMON LAUDER: The discovery has the potential to help hundreds of thousands of people, including diabetes patients, who suffer from chronic wounds.

MICHAEL SAMUEL: They tend not heal over for many months and some people actually have them for years.

It's a major problem because obviously it leads the body open to infection.

SIMON LAUDER: Dr Samuel and his colleagues at the Centre for Cancer Biology in Adelaide have found that they can help restore the extracellular matrix and speed up wound healing by inhibiting a particular protein.

MICHAEL SAMUEL: So we've been looking at how quickly wounds heal in a variety of different context in the lab and we found that when a particular protein called 14-3-3 zeta was not present wounds healed a lot quicker in our models of wound healing.

And so we decided to go away and find out exactly why this is the case and we worked out the mechanism by which this happens.

We found that when 14-3-3 zeta was either not there or when it was inhibited using a pharmacological inhibiter that the scaffolding was actually set up a lot quicker and this was the reason why the wounds were healing faster.

So that's the promise of this research.

SIMON LAUDER: How much of a difference does the absence of 14-3-3 zeta make?

MICHAEL SAMUEL: It halves the wound healing time.

SIMON LAUDER: So that's huge.

MICHAEL SAMUEL: It is huge; it's quite a significant difference.

SIMON LAUDER: What was your reaction when you discovered this?

MICHAEL SAMUEL: Well actually it was quite unexpected because we had anticipated that in the absence of 14-3-3 zeta wounds would take longer to heal so it was really quite surprising.

It's actually one of those things where you have a hypothesis and you're testing it in several ways and often you find out that you weren't actually thinking along the right lines that you discovered something quite the opposite.

But it's a surprising finding and that's why there's been a lot of interest in it in the academic field.

SIMON LAUDER: Dr Samuel says his research on mice raises hope that a cheap and easy to use treatment may be available for humans with chronic wounds in five to ten years and he now wants to work towards human trials.

MICHAEL SAMUEL: I can imagine it would be really useful to a lot of people and actually save a lot of health systems a lot of money.

SIMON LAUDER: The research is published today in the scientific journal Developmental Cell.

KIM LANDERS: Simon Lauder reporting.



http://www.adelaidenow.com.au/news/...k=7f7a81853cbbd2b363e0d2f244faa83c-1450767648

Researchers discover link between inhibiting 14-3-3zeta protein and faster wound healing

December 22, 2015 4:30am
CLARE PEDDIESCIENCE REPORTERThe Advertiser



Research assistant Kaitlin Scheer looks at skin cells on a computer at the Centre for Cancer Biology. Picture: Stephen Laffer

SCIENTIFIC serendipity has led to an Adelaide discovery that promises to accelerate the healing of wounds.

Researchers at the Centre for Cancer Biology who were studying a protein linked to the spread of cancer found that inhibiting it could make wounds heal faster.
Scientists believe high levels of the skin protein, called 14-3-3zeta, may be the reason chronic wounds fail to heal, as in diabetes.
Research leader Dr Michael Samuel said inhibiting the protein helped speed construction of a stiff cellular “scaffold” to support new skin.
“The scaffolding is required for the surface skin to grow over, because otherwise you’ve got a hole,” he said.
“You need to fill that gap with the scaffold before the skin can grow over the top.”

The therapy is a protein inhibitor applied to the skin “for as long as it takes to close the wound”, which has been about five days in tests on mice.
A derivative or “improved version” of this inhibitor will need to go through clinical trials before it is available for use in humans, in possibly five to ten years.
Experiments using human tissue samples from people with chronic wounds have been successful.

Dr Samuel said his laboratory was initially interested in the protein because “cancer manipulates the way the scaffold works, to promote its spread”.
“It’s one of those things where you’re looking at cancer and then you find something else about wound healing,” he said.
“It’s an interesting thing that happens in science quite a lot.”
Research assistant Kaitlin Scheer was the first to observe that mice lacking the protein had faster-healing wounds.
It was the opposite to what she had expected and inspired a new line of research in wound healing.
“As a biologist you have to have a natural sense of curiosity I think,” she said.
“I love it because we’re always learning new things, even doing little experiments and thinking no one in the world has ever observed this particular phenomenon before. I think that’s amazing.”
The research is published today in the journal Developmental Cell.