ASSCR
Chairpersons: Robyn Meech & Stan Gronthos
The Australasian Society for Stem Cell Research is holding a scientific meeting within the AH & MR Congress 2012.
More information about ASSCR is available at www.asscr.org
Themes:
Stem Cells and Transplantation (a collaboration with TSANZ) Haematopiesis Stem Cells and Vascular Biology (a collaboration with AVBS) Pluriopotency and Reprogramming
Invited Speakers
International
- Dr Peter Psaltis, Mayo Foundation for Medical Education and Research, USA
- Dr Allan Robins, ViaCyte - San Diego, USA
- Prof Connie Eaves, University of British Columbia, Canada
- Prof Elaine Dzierzak, Erasmus Stem Cell Institute, Netherlands
- Prof Huck Hui Ng, Agency for Science, Technology and Research, Singapore
National
- A/Prof Louise Purton, St Vincent's Institute
- Prof Peter Ghosh, Institute of Nutraceutical Research
- A/Prof Sharon Ricardo, Monash University
- Prof Luen Bik To, IMVS Pathology
- Dr John Pimanda, University of New South Wales
- Prof Andrew Zannettino, University of Adelaide
- Dr Ben Hogan, University of Queensland
- Dr Quenten Schwarz, University of Adelaide
- Prof Emma Whitelaw, Queensland Institute of Medical Research
- Dr Jo Bowles, University of Queensland
- A/Prof Sheryl deLacy, Flinders University
- Prof Catherine Waldby, University of Sydney
Social Function
A dinner will be held to allow for networking in a relaxed social atmosphere. It will be held on Monday 26th November. Click here to see the menu for the conference dinner.
Annual General Meeting
The ASSCR Annual General Meeting will be held on Tuesday 27th November at 1:30pm in Riverbank Room 2.
Dr. Brash received his BS in Engineering Physics from the University of Illinois, minoring in Physiological Psychology. After a PhD in Biophysics, he began elucidating the steps leading from ultraviolet light photons to human skin cancer. As a postdoc at Harvard, he found that UV-induced mutation hotspots in E. coli occur at the same gene positions as (6-4) photoproducts and cyclobutane dimers: UV wasn't elevating random genomic instability. At the National Cancer Institute, he proved these photoproducts were mutagenic. Upon moving to Yale, the lab used the distinctive UV mutation pattern to identify genes mutated by sunlight in causing skin cancer: p53 in squamous cell carcinoma and its actinic keratosis precursor, and p53 and PTCH in basal cell carcinoma. They then showed P53 to be a key element of UV-induced apoptosis, preventing damaged cells from becoming mutants. The multiple-genetic-hit model of cancer predicts that our bodies harbor cells mutated in just one or another of the genes needed for cancer, so the lab sought p53-mutant cells in normal skin. Astonishingly, these cells were already proliferating as clones and were common – many people carry ~60,000 clones, occupying almost 5% of their epidermis. Switching to mice revealed that clonal expansion is driven by physiology, not by adding mutations. One mechanism is the mutant's resistance to UV-induced apoptosis. Another is UV's ability to tilt a clone's balance between progenitor cells and differentiating cells toward self-renewal of the progenitors. Understanding the role of P53 and UV in this cell fate decision is the lab's current focus. These results contribute to what is perhaps the best picture available of how a human carcinogen works.