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 is available at: www.asscr.org

Invited Speakers

International

National


Social Function

A dinner will be held to allow for networking in a relaxed social atmosphere. More detailsl be posted closer to the date.


Annual General Meeting

The ASSCR Annual General Meeting will be held at the AH&MR Congress.





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.