Dr. Henikoff will talk about histone variants, nucleosome dynamics and epigenetics.

Although Paul Davies wanted me to talk about 10 Crazy Ideas for the Physics of Cancer, I have decided to pare the list down to 5. I am coming to the opinion that there are very deep concepts in biology which, while they may not be “new physics”, in a sense transcend what we usually view as things easily explained by the standard physics world-view. I also am forming the opinion that our failure to “cure” cancer, or even make substantial inroads into the mortality rate, indicates that there are things about biology and cancer that we as physicists miss using the standard physics world-view.

Cancer is a disease of considerable complexity. Cancer originates from and is supported by a wide variety of alterations in the genome that often lead to drastic alterations of the cell’s control circuitry, producing a great deal of diversity in the molecular mechanisms operating in cancer cells. When attempting to make inferences from a diverse population, heterogeneity in either the network regulatory connections or operating rules blurs the relationships and rapidly reduces the ability to accurately discern regulatory interactions. This provides a considerable challenge to those attempting to determine which, of all the changes that can be seen, are consequential.

The seminar followed a 3 day conference at ASU on the mechanical properties of cancer. Don Coffey spoke to Pauline Davies from the Hugh Downs School of Human Communication about the conference. A transcript of the interview follows.

For more information on John D. Nagy please visit his website at: www.scottsdalecc.edu/nagy

Cancer, in general, is thought to evolve from natural selection of cells within a neoplasm. While this hypothesis is still being refined, it is widely accepted that competition amongst neoplastic clones, coupled with genetic changes and environment, are integral to cancer. Genomic instability appears to cooperate with Darwinian selection to promote cancer formation through a process in which genomic aberrations occur at accelerated rates, and those alterations that provide a selective growth advantage lead to clonal evolution and expansion.

Gene expression, cell specialization, and, presumably, the progress to cancer, are controlled by a heritable, but environmentally modifiable code that “lies on top of” the genome. This is called the epigenetic code. Some known epigenetic markings consist of chemical modifications of amino acid residues in proteins. For example, a lysine residue on a histone protein (a protein that packages DNA) may have an amine group replaced ay an acetyl group. DNA itself is also modified.

We are pursuing studies to identify and characterize genes that regulate critical events involved in the development of resistance to hormonal therapies in breast cancer. Approximately two-thirds of breast cancers require estrogen to grow. Estrogen receptor (ER) – the protein activated by estrogen, and the proteins that it activates – are excellent targets for hormonal therapy in these patients.

Speaker: Jack Tuszynski, Ph.D. is a professor of biophysics at the University of Alberta, cross-appointed in the Faculties of Science and Medicine.

Paul Davies, director of ASU’s PSOC, introduces Dr. Stephen Wolfram, the creator of Mathematica, Wolfram|Alpha and the author of ‘A New Kind of Science’. He is the founder and CEO of Wolfram Research. Dr. Wolfram’s seminar is entitled “Biomedicine in the Computational Universe”

For more information contact:
Vanessa Baack, Center for the Convergence of Physical Science and Cancer Biology