Speaker: Alex K-Y. Jen, MSE Chair, Boeing/Johnson Chair Professor of Materials Science & Engineering Professor of Chemistry, University of Washington.

One of the most compelling steps in the post-genomic era is learning the functional roles for all proteins. We have developed the FLEXGene Repository (for Full-Length Expression-ready), which comprises over 8000 full length clones for human genes, as well as complete genomes collections for several microorganisms enabling the high-throughput (HT) screening of protein function for the entire set (or any customized subset) of genes using any method of in vitro or in vivo expression.

Dr. Mikhael’s’ primary research interests are in multiple myeloma and related conditions.

Macrophages are versatile plastic cells that are key components of the body’s immune system. The interaction of engineered nanoparticles with macrophages is important because these cells clear nanoparticles from the circulation, and because they are potential therapeutic targets in inflammatory conditions, atherosclerosis and cancer.

There has been a great interest in the United States and other parts of the world for non-surgical endoscopic techniques such as endoscopic mucosal resection or ablation to manage and eliminate early esophageal cancers. Results from some of these studies will be discussed. The collaborations between Mayo Clinic and Arizona State University provide an exciting opportunity for advances to diagnose, manage and ultimately prevent esophageal cancer.

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.

The final stage of the metastatic cascade, colonization of secondary tissue sites, is very hard to address experimentally and is thus poorly understood. Given the long time-scale of most metastatic disease, it is commonly presumed that colonization arises from rare genetically pre-adapted founding cells. We construct a null model to estimate the relative probability of colonization from common non-pre-adapted cancer cells.

Colorectal cancer arises as the consequence of the accumulation of genetic alterations (e.g. gene mutations, gene amplification, etc.) and epigenetic alterations (e.g. aberrant DNA methylation, chromatin modifications, etc.) that transform colonic epithelial cells into colon adenocarcinoma cells. The loss of genomic and epigenomic stability and resulting gene alterations appears to be a key molecular and pathogenic step that occurs early in the tumorigenesis process and permits the acquisition of a sufficient number of alterations in tumor suppressor genes and oncogenes in a clone of cells to result in their ultimate transformation into cancer. It has also become clear that epigenetic alterations are common in many cancers and affect the formation and behavior of the tumors. With regards to DNA methylation, it is present normally throughout the majority of the genome and is maintained in relatively stable patterns that are established during development.

Breast cancer is the second leading cause of deaths among women. In the United States, an estimated 230,480 are diagnosed with breast cancer each year and, of these, 39,520 are expected to die from the disease. This devastating consequence is partly due our inability to detect and provide treatments while the tumor is localized to the breast. As a result, numerous efforts have been made to identify early breast cancer biomarkers. In my talk I will discuss the implications of a number of potential breast cancer biomarkers specifically focusing on the functions of prolactin and its downstream target, Stat5.

How Endothelial Cells Regulate Leukocyte Transmigration: Application to Cancer Metastasis