Pathologists observe the biology of cancer on a daily basis, diagnosing new cancers and staging known cancers simply by looking into a simple tool invented nearly 500 years ago. The low tech microscope yields nothing more than a magnified picture, but careful observation will allow specific patterns to emerge.

Cancer is a disruption of normal cell development. In the view of the quasi-potential landscape of gene networks, cancer arises because cells are pushed into developmentally inaccessible, evolutionary ancient “side-valleys” – the cancer attractors. I will present experiments supporting this alternative view and apply such non-genetic dynamics to show how Lamarckian (as opposed to Darwinian) dynamics initiates development of cancer drug resistance.

Cancer is the second leading cause of death in the US exceeded only by cardiovascular diseases. About 1.6 million people will be diagnosed with cancer (excluding non-melanoma skin cancers) and 580,000 people will die of the disease in 2013. A significant number of cancer deaths can be prevented by controlling smoking behaviors, alcohol consumption and exposure to certain viruses.

The genome has traditionally been treated as a Read-Only Memory (ROM) subject to change by copying errors and accidents. I propose that we need to change that perspective and understand the genome as an intricately formatted Read–Write (RW) data storage system constantly subject to cellular modifications and inscriptions.

Absorption of light by endogenous or exogenous cells and/or tissue-associated chromophores creates photophysical processes that are captured for diagnostic uses and for surgical guidance, in addition to treatment purposes. Such a process also provides a tool for the mechanistic understanding of disease pathology and tissue responses to various therapeutic interventions.

Cancer is a complex disease, the understanding of which is further challenged by the complexity of the biological samples that serve as disease surrogates for molecular study. Acquiring cancer biospecimens for study is, itself, governed by complex medical, ethical and legal issues. The samples, themselves, typically represent only small foci of a much larger and heterogeneous process that makes sampling bias an inescapable challenge

Cancer’s evolutionary roots can be traced by at least to the dawn of multicellularity 1.5 billion years ago. In that evolutionary context, cancer appears to be a type of atavism, or reversion to an ancestral phenotype, in which gain of function is really regain of deeply-embedded ancient functionalities.

Over the last decade, there has been an explosion in interest in the human microbiome both from the scientific community and the general public. This interest has been driven, in part, by the development of tools for identifying and studying the composition and functional capacity of microbes that coexist with the human host.

The epigenome is reset during embryogenesis and matures around the end of development. Large scale genomic studies have now shown considerable proliferation dependent epigenome changes (drift) in aging cells (DNA methylation instability, chromatin instability).

Most of the diversity of life on earth is contained within the genomes of the planet’s microbes, including bacteria and particularly viruses, which infect every known form of cellular life on the planet. Arguably the most important biological realm for exploration is the microbial world on earth