Dr.Kimberly Bussey, Ph.D.

Cancers or cancer-like phenomena are found across the tree of life in multicellular organisms. The hallmarks of cancer describe the functions a cell or group of cells must express to become a cancerous tumor, including uncontrolled growth, uninhibited mobility, and resistance to cell death. The current paradigm ascribes the acquisition of such behavior to the gradual accumulation of genomic changes. This gene-centric view has been useful up to a point, but it suffers from the problem that most oncogenic changes are neither necessary, sufficient, nor context-independent. Furthermore, such behaviors can be suppressed in a physiologically normal environment.

We propose thinking about cancer as an atavism, in this case the re-expression of single-cell biology in a multicellular context. The re-expression of unicellular behavior is the consequence of a speciation event. Cancer is not normal gone wrong. It is the emergence of a new unicellular parasitic collective where adaptability is itself a selected trait. Under this context, we hypothesize that we can detect evidence of single-cell stress-responses, such as stress-induced mutation (SIM), in cancer genomes, identify how unicellular information flows have been restored through integrating "omic" data sets and testing the resulting predictions in the lab, and apply this understanding clinically.
Cancer
Genomics
Bioinformatics