An average cancer cell is driven by 5–10 mutations, roughly similar to the number of proteins encoded by an average virus.  Transformation or viral infection reconfigures cellular phenotype, but the logic of either complex perturbation is difficult to explain by inspection and intuition.  Our laboratory tackles these challenges with a systems bioengineering approach that combines quantitative measurements, computational models, experimental manipulations, and data mining.  We pursue systems bioengineering research that scales from genes and proteins in cells to tissues and tumors in animals to large-scale observations in human populations.  Explanatory and predictive understanding at the systems level will one day lead to therapeutic strategies that are innovative and tailored to the complexity of each disease.

Recent Publications

Marohl T, Atkins KA, Wang L†, Janes KA†. (2026) PCSK5M452I is a recessive hypomorph exclusive to MCF10DCIS.com cellsMol Cancer Res, 24, 106-118.  Cover article.  [Link] [Pubmed] [Article]
Power LN, Zawrotna N, Dinda M, Weir AE, Paudel BB, Ghimire O, Kisiel K, Letai CT, Janes KA, Smith JS. (2026) Age-dependent topoisomerase I depletion alters recruitment of rDNA silencing complexesJ Biol Chem, 302, 111062.  [Link]   [Pubmed] [Article]
Wells CJ, Labban N, Showalter SL, Przanowska RK, Janes KA. (2026) Fast learning-free organoid quantification and tracking with OrganoSeg2Sci Rep, 16, 7928.  [Link]   [Pubmed] [Article]