Proceedings of the National Academy of Sciences of the United States of America

About the PNAS Member Editor
Name Bissell, Mina J.
Location University of California, Berkeley
Primary Field Cellular and Developmental Biology
Secondary Field Medical Genetics, Hematology and Oncology
 Election Citation
Bissell is a leader in the field of tissue-specificity regulation in tumor microenvironments. Her research into tissue architecture, the extracellular matrix, and gene expression has identified mechanisms that link genomic instability with cancer in mammary cells.
 Research Interests
The fundamental questions we have addressed in my laboratory are: How tissue-specificity is maintained and how these processes go awry in cancer. Early work (70s) on Warburg effect indicated that it is the rate of glucose uptake that regulates rates of glycolysis in normal and transformed cells and that pattern of glucose metabolism was tissue-specific. Work in the 80s indicated that the context determines whether a potent oncogene is oncogenic or whether it could coexist within a normal host. Work in the 80s and 90s indicated that both malignant and normal cells are plastic and dependent on their microenvironment. We could "revert" malignant human breast cells in 3-dimensional extracellular-matrix (ECM) gels (an assay we developed in 1989 for mice mammary and in 1992 for human breast cells). Conversely we could make normal mice develop tumors by destroying the mammary structure by metalloproteinases in engineered mice. We thus established that: 1-ECM signals to tissue-specificity, 2-context matters, 3-phenotype is dominant over genotype, and 4- tissue structure is the ultimate regulator of tissue-specificity. Current work concentrates on the mechanism(s) of "dynamic reciprocity" (a model we proposed in 1982) between how the microenvironment signals and in return receives signals from the chromatin and the nucleus.

 
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