Mina J. Bissell

E. O. Lawrence Berkeley National Laboratory


Election Year: 2010
Primary Section: 22, Cellular and Developmental Biology
Secondary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type: Member

Biosketch

MINA J. BISSELL is Distinguished Scientist, the highest rank bestowed at Lawrence Berkeley National Laboratory (LBNL) and serves as Senior Advisor to the Laboratory Director on Biology. She is also Faculty of four Graduate Groups in UC Berkeley: Comparative Biochemistry, Endocrinology, Molecular Toxicology, and Bioengineering (UCSF/UCB joint). Having challenged several established paradigms, Bissell is a pioneer in breast cancer research and her body of work has provided much impetus for the current recognition of the significant role that extracellular matrix (ECM) signaling and microenvironment play in gene expression regulation in both normal and malignant cells. Her laboratory developed novel 3D assays and techniques that demonstrate her signature phrase: after conception, “phenotype is dominant over genotype.” Bissell earned her doctorate from Harvard Medical, won an American Cancer Society fellowship, and soon after joined LBNL. She was founding Director of the Cell and Molecular Biology Division and later Associate Laboratory Director for all Life Sciences. Bissell has published more than 400 publications, received numerous honors and awards and is one of the most sought-after speakers in the field. She is not only an elected Fellow of most U.S. honorary scientific academies, but she also sits on many national and international scientific boards.

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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