gilmore@bu.edu

Cell Signaling and Gene Regulation Biochemistry Cancer Biology Genetics

Professor of Biology
Ph.D., University of California, Berkeley, 1984

Molecular biology, cell biology, virology, signal transduction, cancer

My research focuses on understanding the cellular and molecular mechanisms by which certain genes can transform normal cells into malignant cells, and the normal control of cellular growth by these genes. In particular, we have concentrated on the Rel/NF-kB family of transcription factors, whose activity is altered in a variety of human cancers, especially lymphoid cell cancers. In recent studies, we have found that the human c-rel gene, which is amplified and overexpressed in many human lymphomas, can also malignantly transform lymphoid cells in tissue culture. Currently, we are determining sequences in the Rel protein that are important for its malignant transforming function, and are developing model systems to study oncogenesis induced by overexpressed c-Rel.

In collaborative studies with Dr. John Porco in the Chemistry Department at Boston University, we are also characterizing natural and synthetic inhibitors of Rel/NF-kB signaling. Many of these inhibitors are derivatives of fungal metabolites, and may have anti-cancer or anti-inflammatory activities.

Recently, we have been studying the evolutionary origins of the NF-kB pathway by characterizing NF-kB genes and proteins in simple marine organisms, such as the sea anemone Nematostella vectensis. This research may also have relevance to the mechanisms by which simple marine organisms deal with the environmental stress that is currently impacting sensitive marine ecosystems. These studies are being carried out in collaboration with Drs. Les Kaufman and John Finnerty (Biology Department, Boston University).

Herscovitch M, W Comb, T Ennis, K Coleman, S Yong, B Armstead, D Kalaitzidis, S Chandani & TD Gilmore. 2008. Intermolecular disulfide bond formation in the NEMO dimer requires Cys54 and Cys347. Biochemical and Biophysical Research Communications, 367: 103-108.

Gilmore TD. 2007. Multiple myeloma: lusting for NF-kB. Cancer Cell 12: 95-97.

Starzynowski DT, H Trautmann, C Pott, L Harder, N Arnold, JA Africa, JR Leeman, R Siebert & TD Gilmore. 2007. Mutation of an IKK phosphorylation site within the transactivation domain of REL in two patients with B-cell lymphoma enhances REL's in vitro transforming activity. Oncogene 26, 2685-2694.

Sullivan JC, D Kalaitzidis, TD Gilmore & JR Finnerty. 2007. Rel homology domain-containing transcription factors in the cnidarian Nematostella vectensis. Development Genes and Evolution, 217: 63-72.

Gilmore TD & M Herscovitch. 2006. Inhibitors of NF-kB signaling: 785 and counting. Oncogene 25: 6887-6899.

Courtois G & TD Gilmore. 2006. Mutations in the NF-kB signaling pathway: implications for human disease. Oncogene 25, 6831-6843.

Perkins ND & TD Gilmore. 2006. Good cop, bad cop: the different faces of NF-kB. Cell Death and Differentiation: 13: 759-772.

Liang M-C, S Bardhan, EA Pace, D Rosman, JA Beutler, JA Porco Jr & TD Gilmore. 2006. Inhibition of transcription factor NF-kB signaling proteins IKKbeta and p65 through specific cysteine residues by epoxyquinone A monomer: correlation with its anti-cancer cell growth activity. Biochemical Pharmacology: 71: 634-645.

Liang M-C, S Bardhan, JA Porco Jr & TD Gilmore. 2006. The synthetic epoxyquinoids jesterone dimer and epoxyquinone A monomer induce apoptosis and inhibit REL (human c-Rel) DNA binding in an IkBalpha-deficient diffuse large B-cell lymphoma cell line. Cancer Letters 241: 69-78.

Questions and comments are always welcome.
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This document was last modified on February 11, 2008.