Faculty Profiles

Thomas Gilmore

Thomas Gilmore

Professor of Biology

PhD, University of California, Berkeley, 1984
Areas of interest: molecular biology, cell biology, signal transduction, cancer, molecular ecology
gilmore@bu.edu
(617) 353-5444
http://www.nf-kb.org

Current Research

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 avian and human lymphoid cells in tissue culture. Currently, we are identifying target genes that are important for c-Rel transformation, and are developing further model systems to study oncogenesis induced by overexpressed c-Rel.

In collaborative studies with Drs. John Porco and Adrian Whitty 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 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).

Courses Taught

  • BB522 Molecular Biology Laboratory
  • BI576 Carcinogenesis

Selected Publications

  • Wolenski FS, Chandani S, Stefanik DJ, Jiang N, Chu E, Finnerty JR, Gilmore TD. (2012). Two polymorphic residues account for the differences in DNA binding and transcriptional activation by NF-kB proteins encoded by naturally occurring alleles in Nematostella vectensis. Journal of Molecular Evolution, in press.
  • Gilmore TD, Wolenski FS (2012). NF-kB: where did it come from and why? Immunological Reviews, in press
  • Gilmore TD, Gerondakis S. (2011). The c-Rel transcription factor in development and disease. Genes & Cancer 7, 695-711.
  • Garbati M, Thompson RC, Haery L, Gilmore TD. (2011). A rearranged EP300 gene in the human B-cell lymphoma cell line RC-K8 encodes a disabled transcriptional co-activator that contributes to cell growth and oncogenicity. Cancer Letters, 302, 76-83.
  • Wolenski F, Garbati MR, Lubinski TJ, Traylor-Knowles N, Stefanik DJ, Dresselhaus E, Goucher H, Finnerty JR, Gilmore TD. (2011). Characterization of the core elements of the NF-kB signaling pathway of the sea anemone Nematostella vectensis. Molecular and Cellular Biology 31, 1076-1087.
  • Gilmore TD, Garbati MR. (2011). Inhibition of NF-kB signaling as a strategy in disease therapy. Current Topics in Microbiology and Immunology 349, 245-263..
  • Thompson RC, Herscovitch M, Zhao I, Ford TJ, Gilmore TD. (2011). NF-kB down-regulates expression of the B-lymphoma marker CD10 through a miR-155/PU.1 pathway. Journal of Biological Chemistry 286, 1675-1681.
  • Sullivan JD, Wolenski FS, Reitzel AM, French CE, Traylor-Knowles N, Gilmore TD, Finnerty JR. (2009). Two alleles encoding transcription factor NF-kB in the sea anemone Nematostella vectensis are widely dispersed in natural populations and encode proteins with distinct activities. PLoS ONE 4, e7311.

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