Faculty of Medicine Cellullar and Mollecular Medicine

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Breast Cancer Research Lab

The laboratory is involved in studying aspects of oncogenic and survival signaling in breast cancer. Expression of genes involved in growth promotion can cause programmed cell death in normal cells but not in cancer cells. We are looking at the mechanism of induction of cell death by a cell cycle protein as well as the contributions and mechanisms of survival signaling at different stages of breast cancer that afford resistance to this cell death.

More than 50% of breast cancers are initially dependent on estrogen for growth and are responsive to anti-estrogen therapy. Eventually, however, this therapy fails as the tumor cells progress to an estrogen-independent state. Another area of focus in the lab is the mechanism involved in breast cancer cell progression with emphasis on cell survival pathways. The NF kappa B family of transcription factors has been implicated in tumorigenesis. Our work involves understanding the role of NF kappa B in conferring estrogen independence to breast cancer cells using both cell culture models of progression and tumor biopsy materials.

Retinoids and retinoid derivatives are promising treatments for certain cancers and may also be beneficial for a wider population of cancers when used in conjunction with standard chemotherapies. We therefore also study the mechanism of action of retinoids and retinoid receptors in apoptosis with emphasis on breast cancer.

We perform a large amount of cell culture and experiments involve both plasmid transfections and immunocytochemistry. The lab uses a wide variety of molecular biology techniques including DNA cloning, polymerase chain reaction, RNA isolation and hybridization, DNA sequencing, electrophoretic mobility gel shifts, etc. Biochemical techniques include affinity chromatography, western blots, enzyme assays, immunoprecipitation, etc.

Selected references:

M.A. Christine Pratt , Tanya E. Bishop, Dawn White, Charles A. Lefebvre, Eric Lacasse, Michel Menard and Robert Clarke. p50-associated NF- B activity is constitutively increased early in breast cancer cell progression and inhibition reverts hormone-independence. Submitted to Molecular and Cellular Biology, October, 2001.

M.-Y. Niu, M. Menard, J.C. Reed, S. Krajewski and M.A.C. Pratt. Ectopic expression of cyclin D1 amplifies a retinoic acid-induced mitochondrial death pathway in breast cancer cells. Oncogene 20:3506-3518 (2001).

M.A.C. Pratt, C.A. Crippen and M. Menard. Spontaneous retinoic acid receptor 2 expression during mesoderm differentiation of P19 murine embryonal carcinoma cells. Differentiation 65: 271-279 (2000).

S. Krajewski, M. Krajewska, B.C. Turner, C. Pratt, B. Howard, J.M. Zapata, V.Frenkel, S. Robertson, Y. Ionov, H. Yamamoto, M. Perucho, S. Takayama and J.C. Reed. Prognostic significance of apoptosis regulators in breast cancer. Endocrine-Related Cancer 6: 29-40 (1999)

M.A. Christine Pratt, Stanislaw Krajewski, Michel Menard, Maryla Krajewska, Heather MacLeod and John C. Reed. Estrogen withdrawal-induced human breast cancer tumour regression in nude mice is prevented by Bcl-2. FEBS Letters 440: 403-408 (1998).

M.A. Christine Pratt, Abheha Satkunaratnam and Denise Novosad. Estrogen activates Raf-1 kinase and induces expression of Egr-1 in MCF-7 breast cancer cells. Molecular and Cellular Biochemistry 189: 119-125 (1998)

Christine Teixeira and M.A. Christine Pratt. Cdk2 is a target for retinoic acid-mediated growth inhibition in MCF-7 human breast cancer cells. Molecular Endocrinology 11: 1191-1202 (1997).

M.A. Christine Pratt, Dave Deonarine, Christine Teixeira, Denise Novosad, Bonnie F. Tate and Joseph F. Gippo. The AF-2 region of the RAR mediates Retinoic acid inhibition of estrogen receptor function in breast cancer cells. Journal of Biological Chemistry 271: 20346-20353 (1996).

Christine Teixeira, John C. Reed and M.A. Christine Pratt. Estrogen promotes chemotherapeutic drug resistance by a mechanism involving Bcl-2 proto-oncogene expression in human breast cancer cells. Cancer Research 55: 3902-3907 (1995).

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