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Molecular and Cellular Biology

Houston, Texas

Image 1: Ovulated mouse cumulus cell oocyte complex immunostained for matrix proteins hyaluronan and versican. By JoAnne Richards, Ph.D.; Image 2: By Yi LI, Ph.D.; Image 3: Mouse oocyte at meiosis I immunostained  for tubulin (red) phosphop38MAPK (green) and DNA (blue). By JoAnne Richards,  Ph.D.;  Image 4: Expanded cumulus cell ooctye ocmplex  immunostained for hyaluronan (red), TSG6 (green) and DAN (blue). By JoAnne  Richards, Ph.D.;  Image 5: Epithelial cells taken from a mouse  mammary gland were cultured in a dish and transduced with a retrovirus  expressing two genes. The green staining shows green fluorescent protein and the red  staining shows progesterone receptor expression. The nucleus of each cell is  stained blue. Photomicrograph taken at 200X magnification.  By Sandra L. Grimm,  Ph.D.; Image 6: Ovarian vasculature (red) is excluded from the granulosa cells (blue) within growing follicles (round structures); Image 7:  Ovulated mouse cumulus cell oocyte  complex immunostained for matrix proteins hyaluronan and versican. By JoAnne Richards, Ph.D.
Department of Molecular and Cellular Biology
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Suzanne AW Fuqua, Ph.D.

Suzanne AW Fuqua, Ph.D. photoProfessor
Departments of Medicine (Lester and Sue Smith Breast Center) and Molecular and Cellular Biology

Education

Ph.D.: University of Texas Graduate School of Biomedical Sciences, Houston
Postdoctoral training: University of Texas Health Science Center, San Antonio

Research Interest

The Role of Estrogen Receptors and Estrogen-regulated Protein in Breast Tumor Progression
Dr. Suzanne AW Fuqua’s laboratory is examining the role of estrogen receptors (ER) α and ß, and the progesterone receptor (PR) A and B isoforms in hormone response, and breast cancer metastasis using clinical material, breast cancer cell lines, and transgenic mouse model systems. Furthermore, she was the first to discover a somatic ER α mutant and alternatively spliced forms of ER α, which are thought to be important in the response of patients to treatment, and the development of breast cancer metastases. She has completed large retrospective clinical studies demonstrating 1) that low levels ERß are associated with resistance to tamoxifen antiestrogen therapy in patients, 2) that PR-positive patients with high levels of the A isoform are also resistant to hormonal therapies, and 3) that a ERα mutation at lysine residue 303 enhances estrogen hypersensitivity and alters treatment responsiveness. These studies are the first to identify these receptors as predictive markers in large, multivariate analyses.

Dr. Fuqua is also elucidating the complex molecular alterations and mechanisms resulting in acquired resistance by utilizing genomics-based methodologies, such as microarray expression analyses. She is Director of the Breast Center microarray core. The main goal of her laboratory remains to understand the central role of the ER and its associated secondary signaling cascades in the progression of breast cancer patients, and the identification of novel markers of disease outcome. She has discovered several novel mechanisms of tamoxifen resistance using metastatic patient tumors. These include the involvement of the androgen receptor (AR) in resistance to antiestrogen, the role of Rho GDIα in resistance and metastatic behavior of ER-positive cells, the role of Dicer—the stem cell and microRNA regulator, in tumor progression, and the impact of metastasis associated protein (MTA) 2 on the metastasis of ER-negative cancer.

Hypersensitivity Tamoxifen Resistance. Model illustration.

Contact Information

Baylor College of Medicine
One Baylor Plaza, Alkek N1220
Houston, TX 77030

Phone: 713-798-1671
E-mail: sfuqua@bcm.edu

Selected Publications

  1. Herynk MH, Parra I, Cui Y, Beyer A, Wu MF, Hilsenbeck SG and Fuqua SAW. (2007). Association between the estrogen receptor α A908G mutation and outcomes in invasive breast cancer. Clinical Cancer Research 13:3235-3243.
  2. Herynk MH, Beyer A, Cui Y, Anderson E, Green TP and Fuqua SAW. (2006). Cooperative action of tamoxifen and c-Src inhibition in preventing the growth of estrogen receptor-positive human breast cancer cells. Mol. Cancer Ther. 5:3023-3031.
  3. Ramos CA, Bowman TA, Boles NC, Merchant AA, Zheng Y, Parra I, Fuqua SA, Shaw CA and Goodell MA. (2006). Evidence for diversity in transcriptional profiles of single hematopoietic stem cells. PLoS Genet. Sep 29; 2(9).
  4. Cui Y, Parra I, Zhang M, Hilsenbeck SG, Tsimelzon A, Furukawa T, Horri A, Zhang ZY, Nicholson R and Fuqua SAW. (2006). Elevated expression of MAPK phosphastase 3 in breast cancer: A mechanism of tamoxifen resistance. Cancer Research 66:5950-5959.
  5. Cui Y, Niu A, Pestell R, Kumar R, Curran EM, Liu Y and Fuqua SAW. (2006). Metastasis-associated protein 2 is a repressor of estrogen receptor α whose overexpression leads to estrogen-independent growth of human breast cancer cells. Molecular Endocrinology Sept; 20(9):2020-2035.
  6. Singh RR, Barnes CJ, Talukder AH, Fuqua SAW and Kumar R. (2005). Negative regulation of ERα transactivation functions by LIM domain only protein LM04. Can. Res. 65:10594-10601.
  7. Cui Y, Zhang M, Pestell R, Curran EM, Welshons WV and Fuqua SAW. (2004). Phosphorylation of estrogen receptor α blocks its acetylation and regulates estrogen sensitivity. Cancer Res. 64:9199-9208.
  8. Hopp TA, Weiss HL, Parra I, Cui Y, Osborne CK and Fuqua SAW. (2004). Low levels of estrogen receptor ß protein predicts resistance to tamoxifen therapy in breast cancer. Clin. Cancer Res. 10:7490-7499.
  9. Hopp TA, Weiss HL, Hilsenbeck SG, Allred DC, Horwitz KB and Fuqua SAW. (2004). Breast cancer patients with progesterone receptor A-rich tumors have poorer disease-free survival rates. Clin. Cancer Res. 10:2751-2760.

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