Profile

Zhila Khalkhali-Ellis, PhD
	zellis@childrensmemorial.org Children's Plaza, Box 222 Room 475 Chicago, IL 60614 Phone: (773) 755-6353 Fax: (773) 755-6594

Education
	Year	Degree	Institution
		Ph.D.	London University, UK

Work Experience
	Period	Description	Organization
	2004 - Present	Research Professor, Dept. of Pediatrics	Children's Memorial Research Center
	1999 - 2004	Associate Research Scientist, Holden Comprehensive Cancer Center member	Dept. of Anatomy and Cell Biology, The University of Iowa
	1994 - 1997	Research Scientist, Dept of Internal Medicine, Division of Rheumatology	Dept. of Pediatrics, St. Louis University
	1992 - 1994	Research Associate, Dept. of Biology	Washington University, St. Louis

Research Interests

Mammary glands undergo structural remodeling and biochemical changes from embryogenesis through aging in females. This process is tightly regulated by hormones and involves a complex cooperation of a variety of genes participating in cell division, proliferation, matrix degradation and remodeling. Like mammary epithelial cells breast cancer tumors require estrogen for continued growth. Anti-estrogen therapy alone or in combination with other drugs, has long been a common procedure for breast cancer treatment and prophylaxis. The clinical efficacy of an anti-estrogen tamoxifen (TAM) has been attributed to growth arrest and induction of apoptosis in breast cancer cells, but the ability of TAM as a potential modulator of tumor suppressor genes has never been reported.
Maspin, a serine protease inhibitor (serpin), is highly expressed in normal mammary and reproductive organs, and is believed to play a critical role in mammary gland development. Maspin is present in high concentrations in normal mammary epithelial (and myoepithelial) cells, but its expression is down-regulated in primary breast cancer and lost in metastatic cells. Maspin promoter contains hormone response element and AP1 sites and maspin induction following androgen ablation and/or radical prostectomy in prostate cancer have been reported. Thus, we hypothesized that that tamoxifen’s anti-tumor action could also be mediated, at least in part, through its ability to induce the tumor suppressor gene maspin. We are currently studying the effect of TAM (over various time period) on maspin expression in normal mammary epithelial cells and breast cancer cell lines and verifying our observations in patients tissue.
Recent studies have also indicated the importance of sex hormones and gender in autoimmune disorders such as rheumatoid arthritis. Regulation of immune response, matrix metalloproteinases and cytokine system by hormones could have a direct effect on cartilage and synovial tissue. Thus, we hypothesized that sex hormones could exert direct and indirect effects on cartilage synthesis and degradation and thus modulate the course of the disease. Studies in our lab are directed to answer such questions.

Lab Affiliations
	Mary J.C. Hendrix Research Laboratory

Recent Publications

Khalkhali-Ellis Z, Christian AL, Kirschmann DA, Edwards EM, Rezaie-Thompson, M, Vasef, MA, Gruman, LM, Seftor, REB, Norwood, LE, Hendrix MJC. (January, 2004). Regulating the tumor suppressor gene maspin expression in normal mammary epithelia and breast cancer cells: a potential mechanism for tamoxifen’s anti-tumor properties.. Clinical Cancer Research: 10:449-454.

Khalkhali-Ellis Z, and Hendrix MJC. (May, 2003). Nitric oxide regulation of maspin in normal mammary epithelial and breast carcinoma.. American J. of Pathology: 162:1411-1418.

Odero V, Khalkhali-Ellis Z, Chunthapong J, Amir, S, Seftor EA, and Hendrix MJC. (2003). Maspin regulates different signalling pathways for motility and adhesion in breast cancer cells. Cancer Biology and Therapy: 2:67-72.

Odero V, Khalkhali-Ellis Z, Schneider GB, Seftor EA, Seftor REB, Koland JG and Hendrix MJC. (2002). Maspin phosphorylation is involved in the regulation of human breast cancer cell motility. Biochem Biophys Res. Communications: 295:800-805.

Khalkhali-Ellis Z, Handa RJ, Price Jr. RH and Hendrix MJC (2002). Androgen receptors in synoviocytes: androgen regulation of IL-1 induced IL-6 production.. J. Rheumatology: 29:1843-1845.

Tobacmann J, Khalkhali-Ellis Z (2001). Steroid sulfatase expression in mammary myoepithelial cells and its regulation by steroid hormones. J. Steroid Biochem. Mol. Biol: 81:65-68.

Khalkhali-Ellis Z, Seftor EA, Handa RJ, Price Jr. RH, Nieva DRC, Kirschmann DA, Baragi VM, Sharma, RV, Bhalla RC, Moore TL and Hendrix MJC. (2000). Estrogen and progesterone regulation of human fibroblast-like synoviocytes in vitro: implications in rheumatoid arthritis. J Rheumatology: 27:1622-1631.

Khalkhali-Ellis Z, Bulla GA, Schlesinger L , Kirschmann DA, Moore TL and Hendrix MJC (1999). C1q containing immune complexes purified from sera of juvenile rheumatoid arthritis patients mediate IL-8 production by human synoviocytes. J Immunology: 163:4612-4620.

Awards/Honors
	2004 - Eisenberg Scholar, Children’s Memorial Research Institute , “Role of secreted maspin" 2000 - Howard Hughes Investigator Research Award 2000 - University of Iowa Florence Lindsay Young Investigator Award

Professional Service

2001 - Present Grant Review services: Department of Defense Study Section on Prostate Cancer, Department of Defense Study Section on breast Cancer, NIH/NCI Special Emphasis Panel on Cancer Metastasis to Bone

1997 - Present Journal Reviewer (Intermittent), Cancer Research, American Journal of Pathology, Journal of Clinical Cancer Research, Clinical and Experimental Metastasis, Arthritis and Rheumatism, Journal of Rheumatology, Journal of Cellular Biology, Oncogene

2002 - 2002 Grant review (Ad hoc), British Research Council