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Kalpana Mujoo, Ph.D.
The focus of our laboratory is to identify and characterize the biological activity of novel compounds from legume plant extracts and study the signal transduction pathways these compounds may target to exert their antitumor activity. In collaboration with the University of Arizona at Tucson, we examined the antitumor activity of number of legume extracts and found one to demonstrate cytotoxicity against a panel of tumor cell lines. After a number of purification steps, we focused on 1 fraction, Fraction 35, which inhibited the growth of human leukemic, breast, ovarian, renal, pancreatic, prostate, and fresh human ovarian cancer cells without significant toxicity for human or mouse fibroblast and normal bone marrow cells. This novel compound significantly inhibited the endothelial cell proliferation with and without stimulation with beta-fibroblast growth factor, suggesting its possible role in inhibition of angiogenesis. Fraction 35 was able to cause cell-cycle arrest and apoptosis of tumor cells. We also conducted studies of the PI-3K signaling pathway in collaboration with Drs. Yinhua Yu and Gordon Mills (this department). Fraction 35 (triterpene glycoside) was able to inhibit the activity of PI-3K by 92%-95% and phosphorylation of AKT, a downstream target of the PI-3K pathway in Jurkat cells and ovarian cell lines. Fraction 35 prevented the formation of 93% of papillomas when we used DMBA as a carcinogen in a skin carcinogenesis model, in collaboration with Drs. Thomas Slaga and Margaret Hanausek (then of the Department of Carcinogenesis). Fraction 35 prevented the mutation of the Ha-ras gene in animals treated with Fraction 35 + DMBA. More recently (in collaboration with Dr. Michael Wargovich, Department of Gastrointestinal Oncology and Digestive Diseases) we have found that, at a daily intake of 1 mg/kg of body weight, Fraction 35 significantly reduced the total number of aberrant crypt foci in the colon carcinogenesis model.

We previously studied the molecular mechanism and therapeutic potential of p53 tumor suppressor gene therapy in human ovarian cancer. More recently, we examined the effect of the p53 adenovirus on growth and survival of cisplatin-resistant human ovarian cancer cells. These cells exhibit greater sensitivity to the p53 adenovirus than to parental OVCAR-3 cells. Marked induction of p21 and apoptosis were observed in drug-resistant OVCAR-3 cells. In addition, we observed 40%-60% greater longevity in animals after injection with p53 adenovirus in an intraperitoneal model of cisplatin-resistant ovarian cells.

Selected Publications:
  1. Mujoo K, Catino JC, Maneval DC, Gutterman JU. Studies of the molecular mechanism of growth inhibition with p53-adenoviral construct in human ovarian cancer cells. International Journal of Gynecologic Cancer 8:233-241, 1998
  2. Mujoo K, Maneval DC, Anderson SC, Gutterman JU. Adenoviral-mediated p53 tumor suppressor gene therapy of human ovarian carcinoma. Oncogene 12:1617-1623, 1996
  3. Murray JL, Kleinerman ES, Jia SF, Rosenblum MG, Eton O, Buzaid A, Lega S, Ross MI, Thompson L, Mujoo K, Reiger PT, Saleh M, Khazaeli MB, Vadhan-Raj S. Phase Ia/Ib trial of anti-GD2 chimeric monoclonal antibody (ch 14.18) and recombinant human granulocyte-macrophage colony stimulating factor (rhGMCSF) in metastatic melanoma. J Immunother Emphasis Tumor Immunol 19:206-217, 1996
  4. Rosenblum MG, Cheung L, Kim SK, Mujoo K, Donato NJ, Murray JL. Mechanisms of resistance to immunotoxins and strategies to target resistant cells. Cancer Immunol Immunother 42:115-121, 1996