PT - JOURNAL ARTICLE AU - XING Q. PAN AU - CHU C. SHIH AU - JOHN HARDAY TI - Chitinase Induces Lysis of MCF-7 Cells in Culture and of Human Breast Cancer Xenograft B11-2 in SCID Mice DP - 2005 Sep 01 TA - Anticancer Research PG - 3167--3172 VI - 25 IP - 5 4099 - http://ar.iiarjournals.org/content/25/5/3167.short 4100 - http://ar.iiarjournals.org/content/25/5/3167.full SO - Anticancer Res2005 Sep 01; 25 AB - Background: It has long been known that the polycarbohydrates on the neoplastic cell surface are different from those on normal cells; differences which allow one to attack tumor cells selectively. Although the exact differences between tumor cells and normal cells are still not clearly known, research into these differences is ongoing for anticancer drug development. Materials and Methods: The human breast cancer cell line MCF-7 in culture and human breast xenograft B11-2 in SCID mice were used in our observations. Two different samples of chitinase from different bacteria were tested in the experiments. Optical observation of regular H & E-stained tumor tissue sections and observations by transmission electron microscopic techniques were used in this study. Results: MCF-7 breast cancer cells in culture showed structural damage within 7 hours after 1.3 unit/ml of chitinase was added to the medium, while normal mice spleen cells did not. The transplanted B11-2 xenograft tissue in mice started to lyse 12 hours after chitinase was injected; the size of the tumor gradually reduced and finally a scab was formed, which came off the skin a few days later. All the tested tumor-bearing mice survived and these cured mice had no tumor re-growth during the following 1-year observation period. Conclusion: Chitinase selectively lysed the tumor cells in vitro and in vivo. Injected chitinase destroyed the tumor tissue and cured the mice. The further development of this type of treatment and of the mechanisms of chitinase action are discussed. Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved