iansmith
May19-04, 06:28 AM
DNA alkylation destroys tumor cells in mice deficient in p53 and BCL-2 | By John Dudley Miller
A University of Pennsylvania research team has shown that it can kill tumor cells in mice by necrosis, rather than by inducing apoptosis, by giving them alkylating agents that block their energy supply. The authors of the study, which appears in the advanced online edition of Genes and Development, say the finding may give researchers another important mechanism with which to destroy cancer cells.
Craig Thompson and colleagues at the university's Abramson Family Cancer Research Institute bred mice to be deficient in two genes that help regulate death by apoptosis, p53, and BCL-2. In a series of experiments, the team proved that alkylating agents caused necrotic death in the tumor cells, according to the report.
The group also showed that providing another source of energy to both apoptotic-deficient tumor cells and tumors from wildtype apoptotic-competent mice prevented both groups of cells from dying, according to the article.
http://www.biomedcentral.com/news/20040517/01
A University of Pennsylvania research team has shown that it can kill tumor cells in mice by necrosis, rather than by inducing apoptosis, by giving them alkylating agents that block their energy supply. The authors of the study, which appears in the advanced online edition of Genes and Development, say the finding may give researchers another important mechanism with which to destroy cancer cells.
Craig Thompson and colleagues at the university's Abramson Family Cancer Research Institute bred mice to be deficient in two genes that help regulate death by apoptosis, p53, and BCL-2. In a series of experiments, the team proved that alkylating agents caused necrotic death in the tumor cells, according to the report.
The group also showed that providing another source of energy to both apoptotic-deficient tumor cells and tumors from wildtype apoptotic-competent mice prevented both groups of cells from dying, according to the article.
http://www.biomedcentral.com/news/20040517/01