Glioma is the most common malignant neoplasm of the central nervous system. Because FPR, which was believed to be mainly involved in proinflammatory and antibacterial responses, was discovered to be expressed by some glioma cells, Ji Ming Wang, M.D., Ph.D., of the National Cancer Institute, and colleagues investigated the relationship between FPR and the biologic behavior of glioma cells.
They found that highly malignant human glioblastoma cell lines, grade IV glioblastoma multiforme, and grade III anaplastic astrocytomas express FPR. Inhibiting FPR with its short interfering RNA substantially reduced tumorigenicity of glioblastoma cells injected into nude mice. The authors conclude that FPR may mediate cell movement and growth and angiogenesis of malignant human gliomas.
Contact: National Cancer Institute Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov
Lack of NM23 Gene Expression Contributes to Metastasis in Mouse Model of Cancer
Lack of expression of the mouse equivalent of the human gene NM23 promotes metastasis in a mouse model of liver cancer, according to a new study.
The NM23 gene is thought to suppress the metastatic spread of solid tumors. Marie-Lise Lacombe, Ph.D., of INSERM in Paris, and colleagues used transgenic mice that lacked the mouse NM23-M1 gene (the mouse equivalent of NM23) in two mouse models of liver cancer to examine the role of NM23 in hepatic tumor development and metastatic dissemination.
They found that in both models, the NM23 protein was overexpressed in the primary liver tumors of mice that had the NM23-M1 gene compared with non-tumor liver tissue. Howe
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Contact: Sarah L. Zielinski
jncimedia@oupjournals.org
301-841-1287
Journal of the National Cancer Institute
31-May-2005