Induction of medulloblastomas in p53-null mutant mice by somatic inactivation of Rb in the external granular layer cells of the cerebellum

Article Abstract:

A mouse model has been generated for medulloblastoma, one of the most common types of malignancies in children. Cre-LoxP-mediated inactivation of Rb and p53 tumor suppressor genes was carried out in the external granular layer (EGL) cells of the cerebellum. Loss of function of RB seems to be essential for medulloblastoma development in the mouse. It is hypothesized that medulloblastomas come from multipotent precursor cells in the EGL.

Nervous system, Cancer in children, Childhood cancer, Mice, mutant strains, Mutant mice, Astrocytes, Medulloblastoma, Brain diseases

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Schwann cell hyperplasia and tumors in transgenic mice expressing a naturally occurring mutant NF2 protein

Article Abstract:

Tumors and Schwann cell hyperplasia have been studied in transgenic mice that express a natural mutant NF2 protein. Certain mutations in some tumor suppressor genes such as p53 can act in a dominant way and whether or not the mechanism may apply also for the neurofibromatosis type-2 gene (NF2 (ital)) has been tested. When mutated, the gene leads to shwannoma development. Mice that express an NF2 protein with an interstitial deletion had high prevalence of Schwann cell-derived tumors and Schwann cell hyperplasia. Those that express a carboxy-terminally truncated protein were normal. Thus some of the mutant NF2 (ital) alleles in patients may encode products that have dominant properties when overexpressed in certain cell lineages.

United States, France, Genetically modified animals, Mutation (Biology), Mutation, Tumors, Tumor suppressor genes, Neurofibromatosis, Schwann cells

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Bmi-1 collaborates with c-Myc in tumorigenesis by inhibiting c-Myc-induced apoptosis via INK4a/ARF

Article Abstract:

Bmi-1 has been shown to collaborate with c-Myc in tumorigenesis through inhibiting c-Myc-induced apoptosis through INK4a/ARF. Regulation of the ink4a-ARF locus by Bmi-1 and whether it is behind the remarkable collaboration of Myc and Bmi-1 in tumorigenesis has been investigated. The hypothesis that relative levels of p16 and p19arf are vital for the tumor suppressive actions has been tested.

Statistical Data Included, Cell death, Bone marrow, Carcinogenesis

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