Nf2 gene inactivation in arachnoidal cells is rate-limiting for meningioma development in the mouse

التفاصيل البيبلوغرافية
العنوان: Nf2 gene inactivation in arachnoidal cells is rate-limiting for meningioma development in the mouse
المؤلفون: Michiko Niwa-Kawakita, Michel Kalamarides, Marco Giovannini, Hélène Leblois, David H. Gutmann, Vincent Abramowski, Gilles Thomas, Michel Perricaudet, Anne Janin
المصدر: Genes & Development. 16:1060-1065
بيانات النشر: Cold Spring Harbor Laboratory, 2002.
سنة النشر: 2002
مصطلحات موضوعية: congenital, hereditary, and neonatal diseases and abnormalities, Genetic Vectors, Biology, medicine.disease_cause, Adenoviridae, Lesion, Meningioma, Mice, Research Communication, Exon, Meningeal Neoplasms, otorhinolaryngologic diseases, Genetics, medicine, Animals, Gene silencing, Meningeal Neoplasm, Gene Silencing, Neurofibromatosis type 2, neoplasms, Neurofibromin 2, Homozygote, Neoplasms, Experimental, medicine.disease, Mice, Mutant Strains, nervous system diseases, Tumor progression, Immunology, Cancer research, Arachnoid, Tumor Suppressor Protein p53, medicine.symptom, Carcinogenesis, Developmental Biology
الوصف: Biallelic NF2 gene inactivation is common in sporadic and in neurofibromatosis type 2 (NF2)-related meningiomas. We show that, beginning at four months of age, thirty percent of mice with arachnoidal cell Cre-mediated excision of Nf2 exon 2 developed a range of meningioma subtypes histologically similar to the human tumors. Additional hemizygosity for p53 did not modify meningioma frequency or progression suggesting that Nf2 andp53 mutations do not synergize in meningeal tumorigenesis. This first mouse model initiated with a genetic lesion found in human meningiomas provides a powerful tool for investigating tumor progression and for the preclinical evaluation of therapeutic interventions.
تدمد: 1549-5477
0890-9369
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::13dc930e0a9859993a0dc896d27af59aTest
https://doi.org/10.1101/gad.226302Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....13dc930e0a9859993a0dc896d27af59a
قاعدة البيانات: OpenAIRE