Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
MICE HETEROZYGOUS FOR A MUTATION AT THE NF2 TUMOR-SUPPRESSOR LOCUS DEVELOP A RANGE OF HIGHLY METASTATIC TUMORS
Autore:
MCCLATCHEY AI; SAOTOME I; MERCER K; CROWLEY D; GUSELLA JF; BRONSON RT; JACKS T;
Indirizzi:
MASSACHUSETTS GEN HOSP,CTR CANC CHARLESTOWN MA 02129 DEPT BIOL CAMBRIDGE MA 02139 MIT CAMBRIDGE MA 02139 TUFTS UNIV,SCH VET MED,DEPT PATHOL,USDA,HUMAN NUTR RES CTR AGING BOSTON MA 02111 MASSACHUSETTS GEN HOSP E,MOL NEUROGENET UNIT CHARLESTOWN MA 02129 HARVARD UNIV,SCH MED CHARLESTOWN MA 02129
Titolo Testata:
Genes & development
fascicolo: 8, volume: 12, anno: 1998,
pagine: 1121 - 1133
SICI:
0890-9369(1998)12:8<1121:MHFAMA>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSGENIC MICE; NEUROFIBROMATOSIS TYPE-2; GENE-PRODUCT; T-ANTIGEN; PROTEIN; MERLIN; EZRIN; MOESIN; CELLS; SCHWANNOMIN;
Keywords:
MERLIN; NF2; TUMOR SUPPRESSOR; CYTOSKELETON; OSTEOSARCOMA; METASTASIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
A.I. Mcclatchey et al., "MICE HETEROZYGOUS FOR A MUTATION AT THE NF2 TUMOR-SUPPRESSOR LOCUS DEVELOP A RANGE OF HIGHLY METASTATIC TUMORS", Genes & development, 12(8), 1998, pp. 1121-1133

Abstract

A role for the membrane/cytoskeleton interface in the development andprogression of cancer is established, yet poorly understood. The neurofibromatosis type II (NF2) turner suppressor gene encodes a member ofthe ezrin/radixin/moesin (ERM) family of membrane/cytoskeleton linkerproteins thought to be important for cell adhesion and motility. We report that in contrast to the narrow spectrum of benign tumors in human NF2 patients, Nf2 heterozygous mice develop a variety of malignant tumors. Using the fact that Nf2 is linked to the p53 tumor suppressor locus in the mouse we have also investigated the effects of genetic linkage of cancer-predisposing mutations on tumorigenesis and examined the genetic pathway to tumor formation involving Nf2 loss. Importantly, we observed a very high rate of metastasis associated with Nf2 deficiency, with or without loss of p53 function, and we provide experimentalevidence supporting a role for Nf2 loss in metastatic potential. Together, our results suggest an important role for the NF2 tumor suppressor, and perhaps the ERM family in tumor formation and metastasis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 10:04:06