Somatic mutations of the RET proto-oncogene are not required for tumor development in multiple endocrine neoplasia type 2 (MEN 2) gene carriers.
Cancer Res
; 56(21): 4853-5, 1996 Nov 01.
Article
in En
| MEDLINE
| ID: mdl-8895732
ABSTRACT
Germ line mutations in one allele of the RET proto-oncogene predispose to the multiple endocrine neoplasia type 2 (MEN 2) syndromes. To investigate whether these inherited mutations alone can cause the development of tumors in vivo (oncogene model) or whether somatic mutations in the homologous RET allele are required for tumorigenesis (tumor suppressor gene model), we analyzed the entire coding region of both alleles of the RET gene in two MEN 2A and two MEN 2B tumors by reverse transcription-PCR and direct sequencing. No tumor-specific mutations could be detected in either allele of the RET gene in these tumors. Unlike the molecular mechanism in other hereditary tumor syndromes, somatic mutations in the homologous allele are apparently not required in MEN 2 tumorigenesis. Thus, RET genes with MEN 2-specific germ line mutations act as dominantly transforming oncogenes in vivo.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Proto-Oncogenes
/
Proto-Oncogene Proteins
/
Receptor Protein-Tyrosine Kinases
/
Multiple Endocrine Neoplasia Type 2a
/
Drosophila Proteins
/
Heterozygote
/
Mutation
Limits:
Humans
/
Male
Language:
En
Journal:
Cancer Res
Year:
1996
Document type:
Article
Affiliation country:
Netherlands