Role of XXXX and @entity817 gene mutations in mucinous @entity43 .

@entity1 @entity43 @entity984 @entity5 @entity817
OBJECTIVES: The goals of this study were to perform a comprehensive assessment of the prevalence of @entity984 oncogene mutations in @entity43 of various histologic subtypes, and for any subgroup(s) in which @entity984 mutation was found to be common, to address the hypothesis that those @entity5 without @entity984 mutation had sustained alternative activation of this signaling pathway through mutation of the @entity817 oncogene. METHODS: A total of 104 primary, @entity43 from a 10-year period at this institution were selected for study based on histologic classification. The histologic cell type was serous in 21 cases, endometrioid in 30 cases, clear cell in 31 cases, and mucinous in 22 cases. Additional clinical and pathological information was abstracted from @entity1 records, and pathology review was performed for all cases. Direct sequence analysis of exon 2 of the @entity984 gene, containing codon 12, was performed using DNA isolated from all @entity5 specimens. Sequence analyses of exons 11 and 15 of the @entity817 gene were performed for the 22 cases of mucinous @entity43 . RESULTS: Activating @entity984 mutations were more common in @entity5 (50%) than in all other histologic types combined (5%; P < 10(-7)). Mutation of @entity984 was more common in @entity5 than in advanced stage @entity5 (P = 0.0004). Of the 11 @entity5 with @entity984 mutations, 6 were of Mullerian (endocervical) type and 5 were of gastrointestinal type. No @entity5 was found to harbor a @entity817 mutation. CONCLUSIONS: These data indicate that @entity984 oncogene mutations exist in several histologic types of @entity43 , especially @entity5 , but are common only in @entity5 of mucinous histology. Mutations are equally prevalent in mucinous @entity43 of M  llerian and gastrointestinal types. In contrast to other solid @entity5 types frequently affected by @entity984 mutation, mucinous @entity43 without a @entity984 mutation have not sustained alternative activation of this signaling pathway through mutation of the @entity817 oncogene.
