Clinicopathological and molecular characterization of XXXX .

@entity1 @entity6756 @entity2355 @entity5344 @entity984 @entity5 @entity2225 @entity406 @entity189 @entity4311 @entity876 @entity982 @entity10580 @entity5822 @entity14 @entity3 @entity817 @entity420 @entity4638
Invasive @entity189 is associated with frequent lymph node @entity3 and adverse clinical outcome. Initially described as a variant of @entity5344 , it has subsequently been found in other organs, most recently the colon. Reports of @entity14 to date are limited in number, and their molecular profile has not been established. The aims of the present study were to analyze their clinicopathological features and molecular profile, and compare them with those of conventional @entity420 . Clinicopathological features of a cohort of 379 @entity1 with primary @entity14 were retrospectively reviewed for the presence of the pattern characteristic of @entity189 . We also assessed the expression of @entity5822 , @entity2225 , @entity10580 , @entity2355 (EMA, clone E29), @entity2355 (clone MA695), @entity6756 , @entity4311 , @entity4638 and @entity876 by immunohistochemistry. Genetic assessments of microsatellite instability, chromosomes 17p and 18q, and mutations in @entity876 , @entity817 and @entity984 were performed using DNA extracted from @entity406 -fixed, @entity982 -embedded sections. In all, 60 of the reviewed cases (16%) had a micropapillary component that ranged from 5 to 95% of the @entity5 , characterized by a higher frequency of an infiltrative pattern, lymphovascular and perineural invasion, a higher depth of invasion and more positive lymph nodes than conventional @entity420 . Immunohistochemistry for @entity2355 (clone MA695) and @entity2355 (EMA, clone E29) enhanced the characteristic inside-out staining pattern of the @entity189 component, whereas the rest of the @entity5 showed luminal staining patterns. @entity5822 expression was slightly increased in @entity189 , but did not reach significance (17-3%, P=0.1967). The molecular parameters showed a higher frequency of @entity876 alterations and a low incidence of microsatellite instability and RER phenotype (loss of mismatch repair protein) in @entity189 . With regard to the histological parameters, @entity189 appears to be more aggressive than conventional @entity14 . The molecular profile supports the hypothesis that @entity189 carcinogenesis develops through the classical chromosomal instability pathway.
