In:
Histopathology, Wiley, Vol. 66, No. 4 ( 2015-03), p. 517-528
Abstract:
To understand the role of and differences in molecular alterations between endometrial and ovarian endometrioid adenocarcinomas. Methods and results We investigated the microsatellite status of 26 ovarian endometrioid adenocarcinomas ( OVEM s), 42 endometrial endometrioid adenocarcinomas ( EMCA s), and 19 concurrent (endometrial and ovarian) endometrioid adenocarcinomas. We evaluated the expression of the mismatch repair proteins, PTEN and ARID 1A, and mutations of PTEN , KRAS , CTNNB 1 , and PIK 3 CA . High levels of microsatellite instability ( MSI ‐H) were present in one of 26 OVEM s, 12 of 42 EMCA s, and four of 19 concurrent endometrioid adenocarcinomas. Only four of 19 concurrent endometrioid adenocarcinomas showed identical molecular alterations in their endometrial and ovarian components. Loss of ARID 1A or loss of PTEN expression, and MSI ‐H, were more common in EMCA s than OVEM s ( P = 0.044, P = 0.004, and P = 0.012, respectively). MSI ‐H in endometrial endometrioid adenocarcinomas was also related to loss of ARID 1A expression ( P 〈 0.001). In the cohort of MSI ‐H endometrioid adenocarcinomas involving the endometrium ( n = 16), MSH 6‐deficient cases showed higher frequencies of CTNNB 1 and PIK 3 CA mutations ( P = 0.008 and P = 0.036, respectively), but lower frequencies of KRAS mutation ( P = 0.011), than PMS 2‐deficient cases. Conclusions The different frequencies of molecular genetic alterations between endometrial endometrioid adenocarcinomas and ovarian endometrioid adenocarcinomas imply that distinct processes may be involved in their tumorigenesis or tumour progression.
Type of Medium:
Online Resource
ISSN:
0309-0167
,
1365-2559
DOI:
10.1111/his.2015.66.issue-4
Language:
English
Publisher:
Wiley
Publication Date:
2015
detail.hit.zdb_id:
2006447-0
