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- Title
ARID1A Loss of Expression in Complex Atypical Hyperplasia and Grade 1 Endometrioid Carcinoma of the Endometrium.
- Authors
Hijazi, Nouf; Almadani, Noorah; Gilks, C. Blake; Huntsman, David G.
- Abstract
ARID1A is a tumor suppressor gene that encodes the BAF250a protein, implicated in various chromatin remodeling processes, and is lost, through mutation, in many gynecological cancers. ARID1A mutation typically results in loss of expression of BAF250a protein encoded by the ARID1A gene. We studied BAF250a expression in 68 cases, consisting of 18 cases of complex atypical hyperplasia (CAH), 13 cases of grade 1 endometrioid adenocarcinoma of the endometrium (Endo Ca), 31 cases of CAH coexisting with Endo Ca, 3 cases of proliferative endometrium and 3 cases of secretory endometrium in an attempt to determine the timing of ARID1A mutation/loss of BAF250a expression during endometrial carcinoma development. Immunostaining for BAF250a protein was performed on whole tissue sections and assessed based on the presence or absence of nuclear staining. In the CAH group, ARID1A staining was retained in 14 cases (78%) with focal loss in 3 cases (17%) and complete loss in 1 case (5%). Of the 13 Endo Ca cases, 6 retained ARID1A expression (46%), five showed focal loss (38%) and two exhibited complete loss of expression (15%). In the group of 31 cases with coexisting CAH and Endo Ca, 6 CAH (19%) and 5 Endo Ca (16%) demonstrated loss of expression, manifesting as either focal or complete loss. Focal loss of expression was manifested as areas within the CAH or Endo Ca showing loss of expression in all epithelial cells within the contiguous area of loss (so-called clonal pattern of loss). Loss of ARID1A expression occurs in endometrial premalignant lesions, i.e. complex atypical hyperplasia, albeit at a low frequency (10/49 cases, 20%) with more frequent loss seen in low-grade Endo Ca (23/44 cases, 52%, p=0.002). ARID1A expression can be lost as an early event in endometrial carcinogenesis, at the premalignant phase (CAH) or later, during progression to endometrial carcinoma.
- Subjects
TUMOR suppressor genes; HYPERPLASIA; ENDOMETRIAL cancer; GENE expression; GENETIC mutation; CANCER invasiveness; CARCINOGENESIS; IMMUNOSTAINING; GENETICS
- Publication
Canadian Journal of Pathology, 2015, Vol 7, Issue 3, p23
- ISSN
1918-915X
- Publication type
Article