Identification of a basal/reserve cell immunophenotype in benign and neoplastic endometrium: a study with the p53 homologue p63.
BACKGROUND
Metaplastic differentiation, including squamous, mucinous, and tubal (ciliated), is common in both benign and neoplastic endometrium, and the cell of origin for this pathway is poorly understood. In this study, expression of a marker for basal and reserve cells in cervical squamous mucosa, designated p63, was investigated in a spectrum of endometrial alterations.


METHODS
One hundred ninety different endometria from 132 patients were examined, including fetal (6), premenarchal (3), benign cyclic (29) and noncyclic (54), hyperplastic (14), and neoplastic (93) endometrial glandular epithelia. The latter included conventional endometrioid carcinomas with and without mucinous, ciliated, and squamous metaplasia, and uterine papillary serous carcinoma (UPSC).


RESULTS
p63 expression was identified in basal/subcolumnar cells in the fetal endometrium in a distribution similar to that in basal/reserve cells of the cervix. Staining was confined to individual scattered basal and suprabasal cells in cycling endometrium. In polyps and postmenopausal endometria, focal clusters of p63-positive cells were identified in inactive glands or surface epithelium. Metaplastic (squamous or mucinous) epithelia, either alone or in conjunction with hyperplasias or carcinomas, exhibited the most intense staining, primarily in basal or subcolumnar cells. In some cases, immediately adjacent nonmetaplastic columnar epithelium also stained positive. UPSCs contained only rare scattered p63-positive cells.


CONCLUSIONS
Cells with a basal or reserve cell phenotype exist in the endometrium during fetal life, are not conspicuous during the reproductive years, but may emerge during shifts in differentiation. Whether these cells signify specialized multipotential endometrial cells is not clear, but the similarity of these cells to basal/reserve cells of the cervix and their association with neoplasia merit further study.
O'Connell
J T
JT
Division of Women's and Perinatal Pathology, Boston, Massachusetts 02115, USA.
Mutter
G L
GL
Cviko
A
A
Nucci
M
M
Quade
B J
BJ
Kozakewich
H P
HP
Neffen
E
E
Sun
D
D
Yang
A
A
McKeon
F D
FD
Crum
C P
CP
D000818:Animals; D014408:Biomarkers, Tumor / Q000096:biosynthesis; D002454:Cell Differentiation / Q000502:physiology; D004268:DNA-Binding Proteins; D016889:Endometrial Neoplasms / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D004717:Endometrium / Q000166:cytology* / Q000196:embryology / Q000502:physiology; D004847:Epithelial Cells / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D005260:Female; D016147:Genes, Tumor Suppressor; D006801:Humans; D016130:Immunophenotyping; D053547:Keratin-14; D007633:Keratins / Q000096:biosynthesis; D008565:Membrane Proteins; D008597:Menstrual Cycle / Q000502:physiology; D008679:Metaplasia / Q000276:immunology / Q000473:pathology; D051379:Mice; D010750:Phosphoproteins / Q000096:biosynthesis*; D015534:Trans-Activators; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins
D014408:Biomarkers, Tumor; C081876:CKAP4 protein, human; D004268:DNA-Binding Proteins; C507540:KRT14 protein, human; D053547:Keratin-14; C507446:Krt14 protein, mouse; D008565:Membrane Proteins; D010750:Phosphoproteins; C115051:TP63 protein, human; D015534:Trans-Activators; D014157:Transcription Factors; C486419:Trp63 protein, mouse; D025521:Tumor Suppressor Proteins; D007633:Keratins