Precancerous lesions of the endometrium

Beutler, Herbert K.; Dockerty, Malcolm B.; Randall, Lawrence M.

doi:10.1016/0002-9378(63)90167-4

Cited by 49 publications

(10 citation statements)

References 13 publications

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“…Factors strongly associated with endometrioid endometrial cancer such as obesity, polycystic ovarian syndrome (PCOS), nulliparity and unopposed use of estrogen are also associated with endometrial hyperplasia (4,5). After years of research focused on endometrial hyperplasia, two facts became obvious; endometrial hyperplasia is a heterogeneous entity varying in its extent of glandular crowding, architectural disorganization and nuclear atypia (6)(7)(8), furthermore, the associated risk of endometrial cancer varies in accordance with the degree of complexity and atypia (9,10).…”

Section: Endometrial Hyperplasiamentioning

confidence: 99%

Mouse models of uterine corpus tumors clinical significance and utility

et al. 2010

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Uterine tumors, whether benign or malignant, are diagnosed in a significant portion of women and are associated with a number of co-morbidities that negatively impact quality of life. Uterine tumors can be derived from the epithelial (endometrial hyperplasia or carcinoma) and mesenchymal (leiomyoma, sarcoma) layers of the uterus. The exact etiologies of the various tumor types are yet to be defined. Collectively their development and progression often results from aberrant steroid hormone exposure or dysregulation of related growth factor signaling and apoptotic pathways, reflecting the role of steroid hormone-dependent signaling and survival pathways in the cycles of cell growth and involution that characterize normal uterine physiology. While molecular analyses of human tumors can identify candidate genetic and epigenetic lesions contributing to uterine tumor initiation and progression, in vivo genetic models are needed to establish the functional significance of such lesions and their contribution to tumorigenesis. For this purpose, genetically-engineered mouse models have proven valuable. Here we review genetically-modified mouse models that develop uterine tumors and compare their pathology, utility/feasibility, and discuss their clinical relevance.

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Section: Endometrial Hyperplasiamentioning

confidence: 99%

Mouse models of uterine corpus tumors clinical significance and utility

et al. 2010

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“…1-10 , 8, 11-14 The World Health Organization (WHO) classification categorizes lesions into hyperplasia without atypia (simple or complex) and hyperplasia with atypia (simple or complex) based on the degree of architectural crowding and complexity and the presence of cytologic atypia. 15 Atypical hyperplasia has the highest risk of progression to or concurrent endometrial carcinoma but unfortunately is also the category with the highest diagnostic disagreement.…”

Section: Introductionmentioning

confidence: 99%

PAX2 Loss by Immunohistochemistry Occurs Early and Often in Endometrial Hyperplasia

Allison

Upson

Reed

et al. 2012

International Journal of Gynecological Pathology

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Background Immunohistochemical markers to assist in the diagnosis and classification of hyperplastic endometrial epithelial proliferations would be of diagnostic use. Methods To examine the possible utility of PAX2 as a marker of hyperplastic endometrium, cases of normal endometrium, simple and complex hyperplasia without atypia, atypical hyperplasia and FIGO grade 1 endometrioid carcinomas were stained for PAX2. Results 206 endometrial samples were available for interpretation of PAX2 staining. The percent of cases with complete PAX2 loss (0% of cells staining) increased with increasing severity of hyperplasia: 0% of normal proliferative and secretory endometrium (n=28), 17.4% of simple hyperplasia (n=23), 59.0% of complex hyperplasia (n=83), 74.1% of atypical hyperplasia (n=54) and 73.3% of FIGO grade 1 endometrioid cancers (n=15). Partial loss of PAX2 expression did occur in normal endometrium (17.9%) but occurred in smaller proportions of tissue and was less frequent than in simple hyperplasia (47.8% with partial loss), complex hyperplasia (32.5%), atypical hyperplasia (22.2%) and FIGO grade 1 carcinomas (20.0%). Uniform PAX2 expression was rare in complex (8.4%) and atypical hyperplasia (3.7%) and carcinoma (6.7%). When evaluating loss of PAX2 in histologically normal endometrium adjacent to lesional endometrium in a given case, statistically significant differences in staining were observed for simple hyperplasia (p=0.011), complex hyperplasia (p< 0.001), atypical hyperplasia (p<0.001) and FIGO grade 1 endometrioid cancer (p=0.003). Conclusion In summary, PAX2 loss appears to occur early in the development of endometrial pre-cancers and may prove useful in some settings as a diagnostic marker in determining normal endometrium from complex and atypical hyperplasia and low grade carcinomas. However, it is not useful in distinguishing between these diagnostic categories.

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“…They studied endometrial tissue samples obtained prior to the diagnosis of endometrial carcinoma and found no abnormal change at more than 15 years before diagnosis, cystic hyperplasia at 6 to 13 years before diagnosis, and adenomatous hyperplasia or anaplastic change at 3 to 5 years before diagnosis. Speert ( 9 ) , Beutler ( 10 ) , and Gambrella ( 11 ) found endometrial hyperplasia in 33.9 to 84.6% of patients more than 1 year before a diagnosis of endometrial carcinoma. Kurman et al ( 2 ) reported that progression to carcinoma occurred in 1.1% of patients with simple hyper‐ plasia, in 3.4% with complex hyperplasia, in 7.7% with atypical simple hyperplasia, and in 28.6% with atypical complex hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

Differential diagnosis between normal endometrium and endometrial hyperplasia with immunostaining cytology using anti-LeY monoclonal antibody

Arai

Nishida

2003

Int J Gynecol Cancer

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We have previously reported that both endometrial cancer and endometrial hyperplasia stain positively for the anti-LeY monoclonal antibody, whereas normal endometrium does not. Endometrial hyperplasia is a premalignant change associated with the eventual development of endometrial carcinoma. However, it can be difficult to differentiate hyperplasia from normal endometrium in cytology. This study illustrates the use of immunocytochemical cytology using anti-LeY monoclonal antibody to differentiate between endometrial hyperplasia and normal endometrium. Immunostaining using anti-LeY monoclonal antibody was performed on cytologic specimens obtained from 17 normal endometria, 25 endometria with endometrial hyperplasia, and 13 endometria with endometrial carcinoma. All normal endometria displayed negative staining for anti-LeY monoclonal antibody, whereas all endometria with endometrial carcinoma displayed positive staining. Of the endometrial hyperplasia cases, 21 displayed positive staining. However, four displayed negative staining due to the small number of cells available for diagnosis. We believe that immunostaining cytology using anti-LeY monoclonal antibody is a useful method for differentiating between normal endometrium and endometrial hyperplasia.

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Precancerous lesions of the endometrium

Cited by 49 publications

References 13 publications

Mouse models of uterine corpus tumors clinical significance and utility

Mouse models of uterine corpus tumors clinical significance and utility

PAX2 Loss by Immunohistochemistry Occurs Early and Often in Endometrial Hyperplasia

Differential diagnosis between normal endometrium and endometrial hyperplasia with immunostaining cytology using anti-LeY monoclonal antibody

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