ArticleCancer research2010
Joint loss of PAX2 and PTEN expression in endometrial precancers and cancer.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Diagnostic accuracy of phosphatase and tensin homolog loss in differentiating between atypical endometrial hyperplasia/endometrioid intraepithelial neoplasia and non-atypical endometrial hyperplasia: A systematic review and meta-analysis.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026Pooled it
- Endometrioid Intraepithelial Neoplasia in the Secretory Phase: Morphologic and Biomarker Diagnostic Features in a Common, Overlooked Setting.The American journal of surgical pathology · 2026Article
- Metabolic Amplification in Endometrial Carcinogenesis: Biological Rationale and Translational Limits of Precision Chemoprevention.Biomedicines · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Immune Suppression and Somatic Mutation in Endometriosis - An Opportunity for Personalized Immunotherapy.International journal of women's health · 2026Article
- The dysregulation of the immune microenvironment during endometrial intraepithelial neoplasia serves as a marker of endometrial carcinogenesis.Frontiers in immunology · 2026Review
- Ovarian endometrioid adenofibroma in a perimenopausal woman with intermittent vaginal bleeding: a case report.Frontiers in reproductive health · 2026Article
- Residual disease volume and prognosis in endometrioid precancer after progestin therapy.Virchows Archiv : an international journal of pathology · 2025Article
- A distinct mechanism of epigenetic reprogramming silences PAX2 and initiates endometrial carcinogenesis.The Journal of clinical investigation · 2025Article
- PDS5B positively regulates PTEN by binding to YTHDC1 to inhibit the malignant progression of endometrial carcinoma.Discover oncology · 2025Article
- PAX2 induces endometrial cancer by inhibiting mitochondrial function via the CD133-AKT1 pathway.Molecular and cellular biochemistry · 2025Article
- Article
- Somatic PTEN and ARID1A loss and endometriosis disease burden: a longitudinal study.Human reproduction (Oxford, England) · 2025Article
- Immunocytochemical examination of Akt, mTOR, and Pax-2 for endometrial carcinoma through thin-layer endometrial cytology.Frontiers in medicine · 2025Article
- Review
- Use of clinicopathological factors to predict prognosis of fertility-sparing treatment for endometrial endometrioid carcinoma and atypical hyperplasia.Oncology letters · 2023Article
- Endometrial polyps are non-neoplastic but harbor epithelial mutations in endometrial cancer drivers at low allelic frequencies.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- Article
- Histopathologic diagnosis of endometrial precancers: Updates and future directions.Seminars in diagnostic pathology · 2022Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Latent endometrial carcinoma precancers are normal-appearing endometrial glands with sporadic loss of tumor suppressor gene function such as PTEN. Progression to carcinoma is inefficient and requires additional genetic damage that creates a histologic precursor lesion called endometrial intraepithelial neoplasia (EIN). In this study, we examined loss of PAX2 expression, a gene required for embryonic uterine development, during endometrial carcinogenesis. Normal proliferative, EIN, and malignant (endometrial adenocarcinoma) endometrial tissues were immunostained for PTEN and PAX2. Proliferative samples with loss of protein in at least one gland were scored as latent precancers. EIN and cancer lesions were scored by the majority pattern. Overall prevalence and topography of joint PAX2-PTEN expression loss was examined. The prevalence of PAX2 protein loss in the sequence of normal to precancer to cancer was 36%, 71%, and 77%, respectively, and for PTEN, it was 49%, 44%, and 68%, respectively. The normal endometrial prevalence of PAX2- or PTEN-deficient latent precancers was unaffected by biopsy indication, but increased significantly with age. Coincident loss of PAX2 and PTEN expression in an individual normal endometrium was seen in 21% of patients, but usually involved different glands. Coincident loss was more common in precancers (31%) and carcinoma (55%), in which case, both markers were protein null in an overlapping clonal distribution. PAX2 and PTEN protein loss occurs independently and accumulates with increasing age in latent precancers of normal premenopausal endometrium. Loss of function of both genes in an overlapping distribution characterizes the clinical emergence of a premalignant lesion which is carried forward to carcinoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.