Objective: To measure association between endometrial carcinoma ER and PR status and endometrial cancer (EC) survival, accounting for inter-observer variation.
Methods: The intensity and proportion of tumor cell expression of ER and PR in ECs were assessed independently and semi-quantitatively by two pathologists using digital images of duplicate tumor tissue microarrays (TMAs). Cases with inconsistent initial assessment were reviewed and final scoring agreed. The association between overall and EC-specific survival and hormone receptor expression (intensity, proportion and combined) was assessed using Cox regression analysis. The C-index was used to evaluate model discrimination with addition of ER and PR status.
Results: Tumor ER and PR analysis was possible in 659 TMAs from 255 patients, and in 459 TMAs from 243 patients, respectively. Initial ER and PR scoring was consistent in 82% and 80% of cases, respectively. In multivariate analyses decreased ER and PR expression was associated with increased tumor-related mortality. Associations reached statistical significance for ER proportion score (P=0.05), ER intensity score (P=0.003), and PR combined score (P=0.04). Decreased expression of combined ER/PR expression was associated with poorer EC-specific survival than decreased expression of either hormone receptor alone (P=0.005). However, hormone receptor status did not significantly improve mortality prediction in individual cases.
Conclusion: ER and PR expression combined, using cut-points that capture variation in scoring and across cores, is significantly associated with EC-specific survival in analyses adjusting for known prognostic factors. However, at the individual level, ER and PR expression does not improve mortality prediction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.ygyno.2017.11.027 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.
Adv Sci (Weinh)
January 2025
Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, 02912, USA.
Pulmonary hypertension (PH) increases the mortality of preterm infants with bronchopulmonary dysplasia (BPD). There are no curative therapies for this disease. Lung endothelial carnitine palmitoyltransferase 1a (Cpt1a), the rate-limiting enzyme of the carnitine shuttle system, is reduced in a rodent model of BPD.
View Article and Find Full Text PDFEndothelial Rho kinase controls blood vessel integrity and angiogenesis.
bioRxiv
November 2024
Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Background: The Rho kinases 1 and 2 (ROCK1/2) are serine-threonine specific protein kinases that control actin cytoskeleton dynamics. They are expressed in all cells throughout the body, including cardiomyocytes, smooth muscle cells and endothelial cells, and intimately involved in cardiovascular health and disease. Pharmacological ROCK inhibition is beneficial in mouse models of hypertension, atherosclerosis, and neointimal thickening that display overactivated ROCK.
View Article and Find Full Text PDFUnlabelled: Focal adhesion kinase (FAK) functions as a signaling and scaffolding protein within endothelial cells (ECs) impacting blood vessel function and tumor growth. Interpretations of EC FAK-null phenotypes are complicated by related PYK2 (protein tyrosine kinase 2) expression, and to test this, we created PYK2 FAK mice with tamoxifen-inducible EC-specific Cre recombinase expression. At 11 weeks of age, EC FAK inactivation resulted in increased heart and lung mass and vascular leakage only on a PYK2 background.
View Article and Find Full Text PDFMTOR maintains endothelial cell integrity to limit lung vascular injury.
J Biol Chem
December 2024
Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. Electronic address:
The functional and structural integrity of the endothelium is essential for vascular homeostasis. Loss of barrier function in quiescent and migratory capacity in proliferative endothelium causes exuberant vascular permeability, a cardinal feature of many inflammatory diseases including acute lung injury (ALI). However, the signals governing these fundamental endothelial cell (EC) functions are poorly understood.
View Article and Find Full Text PDFEndothelial KLF11 is a novel protector against diabetic atherosclerosis.
Cardiovasc Diabetol
October 2024
Frankel Cardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Article Synopsis
- Atherosclerotic cardiovascular diseases are the top cause of death for diabetic patients, with dysfunctional endothelial cells being a key factor in their development, especially in diabetes.
- KLF11, a protein linked to diabetes, is found to play a protective role in vascular health, but its involvement in diabetic atherosclerosis was previously unknown.
- Research reveals that a lack of KLF11 worsens atherosclerosis in diabetic mice, while increased KLF11 levels help prevent it; this suggests that targeting KLF11 could lead to new treatments for cardiovascular issues in diabetes.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!