Adjacent frozen sections of 102 consecutive female breast carcinomas were examined for the expression of the Ki-67 antibody-reactive proliferation-associated nuclear antigen and of estrogen and progesterone receptors with the use of monoclonal antibodies and peroxidase histochemistry. The results of steroid receptor stainings were semiquantitatively assessed (histoscore) on the basis of nuclear staining intensity and the percentage of positively stained carcinoma cell nuclei. Carcinomas negative for either receptor had significantly higher percentages of Ki-67-positive cells. The highest percentages of Ki-67-positive cells were observed in carcinomas negative for both estrogen and progesterone receptors. There was a highly significant decrease in receptor histoscores with increasing proliferative cell fractions as determined by Ki-67 positivity. No significant (progesterone receptor) or poor negative correlation (estrogen receptor) was observed when proliferative cell fractions were related to receptor concentrations from conventional steroid-binding assays. Immunoperoxidase staining for the Ki-67 antibody-defined proliferation antigen and steroid receptors in tissue sections provides a simple means to gain information of therapeutic and prognostic importance.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Targeting unique ligand binding domain structural features downregulates DKK1 in Y537S ESR1 mutant breast cancer cells.
Breast Cancer Res
January 2025
Department of Cancer Biology, Loyola University Chicago Stritch School of Medicine, Maywood, IL, 50153, USA.
Resistance to endocrine therapies remains a major clinical hurdle in breast cancer. Mutations to estrogen receptor alpha (ERα) arise after continued therapeutic pressure. Next generation selective estrogen receptor modulators and degraders/downregulators (SERMs and SERDs) show clinical efficacy, but responses are often non-durable.
View Article and Find Full Text PDFPrognostic value of adjuvant chemotherapy for hormone receptor-negative T1a and T1bN0M0 breast cancer patients.
Sci Rep
January 2025
Department of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi Province, China.
The benefit of adjuvant chemotherapy (CT) for hormone receptor-negative T1a and T1bN0M0 breast cancer remains uncertain. Our study was to explore prognostic value and identify candidates of adjuvant CT for these patients. The data of hormone receptor-negative T1a and T1bN0M0 breast cancer patients were extracted from the Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2015.
View Article and Find Full Text PDFNr4a1 and Nr4a3 redundantly control clonal deletion and contribute to an anergy-like transcriptome in auto-reactive thymocytes to impose tolerance in mice.
Nat Commun
January 2025
Division of Rheumatology, Rosalind Russell and Ephraim P. Engleman Arthritis Research Center, Department of Medicine, University of California, San Francisco, CA, 94143, USA.
The Nr4a nuclear hormone receptors are transcriptionally upregulated in response to antigen recognition by the T cell receptor (TCR) in the thymus and are implicated in clonal deletion, but the mechanisms by which they operate are not clear. Moreover, their role in central tolerance is obscured by redundancy among the Nr4a family members and by their reported functions in Treg generation and maintenance. Here we take advantage of competitive bone marrow chimeras and the OT-II/RIPmOVA model to show that Nr4a1 and Nr4a3 are essential for the upregulation of Bcl2l11/BIM and thymic clonal deletion by self-antigen.
View Article and Find Full Text PDFmiR-18a-5p/PXR/SREBP2 Was Involved in MAFLD Associated With Methyl Tert-Butyl Ether Among Petrol Station Workers.
Liver Int
February 2025
Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing, China.
Background: Metabolic associated fatty liver disease (MAFLD), previously defined as non-alcoholic fatty liver disease (NAFLD), has been shown to be closely related to many environmental pollutants. Lately, we found methyl tert-butyl ether (MTBE), a new environmental pollutant, could increase NAFLD risk in American adults, which still needs more population epidemiological studies to verify, and its pathogenic mechanism is not yet clear.
Methods: We conducted a cross-sectional study among petrol station workers, diagnosed their MAFLD according to internationally recognised diagnostic criteria, assessed the potential association of MTBE exposure with MAFLD risk, and explored the miR-18a-5p/PXR/SREBP2 pathway as possible pathogenic mechanisms in male Wistar rats and HepaRG cells treated with MTBE.
IL-8 promotes pyroptosis through ERK pathway and mediates glucocorticoid resistance in chronic rhinosinusitis with nasal polyps.
Inflamm Res
January 2025
Institute of Otolaryngology head and neck surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Objective: This study seeks to elucidate the role and molecular mechanisms of IL-8 in nasal epithelial cell pyroptosis and its impact on glucocorticoid (GC) resistance.
Methods: We assessed the expression of pyroptosis-related biomarkers and IL-8 in tissues and human nasal epithelial cells (hNECs) from both control and nasal polyp patients using western blot. Their localization was determined through immunohistochemistry and immunofluorescence.
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!