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Objective: To investigate the effect of experimentally created occlusal disorders (ECOD) on the expression of estrogen in rat condylar cartilage.
Methods: The model of ECOD was created by moving right upper and left lower first molars anteriorly. The animals in ECOD were sacrificed at 2, 4, 6, 8 weeks later. In removed occlusal disorders group, the moved first molars were extracted at 6 weeks later, and the animals were sacrificed 2 weeks later. The expression of estrogen was detected by SABC technique of immunocytochemistry, and then was analyzed by the density of estrogen-positive chondrocytes.
Results: 1) Estrogen was abundant in mature layer and hypertrophic layer of rat mandibular condylar cartilage. 2) In control group, the expression of estrogen decreased gradually from 6-week-old to 16-week-old. 3) In both childhood and puberty rats, the expression of estrogen in experiment group was significantly higher at 2 weeks after treatment, while no difference was found at 4, 6, 8 weeks after treatment. However, the expression in removed occlusal disorder group was higher than that in control group and 8 weeks of ECOD group.
Conclusion: In rat condylar cartilage, the expression of estrogen de-creases with age. Induced by ECOD, the expression of estrogen increases in early stage of remodelling activity.
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Breast J
September 2025
University of Hawai'i Cancer Center, Honolulu, Hawaii, USA.
The Oncotype DX test is standardly used for patients with early-stage, hormone-receptor-positive, HER2-negative breast cancers to determine the benefit from chemotherapy and the likelihood of distant recurrence. The relationship between Oncotype DX recurrence scores and race/ethnicity is still being studied. This retrospective study aims to evaluate the relationship between Oncotype DX recurrence scores, race/ethnicity, and clinicopathological factors and to support the applicability of the Oncotype DX test for a diverse breast cancer population of Hawaii.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
September 2025
Guangxi Key Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin, China.
Endometrial cancer (EC) is one of the most common gynecological cancers in developed countries. Like EC, most female reproductive tract malignancies are thought to be hormonally driven, with estrogen signaling acting as an oncogenic signal. The actions of estrogen are mediated through the classical nuclear estrogen receptors α (ER-α) and β (ER-β) as well as transmembrane G protein-coupled estrogen receptors (GPR30 and GPER).
View Article and Find Full Text PDFJ Appl Toxicol
September 2025
School of Public Health, Key Laboratory of Special Environmental and Health Research, Xinjiang Medical University, Urumqi, China.
Humans' exposure to arsenic (As) has been associated with the development of various diseases. Some health effects may be mediated by arsenic-induced toxicity to the thyroid and endocrine systems, but its underlying mechanisms remain unclear. The overall aim of our study was focused on using sodium arsenite (NaAsO)-exposed rats to investigate the involvement of the phosphatidylinositol 3-kinase (PI3K) and transcription factor NF-E2-related factor 2 (Nrf2) pathways in toxicity to the thyroid and endocrine systems.
View Article and Find Full Text PDFJ Pathol
September 2025
Sidney Kimmel Comprehensive Cancer Center and Department of Oncology, Johns Hopkins University, Baltimore, MD, USA.
Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR), and HER2, and remains one of the most aggressive and therapeutically challenging breast cancer subtypes, marked by early relapse, metastasis, and limited targeted treatment options. In a recent study published in The Journal of Pathology, Kuo et al provide compelling evidence that nicotine exposure, whether from tobacco smoke or e-cigarette vapor, drives TNBC progression by promoting stem-like and metastatic phenotypes. Integrating clinical datasets, patient tissues, cell lines, and in vivo models, the authors demonstrate that nicotine enhances tumor aggressiveness via coordinated upregulation of CHRNA9 and IGF1R.
View Article and Find Full Text PDFCancer Pathog Ther
September 2025
Department of Biotechnology, Motilal Nehru National Institute of Technology, Allahabad 211004, India.
Background: Colorectal cancer (CRC) is a complex, heterogeneous disease characterized by frequent relapses and metastasis. Previous studies have reported that the invasion and progression of CRC in several cases can be controlled by targeting fusion genes. This study aimed to screen for potent fusion transcripts as potential molecular biomarkers and therapeutic targets for metastatic CRC (mCRC) using an approach.
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