Aim: Enormous attempts have been made to develop and establish markers that determines the susceptibility of potentially malignant tissues to transform to oral cancer. E - cadherin encoded by CDH1 gene is a protein which plays an important role in cellular adhesion. This study aimed to assess the relationship between the expression of E- cadherin and different grades of epithelial dysplasia in oral leukoplakia.
Materials And Methods: Tumour biopsies from fifty leukoplakia patients was collected. Half of the tissue was sent for histopathological examination and other half was subjected to see E - cadherin expression by real time PCR.
Results: On assessing, the expression of E - cadherin was found to be high in samples with mild dysplasia followed by samples with moderate dysplasia. Samples with severe dysplastic feature showed least expression of E - cadherin. All statistical analyses were performed using Statistical Package for Social science (SPSS) and was proven that there is significant decrease in the expression of E - cadherin as the degree of dysplasia increases with a p value 0.001 and confidence interval 95%.
Conclusion: We conclude that loss of E - cadherin can be used as a tumour marker that could determine the susceptibility of normal and potentially malignant tissues to transform into oral cancers. To generalise our results, further prospective studies with a large sample size using quantitative real time PCR to read the gene expression should be carried out at multi centre levels.
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http://dx.doi.org/10.31557/APJCP.2020.21.2.405 | DOI Listing |
World J Gastroenterol
January 2025
Department of General Surgery, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300052, China.
Background: Regulator of G protein signaling (RGS) proteins participate in tumor formation and metastasis by acting on the α-subunit of heterotrimeric G proteins. The specific effect of RGS, particularly , on the progression of gastric cancer (GC) is not yet clear.
Aim: To explore the role and underlying mechanisms of action of in GC development.
J Immunother Precis Oncol
February 2025
Sarah Cannon Research Institute (SCRI) at HealthONE, Denver, CO, USA.
The cadherin superfamily of proteins is critical for cell-cell interactions and demonstrates tissue-specific expression profiles. In cancers, disruption of cell-cell adhesion is frequently associated with oncogenesis and metastasis. As such, these proteins have been the targets of multiple attempts to develop novel therapeutics in malignancy.
View Article and Find Full Text PDFTransl Psychiatry
January 2025
Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
Anxiety disorder, a prevalent mental health issue, is one of the leading causes of disability worldwide. Damage to the blood-brain barrier (BBB) is implicated in anxiety, but its regulatory mechanisms remain unclear. Herein, we show that adrenomedullin 2 (ADM2), a novel angiogenic growth factor, alleviates autistic and anxiety-like behaviors in mice.
View Article and Find Full Text PDFThromb Haemost
January 2025
Hemostasis and Erythropathology Laboratory, Hematopathology, Pathology Department, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Background: V617F-mutated myeloproliferative neoplasms (MPN) exhibit abnormal proliferation of bone marrow progenitors and increased risk of thrombosis, specifically in splanchnic veins (SVT). The contribution of the endothelium to the development of the prothrombotic phenotype was explored.
Material And Methods: Plasma and serum samples from V617F MPN patients with (n=26) or without (n=7) thrombotic debut and different treatments, were obtained (n=33).
Eur J Pharmacol
January 2025
College of Korean Medicine, Gachon University, Seongnam, 13120, South Korea. Electronic address:
Obesity due to excessive body fat accumulation remains a global problem. Patients with obesity have high cortisol levels, and its dysregulation is caused by increased 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) levels. The effects and mechanism of J2H-1702, an 11β-HSD1 inhibitor, on nonalcoholic steatohepatitis (NASH) were explored.
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