Six bronchopulmonary carcinomas of various histological types (macrocellular, epidermoid) were electronmicroscopically studied on bronchial biopsy samples. The scarcity of intercellular junctions was observed in all of them, especially in carcinoma types or zones (i.e. of epidermoid carcinoma) less differentiated. Close and gap junctions, zonulae adherentes and maculae adherentes dominated the structure of poorly differentiated carcinomas, while the differentiated types also presented frequent desmosomes. Also the reduction of intercellular junctions frequency was accompanied by their ultrastructural aberrations. The ultrastructural changes observed were correlated to the capacity for invasion of investigated carcinomas without reducing this basic property of cancer cells to the former.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Linking altered neuronal and synaptic properties to nicotinic receptor Alpha5 subunit gene dysfunction: a translational investigation in rat mPFC and human cortical layer 6.
Transl Psychiatry
January 2025
Research Center Juelich, Institute of Neuroscience and Medicine 10, Research Center Juelich, Juelich, Germany.
Genetic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit of mice results in behavioral deficits linked to the prefrontal cortex (PFC). rs16969968 is the primary Single Nucleotide Polymorphism (SNP) in CHRNA5 strongly associated with nicotine dependence and schizophrenia in humans. We performed single cell-electrophysiology combined with morphological reconstructions on layer 6 (L6) excitatory neurons in the medial PFC (mPFC) of wild type (WT) rats, rats carrying the human coding polymorphism rs16969968 in Chrna5 and α5 knockout (KO) rats.
View Article and Find Full Text PDFTail Anchored protein insertion mediated by CAML and TRC40 links to neuromuscular function in mice.
PLoS Genet
January 2025
Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 1st St. SW, Rochester, Minnesota 55905, United States of America.
Motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) and progressive bulbar palsy, involve loss of muscle control resulting from death of motor neurons. Although the exact pathogenesis of these syndromes remains elusive, many are caused by genetically inherited mutations. Thus, it is valuable to identify additional genes that can impact motor neuron survival and function.
View Article and Find Full Text PDFControl of striatal circuit development by the chromatin regulator .
Sci Adv
January 2025
Department of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
The pathophysiology of neurodevelopmental disorders involves vulnerable neural populations, including striatal circuitry, and convergent molecular nodes, including chromatin regulation and synapse function. Despite this, how epigenetic regulation regulates striatal development is understudied. Recurrent de novo mutations in are associated with intellectual disability and autism.
View Article and Find Full Text PDFIon permeability profiles of renal paracellular channel-forming claudins.
Acta Physiol (Oxf)
February 2025
Clinical Physiology/Nutritional Medicine, Medical Department, Division of Gastroenterology, Infectiology, Rheumatology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Aim: Members of the claudin protein family are the major constituents of tight junction strands and determine the permeability properties of the paracellular pathway. In the kidney, each nephron segment expresses a distinct subset of claudins that form either barriers against paracellular solute transport or charge- and size-selective paracellular channels. It was the aim of the present study to determine and compare the permeation properties of these renal paracellular ion channel-forming claudins.
View Article and Find Full Text PDFE-Cadherin-Mediated Cell-Cell Adhesion and Invasive Lobular Breast Cancer.
Adv Exp Med Biol
January 2025
Cancer Research UK Scotland Centre (Edinburgh), Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK.
E-cadherin is a transmembrane protein and central component of adherens junctions (AJs). The extracellular domain of E-cadherin forms homotypic interactions with E-cadherin on adjacent cells, facilitating the formation of cell-cell adhesions, known as AJs, between neighbouring cells. The intracellular domain of E-cadherin interacts with α-, β- and p120-catenins, linking the AJs to the actin cytoskeleton.
View Article and Find Full Text PDFWant 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!