Literature DB >> 9891919

Altered gap and tight junctions in human thyroid oncocytic tumors: a study of 8 cases by freeze-fracture.

B Cochand-Priollet1, D Raison, V Molinie, P J Guillausseau, M Wassef, C Bouchaud.   

Abstract

Human oncocytic tumors of the thyroid gland may be either adenomas or carcinomas. The morphology and the ultrastructure of these oncocytes are well-known. Numerous studies have demonstrated the role of gap and tight junctions in experimental and human carcinogenesis; however, the junctional complexes of the oncocytic tumors have never been studied. The aim of this study is to analyze gap and tight junctions in the oncocytic tumors of the thyroid. Because they are morphologically similar, whether benign or malignant, they offer an attractive model for studying the junctional complexes in both benign and malignant lesions. Eight oncocytic human thyroid tumors were collected and studied by freeze-fracture. Four of these cases were benign and four were malignant. Four cases of normal gland were also studied to represent the control group. Normal tight and gap junctions were described for the control group. No gap junctions could be found for the oncocytic tumors. Furthermore, alterations of the tight junctions were described; especially focal tights in the oncocytic adenomas and well organized and labyrinthic tight junctions in the oncocytic carcinomas. The lack of gap junction in the benign as well as in the malignant oncocytomas may suggest that the absence of gap junction is not sufficient for malignancy. The alterations of the tight junctions found in the oncocytic tumors of the thyroid are similar to those observed in poorly differentiated tissues or tumors, and may suggest a cellular regression rather than a tumorogenic factor.

Entities:  

Mesh:

Year:  1998        PMID: 9891919     DOI: 10.3109/01913129809032276

Source DB:  PubMed          Journal:  Ultrastruct Pathol        ISSN: 0191-3123            Impact factor:   1.094


  5 in total

1.  Viral oncoprotein-induced mislocalization of select PDZ proteins disrupts tight junctions and causes polarity defects in epithelial cells.

Authors:  Isabel J Latorre; Michael H Roh; Kristopher K Frese; Robert S Weiss; Ben Margolis; Ronald T Javier
Journal:  J Cell Sci       Date:  2005-09-01       Impact factor: 5.285

Review 2.  Emerging theme: cellular PDZ proteins as common targets of pathogenic viruses.

Authors:  Ronald T Javier; Andrew P Rice
Journal:  J Virol       Date:  2011-07-20       Impact factor: 5.103

Review 3.  Cell polarity proteins: common targets for tumorigenic human viruses.

Authors:  R T Javier
Journal:  Oncogene       Date:  2008-11-24       Impact factor: 9.867

4.  The human adenovirus E4-ORF1 protein subverts discs large 1 to mediate membrane recruitment and dysregulation of phosphatidylinositol 3-kinase.

Authors:  Kathleen Kong; Manish Kumar; Midori Taruishi; Ronald T Javier
Journal:  PLoS Pathog       Date:  2014-05-01       Impact factor: 6.823

Review 5.  Tight junctions and the modulation of barrier function in disease.

Authors:  Carola Förster
Journal:  Histochem Cell Biol       Date:  2008-04-16       Impact factor: 4.304

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.