Expression of cell adhesion molecules alpha-2, alpha-5 and alpha-6 integrin, E-cadherin, N-CAM and CD-44 in renal cell carcinomas

1993 ◽  
Vol 422 (3) ◽  
pp. 219-224 ◽  
Author(s):  
Hans-Joachim Terpe ◽  
Kian Tajrobehkar ◽  
Ursula Günthert ◽  
Michael Altmannsberger
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Renal Cell ◽  
Cell Adhesion Molecules ◽  
Renal Cell Carcinomas ◽  
E Cadherin

scholarly journals Differences in E-Cadherin and Syndecan-1 Expression in Different Types of Ameloblastomas

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ramón G. Carreón-Burciaga ◽  
Rogelio González-González ◽  
Nelly Molina-Frechero ◽  
Sandra López-Verdín ◽  
Vanesa Pereira-Prado ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Tumor Size ◽  
Cell Adhesion Molecules ◽  
Strong Association ◽  
Tumor Aggressiveness ◽  
Future Studies ◽  
Unicystic Ameloblastoma ◽  
Different Types ◽  
E Cadherin

Ameloblastomas are a group of benign, locally aggressive, recurrent tumors characterized by their slow and infiltrative growth. E-Cadherin and syndecan-1 are cell adhesion molecules related to the behavior of various tumors, including ameloblastomas. Ninety-nine ameloblastoma samples were studied; the expression of E-cadherin and syndecan-1 were evaluated by immunohistochemistry. E-Cadherin and epithelial syndecan-1 were more highly expressed in intraluminal/luminal unicystic ameloblastoma than in mural unicystic ameloblastoma and solid/multicystic ameloblastoma, whereas the stromal expression of syndecan-1 was higher in mural unicystic ameloblastoma and solid/multicystic ameloblastoma. Synchronicity was observed between E-cadherin and epithelial syndecan-1; the expression was correlated with intensity in all cases. There was a strong association between expression and tumor size and recurrence. The evaluation of the expression of E-cadherin and syndecan-1 are important for determining the potential aggressiveness of ameloblastoma variants. Future studies are required to understand how the expression of these markers is related to tumor aggressiveness.

scholarly journals Ultrastructural localization of E-cadherin cell adhesion molecule on the cytoplasmic membrane of keratinocytes in vivo and in vitro.

1994 ◽  
Vol 42 (10) ◽  
pp. 1333-1340 ◽  
Author(s):  
Y Horiguchi ◽  
F Furukawa ◽  
M Fujita ◽  
S Imamura
Keyword(s):  
Cell Adhesion ◽  
Free Surface ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Cytoplasmic Membrane ◽  
Ultrastructural Localization ◽  
In Vivo Studies ◽  
E Cadherin

We examined the ultrastructural localization of E (epithelial)-cadherin cell adhesion molecules by immunoperoxidase electron microscopy on the epithelium of mouse intestine, epidermis of human skin, and cultured human keratinocytes. The in vivo studies demonstrated that E-cadherin was present at the intermediate junction but not at the desmosome of the mouse intestinal single epithelium, and was found on the cytoplasmic membranes of keratinocytes with condensation in the intercellular space of the desmosomes, except for the basal surface of the basal cells. In vitro studies demonstrated that keratinocytes cultured in medium containing a low Ca2+ concentration (0.1 mM) lacked the tight connection through desmosomes, and that E-cadherin showed diffuse distribution and dot-like accumulation around the free surface of the cytoplasmic membrane. In culture medium containing a high concentration of Ca2+ (0.6 mM), keratinocytes formed desmosomal adhesion structures in which E-cadherin was accumulated. The free surface of the keratinocytes in this medium showed weaker distribution and a lesser amount of dot-like accumulation of E-cadherin than that in a low Ca2+ condition. These findings suggest that the distribution pattern of the E-cadherin cell adhesion molecules on the keratinocytes is different from that on the single epithelium of the intestine, and that E-cadherin on the cytoplasmic membrane of the keratinocytes shifts to the desmosomes under physiological conditions, participating in adhesion in association with other desmosomal cadherins.

Attenuated expression of epithelial cell adhesion molecules in murine polycystic kidney disease

1992 ◽  
Vol 262 (4) ◽  
pp. F679-F686 ◽  
Author(s):  
M. V. Rocco ◽  
E. G. Neilson ◽  
J. R. Hoyer ◽  
F. N. Ziyadeh
Keyword(s):  
Cell Adhesion ◽  
Growth Factors ◽  
Kidney Disease ◽  
Adhesion Molecules ◽  
Polycystic Kidney Disease ◽  
Cell Adhesion Molecules ◽  
Structural Proteins ◽  
Polycystic Kidney ◽  
Cystic Kidneys ◽  
E Cadherin

Polycystic kidney disease is an inherited disorder of parenchymal structure that leads to renal failure. Cysts begin as focal dilations in proximal tubules and collecting ducts, giving rise to cyst walls lined by a phenotypically disturbed epithelium that expresses dysfunctional transport and matrix proteins. We used an mRNA search protocol to probe efficiently for tissue-specific disturbances that might underlie the formation of cysts. This search assessed the relative abundance of transcripts encoding a variety of growth factors (transforming growth factor-beta 1, interleukin-6, tumor necrosis factor, and endothelin-1), structural proteins (collagen IV, nidogen, fibronectin, and laminins A and B1), and cell adhesion molecules (CAMs; E-cadherin, N-CAM, laminin receptor, and fibronectin receptor) in the cystic kidneys of cpk/cpk mice and uncovered a previously unrecognized early reduction in mRNA encoding N-CAM (54%) and E-cadherin (56%) (n = 5; P less than 0.001). Levels of transcripts for growth factors, structural proteins, and for fibronectin and laminin receptors in normal and cystic kidneys were generally similar. The reduction in transcripts for N-CAM and E-cadherin in kidneys from cystic mice was not observed in autologous liver. The immunofluorescent staining of cystic kidneys confirmed that the decrease in N-CAM and E-cadherin was generally confined to regions abundant in developing cystic epithelium. The presence of both N-CAM and E-cadherin appears to guide the sequential differentiation and polarization of normal renal epithelium, and their attenuated expression in the kidney of cpk/cpk mice may be a material factor contributing to the pathogenesis of cyst formation.

scholarly journals Molecular Expression of bone marrow angiogenic factors, cell-cell adhesion molecules and matrix-metallo-proteinase plasma cellular disorders: a molecular panel to investigate disease progression

2018 ◽  
Vol 10 ◽  
pp. e2018059
Author(s):  
Maria Cristina Rapanotti
Keyword(s):  
Multiple Myeloma ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Plasma Cells ◽  
Angiogenic Factors ◽  
Specific Cell ◽  
Angiogenic Potential ◽  
E Cadherin ◽  
Cell Cell

Increasing levels of angiogenesis play an important role in the pathogenesis and progression of multiple myeloma (MM). Malignant plasma cells promote a gradual increase in the degree of angiogenesis, modulation of specific cell-cell adhesion molecules and secretion of matrix-metallo-proteinases (MMPs), changing the BM composition from benign conditions, such as MGUS, to smouldering multiple myeloma (SM) and to active MM. We aimed to identify a gene expression profile, helpful to discriminate the “angiogenic potential” in BM and PB plasma cells from MGUS, SMM and active MM patients analyzed at diagnosis. We analyzed the expression of cell-cell adhesion molecules such as VE-Cadherin, E-Cadherin MCAM/MUC18/CD146 and of the MMP-2 and MMP-9. MCAM/MUC18 expression resulted mostly associated with that of the pivotal angiogenic factors VEGF and Ang2, and in MGUS the pattern was different in steady state, compared to progression towards SM. Furthermore, E-Cadherin, the main epithelial cell-cell-adhesion molecule, unexpectedly resulted overexpressed in MM.                                                                                                                                                                                                                                                

Immunohistochemical detection of the expression of the cell adhesion molecules E-cadherin, desmoglein-2, beta4-integrin, ICAM-1 and HCAM (CD44s) in Warthin’s tumour of the parotid gland

Oral Oncology ◽  
2005 ◽  
Vol 41 (8) ◽  
pp. 799-805 ◽  
Author(s):  
Dimitrios Andreadis ◽  
Apostolos Epivatianos ◽  
Athanasios Poulopoulos ◽  
Alexandros Nomikos ◽  
Konstantinos Christidis ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Parotid Gland ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Immunohistochemical Detection ◽  
Warthin’S Tumour ◽  
E Cadherin

scholarly journals Expression of Three Cell Adhesion Molecules in Bladder Carcinomas: Correlation with Pathological Features

1997 ◽  
Vol 13 (3) ◽  
pp. 125-136 ◽  
Author(s):  
Agnès Mialhe ◽  
Josette Louis ◽  
Dominique Pasquier ◽  
Jean‐Jacques Rambeaud ◽  
Daniel Seigneurin
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Tumour Progression ◽  
Histological Grade ◽  
Immunohistochemical Analysis ◽  
Aberrant Expression ◽  
Bladder Carcinomas ◽  
Bladder Tumours ◽  
E Cadherin

Recently, independent studies have shown that the expression of two integrin chains,β4 andα2, plus the epithelial cadherin are related to tumour progression in human bladder carcinomas. For the first time, we compare the expression of these three cell adhesion molecules using immunohistochemical analysis of consecutive cryosections from a series of 50 bladder tumours. E‐cadherin,β4, andα2 were strongly expressed in normal urothelium. A majority of non‐invasive bladder cancers stained positively for E‐cadherin (62%), whereas only 29% expressed normal positivity forα2, and only 35% forβ4. However, most invasive tumours presented an aberrant expression ofα2 (81%),β4 (100%), and E‐cadherin (75%). We studied the correlation of immunoreactivity with histological grade and stage. Theα2 pattern was not correlated with stage and grade. In contrast, loss of normalβ4 expression was significantly related to increasing tumour grade and deep invasion with a higher correlation for grade. Finally, E‐cadherin expression was highly correlated with stage, but not with grade. Thus our results indicate that, although many invasive bladder tumours presented a disorder in expression of the two integrinsα2 andβ4, E‐cadherin appeared to be a better marker of invasiveness in bladder carcinomas.

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