A monoclonal antibody that defines basal cells of stratified epithelia in various human and rabbit tissues

1989 ◽  
Vol 92 (4) ◽  
pp. 319-324 ◽  
Author(s):  
K. Maeda ◽  
K. Sueishi
1985 ◽  
Vol 157 (2) ◽  
pp. 293-306 ◽  
Author(s):  
Scott A. Settle ◽  
Ingegerd Hellström ◽  
Karl Erik Hellström

1997 ◽  
Vol 30 (5/6) ◽  
pp. 601-608 ◽  
Author(s):  
Shuji Yamashita ◽  
Takashi Sogo ◽  
Kenjiro Yasuda

2016 ◽  
Vol 19 (5) ◽  
pp. 283-286
Author(s):  
Alexandra K. Aleksandrova ◽  
G. I Sukolin ◽  
V. A Smolynnikova

The significant role in the pathogenesis of seborrheic keratosis (SK) plays the violation of the cell cycle regulation. According to the research unit the cell proliferation in acanthotic and irritated histological types of SK is regulated by p27 (Kip1), cyclin-dependent kinase inhibitor. Considering the variety of histological types of SK, definition of p27 expression will reveal the characteristic features of the cell cycle disorders and proliferation for each type of tumor. Material and Methods. Of the 102 tumors from patients with SK, according to the results of histological examination, were selected 10 specimens of each histological types of SK: acanthotic, hyperkeratotic, adenoid, irritated, and clonal. We assessed all specimens for p27 (Kip1) expression using immunohistochemistry (monoclonal antibody p27 at a dilution of 1:20 (Novocastra Laboratories Ltd.). Three skin biopsy samples of healthy individuals were included. Results. Severe diffuse nuclear expression of p27 was present in all cases of adenoid, irritated, and 4 cases of clonal histological types of SK. In other tumor types positive reaction with monoclonal antibody to p27 was reduced as compared with healthy skin were recorded single positively stained nuclei of basal cells. Conclusions. Thus, we have found a violation of p27 protein expression in all types of seborrheic keratosis as with the excess (adenoid, irritated, clonal SK type) and in p27 protein deficiency (acanthotic, hyperkeratotic) normal course of cell cycle phases is broken. This leads to the disappearance of control over the cell proliferative activity and apoptosis, facilitating a slow, uncontrolled growth of SK cells.


2002 ◽  
Vol 65 (2) ◽  
pp. 201-208 ◽  
Author(s):  
Jiro HITOMI ◽  
Fumio ISHIZAKI ◽  
Eiji KIMURA ◽  
Nobuyuki SATO

1985 ◽  
Vol 76 (5) ◽  
pp. 1978-1983 ◽  
Author(s):  
V B Morhenn ◽  
A B Schreiber ◽  
O Soriero ◽  
W McMillan ◽  
A C Allison

1990 ◽  
Vol 1 (5) ◽  
pp. 387
Author(s):  
Xiao-Min Zhang ◽  
Yuji Horiguchi ◽  
Sadao Imamura

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