In situ detection of telomeres by fluorescence in situ hybridization and telomerase activity in glioblastoma multiforme: Correlation with p53 status, EGFR, c-myc, MIB1, and Topoisomerase IIα protein expression

Author(s):  
Clelia Miracco ◽  
M. De Santi ◽  
Pietro Luzi ◽  
Anna Lalinga ◽  
Lorella Laurini ◽  
...  
2003 ◽  
Vol 47 (5) ◽  
pp. 129-132
Author(s):  
N. Noda ◽  
Y. Ebie ◽  
M. Matsumura ◽  
S. Tsuneda ◽  
A. Hirata ◽  
...  

The in situ fluorescent antibody and fluorescence in situ hybridization (FISH) methods are very useful in the in situ detection of specific bacteria like nitrifiers in a biofilm. In this study, simultaneous staining using the FISH and in situ fluorescent antibody methods was examined. As a result, no specific fluorescence was observed with either method when FISH was performed followed by the in situ fluorescent antibody method; however, when the in situ fluorescent antibody method was performed first followed by FISH, specific fluorescence was observed in both cases. Moreover, it was suggested that the detection specificities of FISH and the in situ fluorescent antibody method are almost identical.


2017 ◽  
Vol 44 (2) ◽  
pp. 14-19
Author(s):  
A. Kotzev ◽  
M. Kamenova

AbstractMolecular biology of esophageal adenocarcinoma (EAC) is not fully elucidated. The aim of this study was to assess the expression of cycle regulator and tumor suppressor p16 in esophageal adenocarcinoma. The expression of p16 at protein and gene level was investigated using immunohistochemistry and fluorescence in situ hybridization in thirteen EAC specimens obtained by endoscopic biopsies and surgical resections. The mean age of enrolled patients was 62 years and a male predominance was observed. Loss of p16 protein expression was detected in 77% of the cases and loss of p16 gene was found in 69% of cases as hemizygous deletion was the most common. Significant correlation was found between the absence of p16 protein expression and p16 allelic loss. Cell cycle disturbances seem to play role in the EAC carcinogenesis and probably p16 gene deletions are connected with the loss of p16 protein expression.


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