scholarly journals Detection of telomerase activity in exfoliated cancer cells in colonic luminal washings and its related clinical implications

1997 ◽  
Vol 75 (4) ◽  
pp. 548-553 ◽  
Author(s):  
K Yoshida ◽  
T Sugino ◽  
S Goodison ◽  
BF Warren ◽  
D Nolan ◽  
...  
Redox Biology ◽  
2016 ◽  
Vol 8 ◽  
pp. 91-97 ◽  
Author(s):  
Pengying Li ◽  
Meilin Wu ◽  
Jing Wang ◽  
Yilun Sui ◽  
Shanlin Liu ◽  
...  

2017 ◽  
Vol 37 (2) ◽  
pp. 445-454 ◽  
Author(s):  
SEYUNG S CHUNG ◽  
DEBBIE ADEKOYA ◽  
IKECHUKWU ENENMOH ◽  
ORETTE CLARKE ◽  
PIWEN WANG ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 949 ◽  
Author(s):  
Marta Recagni ◽  
Joanna Bidzinska ◽  
Nadia Zaffaroni ◽  
Marco Folini

Telomere maintenance mechanisms (i.e., telomerase activity (TA) and the alternative lengthening of telomere (ALT) mechanism) contribute to tumorigenesis by providing unlimited proliferative capacity to cancer cells. Although the role of either telomere maintenance mechanisms seems to be equivalent in providing a limitless proliferative ability to tumor cells, the contribution of TA and ALT to the clinical outcome of patients may differ prominently. In addition, several strategies have been developed to interfere with TA in cancer, including Imetelstat that has been the first telomerase inhibitor tested in clinical trials. Conversely, the limited information available on the molecular underpinnings of ALT has hindered thus far the development of genuine ALT-targeting agents. Moreover, whether anti-telomerase therapies may be hampered or not by possible adaptive responses is still debatable. Nonetheless, it is plausible hypothesizing that treatment with telomerase inhibitors may exert selective pressure for the emergence of cancer cells that become resistant to treatment by activating the ALT mechanism. This notion, together with the evidence that both telomere maintenance mechanisms may coexist within the same tumor and may distinctly impinge on patients’ outcomes, suggests that ALT may exert an unexpected role in tumor biology that still needs to be fully elucidated.


2001 ◽  
Vol 165 (5) ◽  
pp. 1802-1805 ◽  
Author(s):  
FLORIAN H. MEID ◽  
CHRISTIAN M. GYGI ◽  
HANS-JUERG LEISINGER ◽  
FRED T. BOSMAN ◽  
JEAN BENHATTAR

2004 ◽  
Vol 82 (4) ◽  
pp. 498-507 ◽  
Author(s):  
Chiara Mondello ◽  
A Ivana Scovassi

Telomeres are specialized high-order chromatin structures that cap the ends of eukaryotic chromosomes. In vertebrates, telomeric DNA is composed of repetitions of the TTAGGG hexanucleotide, is bound to a set of specific proteins, and is elongated by the reverse transcriptase enzyme telomerase. Telomerase activity is promptly detected in cells with an indefinite replicative potential, such as cancer cells, while is almost undetectable in normal cells, which are characterized by a limited life span. Mounting evidence indicates that the maintenance of telomere integrity and telomerase protect cells from apoptosis. Disruption of the telomere capping function and (or) telomerase inhibition elicit an apoptotic response in cancer cells, while restoration of telomerase activity in somatic cells confers resistance to apoptosis. The possible mechanisms linking telomeres, telomerase and apoptosis are discussed in this review, together with the impact of this field in anticancer research.Key words: telomeres, telomerase, telomeric proteins, apoptosis, tumorigenesis.


2011 ◽  
Author(s):  
Orit Uziel ◽  
Gil Kanfer ◽  
Einat Beery ◽  
Jardena Nordenberg ◽  
Meir Lahav

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