Host manipulation by cancer cells: Expectations, facts, and therapeutic implications

BioEssays ◽  
2016 ◽  
Vol 38 (3) ◽  
pp. 276-285 ◽  
Author(s):  
Tazzio Tissot ◽  
Audrey Arnal ◽  
Camille Jacqueline ◽  
Robert Poulin ◽  
Thierry Lefèvre ◽  
...  
1995 ◽  
Vol 14 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S Y James ◽  
A G Mackay ◽  
K W Colston

ABSTRACT The effects of the novel vitamin D analogue, EB1089 alone, or in combination with the retinoid, 9-cis retinoic acid (9-cis RA) on indices of apoptosis in MCF-7 breast cancer cells have been examined. EB1089 was capable of reducing bcl-2 protein, a suppressor of apoptosis, and increasing p53 protein levels in MCF-7 cell cultures following 96h treatment. In the presence of 9-cis RA, EB1089 acted to further enhance the down-regulation and up-regulation of bcl-2 and p53 respectively. Furthermore, EB1089 induces DNA fragmentation in MCF-7 cells, a key feature of apoptosis, alone and in combination with 9-cis RA in situ. The observation that EB1089 and 9-cis RA act in a cooperative manner to enhance induction of apoptosis in these cells may have therapeutic implications.


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.


Author(s):  
Junjiang Liu ◽  
Lei Wang ◽  
Yunxia Zhang ◽  
Shoubin Li ◽  
Fuzhen Sun ◽  
...  

The Breast ◽  
2015 ◽  
Vol 24 ◽  
pp. S37-S38
Author(s):  
M.H. Bashari ◽  
F. Fan ◽  
M. Arn ◽  
S. Vallet ◽  
J. Opferman ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 7 (43) ◽  
pp. 70639-70653 ◽  
Author(s):  
Suellen Ferro ◽  
João Azevedo-Silva ◽  
Margarida Casal ◽  
Manuela Côrte-Real ◽  
Fatima Baltazar ◽  
...  

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