Evaluating the Significance of CDK2-PELP1 Axis in Tumorigenesis and Hormone Therapy Resistance

2011 ◽  
Author(s):  
Binoj Nair
2014 ◽  
Vol 21 (2) ◽  
pp. 373-385 ◽  
Author(s):  
Philip C. Miller ◽  
Jennifer Clarke ◽  
Tulay Koru-Sengul ◽  
Joeli Brinkman ◽  
Dorraya El-Ashry

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1028 ◽  
Author(s):  
David Rodriguez ◽  
Marc Ramkairsingh ◽  
Xiaozeng Lin ◽  
Anil Kapoor ◽  
Pierre Major ◽  
...  

Breast cancer stem cells (BCSC) play critical roles in the acquisition of resistance to endocrine therapy in estrogen receptor (ER)-positive (ER + ve) breast cancer (BC). The resistance results from complex alterations involving ER, growth factor receptors, NOTCH, Wnt/β-catenin, hedgehog, YAP/TAZ, and the tumor microenvironment. These mechanisms are likely converged on regulating BCSCs, which then drive the development of endocrine therapy resistance. In this regard, hormone therapies enrich BCSCs in ER + ve BCs under both pre-clinical and clinical settings along with upregulation of the core components of “stemness” transcriptional factors including SOX2, NANOG, and OCT4. SOX2 initiates a set of reactions involving SOX9, Wnt, FXY3D, and Src tyrosine kinase; these reactions stimulate BCSCs and contribute to endocrine resistance. The central contributions of BCSCs to endocrine resistance regulated by complex mechanisms offer a unified strategy to counter the resistance. ER + ve BCs constitute approximately 75% of BCs to which hormone therapy is the major therapeutic approach. Likewise, resistance to endocrine therapy remains the major challenge in the management of patients with ER + ve BC. In this review we will discuss evidence supporting a central role of BCSCs in developing endocrine resistance and outline the strategy of targeting BCSCs to reduce hormone therapy resistance.


2009 ◽  
Author(s):  
B Chandrasekharan Nair ◽  
SS Nair ◽  
D Chakravarty ◽  
RP Yew ◽  
RR Tekmal ◽  
...  

2020 ◽  
Author(s):  
Kathryn E. Ware ◽  
Santosh Gupta ◽  
Jared Eng ◽  
Gabor Kemeny ◽  
Bhairavy J. Puviindran ◽  
...  

SummaryAdaptation of cancer cells to targeted therapy follows ecological paradigms observed in natural populations that encounter resource depletion and changing environments, including activation of pro-survival mechanisms, migration to new locations, and escape of predation. We identified the p38 MAPK pathway as a common molecular driver of these three responses during the adaptation to hormone therapy resistance in prostate cancer. The p38 pathway is activated in therapy-resistant cells and mechanistically drives these three convergent responses through sustained AR activity, enhanced invasion and metastasis, and immune evasion. Targeting p38 signaling may represent a new therapeutic strategy to treat men with metastatic, hormone therapy-resistant prostate cancer.


2015 ◽  
Vol 06 (09) ◽  
pp. 773-782
Author(s):  
Sally A. Litherland ◽  
Louis Barr ◽  
Robert Reynolds ◽  
Elizabeth Griffith ◽  
Ryan Sause ◽  
...  

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