Role of toll-like receptor 3 in prostate cancer therapy-resistance

2019 ◽  
Vol 18 (8) ◽  
pp. e3124
Author(s):  
X.M. Muresan ◽  
S. Drapela ◽  
E. Slabakova ◽  
J. Remsik ◽  
R. Fedr ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Toll Like Receptor ◽  
Prostate Cancer Therapy

scholarly journals The role of lineage plasticity in prostate cancer therapy resistance

2019 ◽  
pp. clincanres.1423.2019 ◽  
Author(s):  
Himisha Beltran ◽  
Andrew Hruszkewycz ◽  
Howard I. Scher ◽  
Jeffrey Hildesheim ◽  
Jennifer Isaacs ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Prostate Cancer Therapy

scholarly journals Cell Plasticity and Prostate Cancer: The Role of Epithelial–Mesenchymal Transition in Tumor Progression, Invasion, Metastasis and Cancer Therapy Resistance

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2795
Author(s):  
Sofia Papanikolaou ◽  
Aikaterini Vourda ◽  
Spyros Syggelos ◽  
Kostis Gyftopoulos
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Tumor Progression ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Tumor ◽  
Therapy Resistance ◽  
Cellular Process ◽  
Cell Plasticity ◽  
Mesenchymal Transition

Prostate cancer, the second most common malignancy in men, is characterized by high heterogeneity that poses several therapeutic challenges. Epithelial–mesenchymal transition (EMT) is a dynamic, reversible cellular process which is essential in normal embryonic morphogenesis and wound healing. However, the cellular changes that are induced by EMT suggest that it may also play a central role in tumor progression, invasion, metastasis, and resistance to current therapeutic options. These changes include enhanced motility and loss of cell–cell adhesion that form a more aggressive cellular phenotype. Moreover, the reverse process (MET) is a necessary element of the metastatic tumor process. It is highly probable that this cell plasticity reflects a hybrid state between epithelial and mesenchymal status. In this review, we describe the underlying key mechanisms of the EMT-induced phenotype modulation that contribute to prostate tumor aggressiveness and cancer therapy resistance, in an effort to provide a framework of this complex cellular process.

scholarly journals Splicing of a Novel Androgen Receptor Exon Generates a Constitutively Active Androgen Receptor that Mediates Prostate Cancer Therapy Resistance

2008 ◽  
Vol 68 (13) ◽  
pp. 5469-5477 ◽  
Author(s):  
Scott M. Dehm ◽  
Lucy J. Schmidt ◽  
Hannelore V. Heemers ◽  
Robert L. Vessella ◽  
Donald J. Tindall
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Prostate Cancer Therapy ◽  
Constitutively Active
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