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resistance PCa, targeting these epigenetic changes that facilitate AR target gene activation has a highly
possible and promising potential in developing novel therapeutic approaches. Though whether targeting
these factors’ stability will produce toxic or ineffective effects is obscure, pre-clinical trial data gathered and
documented by our lab indicates that clinical trial participation could result in highly efficient and optional
treatment methods.
DECLARATIONS
Authors’ contributions
Made substantial contributions to conception, material articulation, and editing of the review: Jones K
Provided administrative, technical, and material support: Zhang Y
Provided material support: Kong Y, Wang R, Farah E, Li C, Wang X, Zhang Z, Wang J, Mao F
Contributed to the conception and design of the review: Liu X, Liu J
Availability of data and materials
Not applicable.
Financial support and sponsorship
The work was supported by NIH grants R01 CA157429 (Liu X), R01 CA192894 (Liu X), R01 CA196835
(Liu X), and R01 CA196634 (Liu X). The work was also supported by the DTCB internal fellowship (Liu J).
Conflicts of interest
All authors declared that there are no conflicts of interest.
Ethical approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Copyright
© The Author(s) 2021.
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