We are analyzing https://link.springer.com/article/10.1186/s13045-015-0225-2.

Title:
Persistent androgen receptor addiction in castration-resistant prostate cancer | Journal of Hematology & Oncology
Description:
It is now understood that persistent activation of the androgen receptor (AR) signaling pathway often underlies the development of castration-resistant prostate cancer (CRPC). This realization led to renewed interest in targeting the AR and ultimately to the development of the potent next-generation AR-directed agents abiraterone and enzalutamide. While these drugs prolong survival in men with CRPC, they are unfortunately not curative. Perhaps not surprisingly, evidence points to persistent AR signaling as one of the key drivers by which resistances to these agents develops. In this context, activation of the AR signaling program can occur through a number of molecular adaptations, including alterations leading to persistent canonical AR signaling (e.g., AR amplification/overexpression, elucidations/concentration of intratumoral androgens), activation of the AR program via feedback pathways (e.g., AKT/mTOR/Pi3K, HER2/Neu), and activation of the AR program via mutation or substitution (e.g., AR ligand binding domain mutation; AR splice variants; glucocorticoid receptor signaling). This review will provide an overview of the more clinical relevant (i.e., druggable) pathways that have been implicated in the emergence of drug resistance in men with CRPC and highlight some of the ongoing efforts towards developing therapeutics to impair these mechanisms.
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Keywords {🔍}

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Topics {✒️}

akt/foxo3a/gsk-3beta/ar signaling network nf-kappab2/p52 induces resistance androgen-il-6-stat3 autocrine loop intense androgen-deprivation therapy multi-targeted anti-angiogenic tki castration-resistant prostate cancer hormone-refractory prostate cancer androgen-independent prostate cancer castrate-resistant prostate cancer castration-resistant tumor growth hormone-sensitive prostate cancer cyclooxygenase-dependent antineoplastic actions androgen-independent prostatic cancer androgen-receptor signaling axis increased full-length ar transforming growth factor-beta1 pi3k/akt/mtor pathway circulating cell-free dna generation ar-directed therapies pi3k/akt/mtor signaling pi3k-akt-mtor signaling initial rate-limiting step n-terminal domain antagonists anti-androgen withdraw effect nuclear hormone receptors anti-helminthic drug niclosamide circulating cell-free ar aldo-keto reductase akr1c3 ar splice variant article download pdf pten-deficient prostate cancer anti-prostate cancer agents clear anti-tumor activity anti-il-6 monoclonal antibody subsequent ligand-independent transcription ligand-independent ar transcription ar-directed therapeutic galeterone pten/akt/pi3k signaling androgen deprivation therapy hsp heat-shock proteins ar n-terminal domain nonsteroidal anti-inflammatory drugs canonical ar-fl signaling enhanced jak/stat signaling paradoxical anti-tumor effect profound anti-tumor effect population-based nonscreened cohort mutant androgen receptors generation ar-directed agents anti-interleukin-6 antibody siltuximab

Questions {❓}

Targeting HER2 in prostate cancer: where to next?

Schema {🗺️}

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         headline:Persistent androgen receptor addiction in castration-resistant prostate cancer
         description:It is now understood that persistent activation of the androgen receptor (AR) signaling pathway often underlies the development of castration-resistant prostate cancer (CRPC). This realization led to renewed interest in targeting the AR and ultimately to the development of the potent next-generation AR-directed agents abiraterone and enzalutamide. While these drugs prolong survival in men with CRPC, they are unfortunately not curative. Perhaps not surprisingly, evidence points to persistent AR signaling as one of the key drivers by which resistances to these agents develops. In this context, activation of the AR signaling program can occur through a number of molecular adaptations, including alterations leading to persistent canonical AR signaling (e.g., AR amplification/overexpression, elucidations/concentration of intratumoral androgens), activation of the AR program via feedback pathways (e.g., AKT/mTOR/Pi3K, HER2/Neu), and activation of the AR program via mutation or substitution (e.g., AR ligand binding domain mutation; AR splice variants; glucocorticoid receptor signaling). This review will provide an overview of the more clinical relevant (i.e., druggable) pathways that have been implicated in the emergence of drug resistance in men with CRPC and highlight some of the ongoing efforts towards developing therapeutics to impair these mechanisms.
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            Hematology
            Cancer Research
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      headline:Persistent androgen receptor addiction in castration-resistant prostate cancer
      description:It is now understood that persistent activation of the androgen receptor (AR) signaling pathway often underlies the development of castration-resistant prostate cancer (CRPC). This realization led to renewed interest in targeting the AR and ultimately to the development of the potent next-generation AR-directed agents abiraterone and enzalutamide. While these drugs prolong survival in men with CRPC, they are unfortunately not curative. Perhaps not surprisingly, evidence points to persistent AR signaling as one of the key drivers by which resistances to these agents develops. In this context, activation of the AR signaling program can occur through a number of molecular adaptations, including alterations leading to persistent canonical AR signaling (e.g., AR amplification/overexpression, elucidations/concentration of intratumoral androgens), activation of the AR program via feedback pathways (e.g., AKT/mTOR/Pi3K, HER2/Neu), and activation of the AR program via mutation or substitution (e.g., AR ligand binding domain mutation; AR splice variants; glucocorticoid receptor signaling). This review will provide an overview of the more clinical relevant (i.e., druggable) pathways that have been implicated in the emergence of drug resistance in men with CRPC and highlight some of the ongoing efforts towards developing therapeutics to impair these mechanisms.
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         Androgen receptor splice variant
         Drug resistance
         Signaling pathway
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         Hematology
         Cancer Research
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