Treatment sequence in castration-resistant prostate cancer: A retrospective study in the new anti-androgen era

Hoshi, Senji; Numahata, Kenji; Ono, Kunio; Yasuno, Nobuhiro; Bilim, Vladimir; Hoshi, Kiyotsugu; Amemiya, Hiroshi; Sasagawa, Isoji

doi:10.3892/mco.2017.1361

Cited by 4 publications

(4 citation statements)

References 18 publications

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“…2). Our result also can give explanations to earlier findings that the clinical activity of enzalutamide can be blunted by previous docetaxel chemotherapy 13–15 . Although initiation of taxane-based chemotherapy may not promptly induce ARV7, long-term exposure to chemotherapy may otherwise induce ARV7, which results in acquisition of resistance to subsequent AR-targeted therapy.…”

Section: Discussionsupporting

confidence: 85%

Taxane-based Chemotherapy Induced Androgen Receptor Splice Variant 7 in Patients with Castration-Resistant Prostate Cancer: A Tissue-based Analysis

Shim

Kim

Park

et al. 2019

Sci Rep

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In total, 95 prostate cancer (Pca) patients who underwent transurethral resection of the prostate from 2000 to 2013 were assigned to four groups: Group 1, hormone-naïve and T1a or T1b Pca (n = 17); Group 2, hormone-sensitive and metastatic Pca (n = 33); Group 3, chemo-naïve castration-resistant Pca (CRPC), (n = 18); and Group 4, CRPC with chemotherapy (n = 27). Full-length androgen receptor (ARfl) transcript levels significantly increased from Group 1 through to Group 3 (p = 0.045), but decreased from Group 3 through to Group 4. AR splice variant 7 (ARV7) and glucocorticoid receptor (GR) transcript levels significantly increased from Group 1 through to Group 4 (p = 0.002 and 0.049, respectively). Kaplan–Meier curve revealed that the high transcript level of these three receptors resulted in significantly poorer cancer-specific survival (CSS) than that by low transcript level, although Cox regression analysis revealed that the ARV7 level alone was an independent prognostic factor for CSS in CRPC patients (high vs. low: hazard ratio, 1.897; 95% confidence interval, 1.102–3.625; p = 0.042). In conclusion, ARV7 and GR transcript levels significantly increase as Pca progresses to CRPC.

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Section: Discussionsupporting

confidence: 85%

Taxane-based Chemotherapy Induced Androgen Receptor Splice Variant 7 in Patients with Castration-Resistant Prostate Cancer: A Tissue-based Analysis

Shim

Kim

Park

et al. 2019

Sci Rep

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“…It has been theorized that early chemotherapy disposes of AR-independent tumor clones hence favoring efficacy of AR targeting AA/E as first-line treatment for mCRPC [6,10]. On the other hand, a few in vivo and in vitro studies observed cross-resistance between D for mCRPC and subsequent AA or E and partly attributed it to the partially overlapping mechanisms of action of these drugs which interfere with AR signaling pathway and inhibit AR nuclear translocation [13-15]. In the present study, D is used for the hormone-sensitive disease but the treatment sequence is the same hence cross-resistance could arise.…”

Section: Discussionmentioning

confidence: 99%

Clinical Outcomes of First-line Abiraterone Acetate or Enzalutamide for Metastatic Castration-resistant Prostate Cancer After Androgen Deprivation Therapy + Docetaxel or ADT Alone for Metastatic Hormone-sensitive Prostate Cancer

Francini

Yip

Ahmed

et al. 2018

Clinical Genitourinary Cancer

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Background The CHAARTED and STAMPEDE trials showed that the addition of docetaxel (D) to androgen deprivation therapy (ADT) prolonged longevity of men with metastatic hormone sensitive prostate cancer (mHSPC). However, the impact of upfront D on subsequent therapies is still unexplored. As abiraterone acetate (AA) and enzalutamide (E) are the most commonly used first-line treatment for metastatic CRPC (mCRPC), we aimed to assess whether they maintained their efficacy after ADT+D versus ADT alone. Patients and Methods A cohort of mCRPC patients treated between 2014 and 2017 with first-line AA or E for mCRPC was identified from three hospitals’ IRB approved databases. Patients were classified by use of D for mHSPC. This time frame was chosen as ADT+D became a valid therapeutic option for mHSPC in 2014 and it inherently entailed a short follow-up time on AA/E. The endpoints included overall survival (OS) from ADT start, OS from AA/E start, and time to AA/E start from ADT start. Differences between groups were assessed using the log-rank test. Results Of the 102 mCRPC patients identified, 50 (49%) had previously received ADT alone, while 52 (51%) had ADT+D. No statistically significant difference in any of the evaluated outcomes was observed between the 2 cohorts. Yet, deaths in the ADT+D group were 12 versus 21 in the ADT alone, after a median follow-up of 24.4 and 29.8 months, respectively. Conclusion In a cohort of ADT/ADT+D treated mCRPC patients with short times to first-line AA/E and follow-up, the efficacy of AA/E is similar regardless of previous use of D.

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“…For treatment of CRPC, currently nine drugs are mainly used, out of which, Docetaxel, Enzalutamide, Apalutamide, Darolutamide and Abiraterone are often used as a first line chemotherapy and Sipleucel-T, Radium-223 dichloride, Cabazitaxel and Olaparib are considered as a second line of defense [3,5,[11][12][13][14][18][19][20]. For the first line of treatment in CRPC patients, the optimal sequencing between next generation anti-androgen drugs with taxane chemotherapy in point of efficacy and cross-resistance still remains unknown [21][22][23]. In this context, no chemotherapeutic drug has been identified more superior in performance than other types of available agents as the first line therapy for advanced prostate cancer.…”

Section: Challenges In Current Sequencing Strategies For Advanced Prostate Cancer and Associated Cross Resistancementioning

confidence: 99%

“…Basically, current therapeutic inconsistencies for CRPC can be explained by several other critical factors which not only increases the complexities of these diseases but also are centrally responsible for observed ineffectiveness of available treatment processes during late stage of CRPC progression. Fundamentally, CRPC progression can be characterized by its extreme levels of inter-tumor & intra-tumor heterogeneity [21][22][23], remarkable variability's in clinical behavior along with mechanistic complexities and presence of redundancies in tumor cell signaling pathways driven by the key functional interplay of multiple oncogenes [8,[50][51][52][53]. In fact, these prostate cancer patient specific intra-tumor heterogeneities also provides the essential challenges for attaining desired clinical effectiveness during metastatic prostate cancer treatment [54,55].…”

Section: Real Facts Behind Prostate Cancer Therapeutic Unsuccessfulnessmentioning

confidence: 99%

A comprehensive mechanistic basis of prostate cancer advancement & its personalized implementation-bridging the gap: present state and future prospect

2021

JOMH

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Despite signiﬁcant achievements in prostate cancer mechanistic understanding and its targeted therapies, currently there exists several major challenges that mainly arises during the therapy of advanced prostate cancer. Present prostate cancer precision medicine strategy principally suffers from several practical concerns, particularly in point of therapeutic resistance, tumor heterogeneity, complex clinical & pathological behavior and an extensive genomic perturbation landscape. Prostate Cancer Systems-Medicine Initiative is a global trans-disciplinary movement taken from corre-sponding scientiﬁc domains to critically determine the nature of this major existing challenges and its corresponding most possible solutions by systematically accumulating the present existing knowledge. Basically, it explains the importance of broad spectrum cancer hallmark based integrative approaches for development of combination therapy associated strategic measures for metastatic castration resistant prostate cancer. The major ﬁndings of this initiative can be summarized by identiﬁcation of 136 therapeutic resistance mediators, 103 prostate cancer driver oncogenes and 8 progression pathways along with 5 terrain factors which centrally drives the basic events in prostate cancer pathogenesis, its further metastatic propagation and ultimate therapeutic resistance. In addition, it also attempts to summarize the critical features and basic challenging aspects of current therapeutic options.

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Treatment sequence in castration-resistant prostate cancer: A retrospective study in the new anti-androgen era

Cited by 4 publications

References 18 publications

Taxane-based Chemotherapy Induced Androgen Receptor Splice Variant 7 in Patients with Castration-Resistant Prostate Cancer: A Tissue-based Analysis

Taxane-based Chemotherapy Induced Androgen Receptor Splice Variant 7 in Patients with Castration-Resistant Prostate Cancer: A Tissue-based Analysis

Clinical Outcomes of First-line Abiraterone Acetate or Enzalutamide for Metastatic Castration-resistant Prostate Cancer After Androgen Deprivation Therapy + Docetaxel or ADT Alone for Metastatic Hormone-sensitive Prostate Cancer

A comprehensive mechanistic basis of prostate cancer advancement & its personalized implementation-bridging the gap: present state and future prospect

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