Is There Evidence of a Relationship between Benign Prostatic Hyperplasia and Prostate Cancer? Findings of a Literature Review

Alcaraz, Antonio; Hammerer, Peter; Tubaro, Andrea; Schröder, Fritz H.; Castro, Ramiro

doi:10.1016/j.eururo.2008.11.011

Cited by 194 publications

(167 citation statements)

References 70 publications

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“…Clinically, a 1 -AR antagonists such as naftopidil and tamsulosin have been widely used to treat BPH, a common prostatic disease in elderly men; naftopidil has high tolerability with few adverse effects (28). As the incidence of BPH increases with age (29), this would suggest that administration of a 1 -AR antagonists for BPH might often precede diagnosis of RCC. Thus, there may be some prospective clinical benefits from long-term use of naftopidil for BPH.…”

Section: Discussionmentioning

confidence: 99%

Oral Naftopidil Suppresses Human Renal-Cell Carcinoma by Inducing G1 Cell-Cycle Arrest in Tumor and Vascular Endothelial Cells

Iwamoto

Ishii

Sasaki

et al. 2013

Cancer Prevention Research

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Renal cell carcinoma (RCC) is an angiogenesis-dependent and hypoxia-driven malignancy. As a result, several targeting agents are being investigated. However, the efficacy of current regimens is generally insufficient for their toxicity and poor overall response rates. We have recently reported that naftopidil exerts growth-inhibitory effects on human prostate cancer cells. In this study, we investigated the biochemical mechanisms by which naftopidil produces growth-inhibitory and antiangiogenic effects on RCC. We first tested the effects of naftopidil on the proliferation of ACHN and Caki-2 RCC cells. Next, we set up a model simulating the tumor microenvironment, in which ACHN cells were grafted onto the renal capsule of mice. We then tested the effects of naftopidil on human umbilical vein endothelial cells' cell proliferation and Matrigel plug vascularization. Finally, to establish the antitumor activity of naftopidil on RCC, we tested the antitumor effects of naftopidil on excised tumor specimens from 20 patients with RCC that were grafted beneath the renal capsule of mice. Naftopidil showed similar in vitro growth-inhibitory effects on all cell lines. Fluorescence-activated cell sorting analysis revealed an increase in G 1 cell-cycle arrest in all naftopidil-treated cell lines. In vivo tumorigenic studies showed a significant reduction of ACHN tumor weight, Ki-67 index, and microvessel density (MVD) in naftopidil-treated mice. Naftopidil attenuated neovascularization in an in vivo Matrigel plug assay. Studies in mouse xenograft models also showed a significant MVD reduction in naftopidil-treated excised human RCC. The growth-inhibitory effects of naftopidil suggest it may be a novel anticancer agent and a potential preventive option for RCC. Cancer Prev Res; 6(9); 1000-6. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

Oral Naftopidil Suppresses Human Renal-Cell Carcinoma by Inducing G1 Cell-Cycle Arrest in Tumor and Vascular Endothelial Cells

Iwamoto

Ishii

Sasaki

et al. 2013

Cancer Prevention Research

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“…In regard to treatment for BPH, a 1 -AR antagonists are the most widely used therapeutic agents. Although the incidence of BPH increases with age, this increase occurs faster than that of PCa (3). In addition, most PCa arises in the prostate concomitant with BPH elsewhere (4).…”

Section: Introductionmentioning

confidence: 95%

Naftopidil, a Selective α1-Adrenoceptor Antagonist, Suppresses Human Prostate Tumor Growth by Altering Interactions between Tumor Cells and Stroma

Hori

Ishii

Kanda

et al. 2011

Cancer Prevention Research

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In prostate cancer, tumor-stroma interactions play a critical role in the promotion of tumorigenesis, and thus the prevention of those interactions is a promising target to suppress tumor growth. Several studies demonstrated that alpha 1 -adrenoceptor (a 1 -AR) antagonists, therapeutic drugs for benign prostatic hyperplasia, have growth inhibitory effects on human prostate cancer (PCa) cells through induction of apoptosis or G 1 cell-cycle arrest. However, their direct actions on stromal cells surrounding cancer cells have not yet been elucidated. In this study, we investigated the effects of subtype-selective a 1 -AR antagonists (naftopidil, tamsulosin, and silodosin) on prostate tumor growth with a focus on the role of stroma, using commercially available fibroblast cells (PrSC). Tumorigenic studies in vivo showed significant reductions in tumor growth when E9 cells (an androgen low-sensitive LNCaP subline) grafted with PrSC were treated with naftopidil. In in vitro analyses, naftopidil and silodosin showed antiproliferative effects on PCa cells regardless of androgen sensitivity and a 1 -AR subtype expression. In PrSC, a strong growth inhibitory effect was observed with naftopidil but not silodosin. Flow cytometric analysis revealed that naftopidil, but not silodosin, induced G 1 cell-cycle arrest in both PCa cells and PrSC. In naftopidil-treated PrSC, total interleukin-6 protein was significantly reduced with increased suppression of cell proliferation. Silodosin induced weak early apoptosis only in PCa cells. These findings demonstrated that naftopidil strongly suppressed cell proliferation of stromal cells, resulting in decreased tumorigenic soluble factor, suggesting that naftopidil might be effective in preventing stromal support of tumor cells.

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“…Mp-MRG'nin bu hasta grubunda BPH-kanser ayrımında, zonal ve tüm prostat volüm değerlendirmesinde, büyüyen segmentin saptanmasında, stromal ve glandü-ler dokunun oranına göre tedavi kararının verilmesinde potansiyel kullanımı alanı vardır [26]. Prostat kanseri ve BPH popülasyonda yaşam süresinin uzaması ve yaşlı nüfusun artışıyla birlikte ciddi bir sağlık problemi haline gelmiştir [27][28][29]. BPH'nın görülme sıklığı 50'lili yaşlar-da 1/4 iken, 60'lı yaşlarda 1/3 oranındadır [30,31].…”

Section: Multiparametrik Prostat Manyetik Rezonans Görüntülemeunclassified

Benign Prostat Hiperplazisi

Danacı¹,

Fakultesi²

2018

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Is There Evidence of a Relationship between Benign Prostatic Hyperplasia and Prostate Cancer? Findings of a Literature Review

Cited by 194 publications

References 70 publications

Oral Naftopidil Suppresses Human Renal-Cell Carcinoma by Inducing G1 Cell-Cycle Arrest in Tumor and Vascular Endothelial Cells

Oral Naftopidil Suppresses Human Renal-Cell Carcinoma by Inducing G1 Cell-Cycle Arrest in Tumor and Vascular Endothelial Cells

Naftopidil, a Selective α1-Adrenoceptor Antagonist, Suppresses Human Prostate Tumor Growth by Altering Interactions between Tumor Cells and Stroma

Benign Prostat Hiperplazisi

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