Hiroshi Matsui

Gunma University, Maebashi-shi, Gunma-ken, Japan

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Publications (52)86.56 Total impact

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    ABSTRACT: Mammalian target of rapamycin inhibitor has exhibited promising anticancer activity for the treatment of renal cell carcinoma (RCC). However, many patients acquire resistance to therapeutic agents leading to treatment failure. The objective of this study was to determine whether treatment with YM155, a novel small molecule inhibitor of survivin, could reverse rapamycin resistance in a rapamycin-resistant RCC.
    Journal of Cancer Research and Clinical Oncology 06/2014; · 2.91 Impact Factor
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    ABSTRACT: Sunitinib is an oral multi-target tyrosine kinase inhibitor approved for treating metastatic renal cell carcinoma (RCC) that is metabolised mainly by CYP3A4 to the pharmacologically active N-desethyl metabolite SU12662. In a phase I clinical trial, the recommended dose of sunitinib with manageable toxicity was determined to be 50 mg day-1 (4 weeks on, 2 weeks off; 4/2 schedule). Although a single dose of up to 350 mg was well tolerated, a case of sunitinib overdose has never been reported. Here, we report the pharmacokinetic analysis of sunitinib and a life-threatening adverse event in a patient with metastatic RCC who took 450 mg of sunitinib as a single dose together with brotizolam.
    British Journal of Clinical Pharmacology 03/2014; · 3.58 Impact Factor
  • Kazuhiro Suzuki, Hiroshi Matsui, Nobuaki Ohtake
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    ABSTRACT: Hereditary and familial prostate cancers respectively account for about 5% and 20% of all prostate cancer in the United States. The most striking characteristic of familial prostate cancer is the early-onset of the disease. In the clinical setting, a family history of prostate cancer is recognized as a high risk for developing prostate cancer, and a risk-based prostate cancer screening program for it has been proposed. Genetic analyses for identifying the susceptible genes have been reported, and it appears that multiple genes are involved in the development of prostate cancer. Recently, genome-wide association studies showed that the single nucleotide polymorphisms located at the 8q24 region had an association with prostate cancer development. Familial prostate cancer, although its incident rate is relatively rare, must be treated as a high-risk group. Further clinical and basic research is warranted to explore the mechanism of prostate cancer development.
    Gan to kagaku ryoho. Cancer & chemotherapy 02/2013; 40(2):159-63.
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    ABSTRACT: The β form of p120 is reported to be a strong coactivator of the androgen receptor. We investigated the gene expression profiles of the α and β forms of p120 in prostate cancer cell lines, benign prostatic hyperplasia (BPH), nontreated prostate cancer (NTPC), and prostate cancer after androgen deprivation therapy (PCA-ADT). We obtained 154 prostate needle biopsy specimens (81 in BPH, 51 in NTPC, and 22 in PCA-ADT). Levels of p120α and β expression were determined by multiplex real-time polymerase chain reaction. Prostate cancer cell lines, LNCaP, PC-3, DU-145, and LNCaP-LA, which is a derivative of LNCaP under androgen deprivation, expressed both p120α and p120β. p120α expression levels were significantly higher than those of p120β in all cell lines examined. In human prostate tissues, p120α expression was significantly higher than that of p120β in BPH and NTPC. p120α expression in BPH was significantly higher than in other groups. In contrast, p120β expression was significantly higher in NTPC and PCA-ADT than in BPH. Expression of the two forms of p120 was not correlated with age, prostate-specific antigen, or Gleason score. The expression profiles of p120α and p120β significantly differ in cancerous and benign prostatic tissues.
    Prostate international. 01/2013; 1(1):10-5.
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    ABSTRACT: Inguinal hernias often occur after radical retropubic prostatectomy (RRP). We present a novel and simple technique for preventing inguinal hernias after RRP, which any surgeon can complete within a few minutes. A total of 230 Japanese prostate cancer patients underwent RRP between January 2007 and September 2011. From July 2009, 115 patients underwent inguinal hernia prevention procedures at the same time as RRP. In this procedure, we released approximately 5 cm of the bilateral vas deferens and spermatic vessels from the peritoneum. In cases in which the processus vaginalis had spread into the abdomen, we ligated it close to the peritoneal cavity and then transected it. The remaining 115 patients who underwent RRP but did not undergo the hernia prevention procedure were used as the control group. The incidence rate of postoperative inguinal hernia was compared between the 2 groups. Inguinal hernias developed during the postoperative follow-up period in 18 of the 115 control patients (15.7%) (median duration, 50 months). The hernia-free survival rate of this group was 89.6% and 84.1% at 1 and 2 postoperative years, respectively. In contrast, only 1 of the 115 patients (0.87%) who underwent the hernia prevention procedure developed an inguinal hernia during the follow-up period (median duration, 27 months). The hernia-free survival rate of this group was 100% at both 1 and 2 postoperative years (P<0.0001). We developed a simple method for preventing post-RRP inguinal hernias. The procedure is easy to perform and produces excellent outcomes.
    Prostate international. 01/2013; 1(2):76-80.
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    ABSTRACT: To investigate the clinical efficacy of low-dose chlormadinone acetate (CMA) in prostate cancer patients who suffer from hot flushes that is a major side effect of androgen deprivation therapy. Our study included 32 prostate cancer patients who had severe hot flush after undergoing hormone therapy for more than 3 months. The average age of the patients was 72.5 years. In the beginning, patients received CMA at 100 mg orally per day. We defined the hot flush as disappeared, improved, or not improved. In patients with disappeared or improved symptoms, we decreased CMA dose to 50 mg per day, and after we reevaluated the effect, we decreased CMA dose to 25 mg per day. When hot flush appeared again at 25 mg per day, we returned the dose of CMA to 50 mg per day. In cases with no change for more than two months, we canceled the treatment of CMA. Hot flush disappeared in 17 patients, improved in 10 patients, and did not improve in 5 patients (reduction in 84% of hot flush patients). The median time to hot flush reduction was 1.16 months. The effect of CMA was maintained at 25 mg per day in 19 patients and at 50 mg per day in 8 patients. No patients had prostate-specific antigen failure in the treatment of CMA. When hot flush appears during treatment with luteinizing hormone-releasing hormone agonist for prostate cancer, it seems that CMA can improve it immediately in most patients.
    Prostate international. 01/2013; 1(3):113-6.
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    ABSTRACT: PURPOSE: One of the most important issues to address when developing an optimal screening system for prostate cancer is investigating appropriate biopsy indications following serum prostate-specific antigen (PSA) measurements in order to maintain high sensitivity and avoid unnecessary biopsy. METHODS: Between April 2004 and December 2007, 239 consecutive men with total PSA levels of 2.0-10.0 ng/mL underwent measurements of PSA, free PSA, and [-2]pro-PSA. We assessed the significance of laboratory-based PSA-related indices including free PSA/total PSA (%f-PSA), p2PSA/free PSA (%p2PSA), p2PSA/%f-PSA, Prostate Health Index (phi, an index combining PSA, free PSA, and p2PSA), total prostate volume (TPV)-adjusted PSA-related indices, including PSA density, %p2PSA density, p2PSA/%f-PSA density, and phi density, and transition zone (TZ) prostate volume-adjusted PSA-related indices such as PSA TZ density (PSATZD), %p2PSA TZD, p2PSA/%fPSA TZD, and phi TZD. RESULTS: The positive biopsy rate was 22.2 %. When sensitivity was fixed at 95 %, unnecessary biopsies could be avoided in 28 % of men when phi was used as a biopsy indication. In cases where total and transition zone prostate volumes were available, the use of %p2PSA density, phi density, p2PSA/%f-PSA TZD, and phi TZD resulted in the avoidance of 48, 47, 54, and 54 % of unnecessary biopsies, respectively, while maintaining a high sensitivity of 90 %. CONCLUSIONS: At 90 and 95 % sensitivity, laboratory-based indices containing p2PSA, particularly phi, showed significantly greater specificity for prostate cancer as compared with %f-PSA. The diagnostic accuracy of prostate volume-adjusted p2PSA-related indices could be excellent, particularly the transition zone volume-adjusted indices at fixed sensitivities of 95 and 90 %.
    World Journal of Urology 08/2012; · 2.89 Impact Factor
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    ABSTRACT: Background:We previously conducted a genome-wide linkage analysis of Japanese nuclear families affected with prostate cancer and showed that the susceptibility to prostate cancer was closely linked to D8S550 at 8p23. The role of farnesyl diphosphate farnesyltransferase (FDFT1), which is located under the peak marker D8S550 at 8p23, and squalene synthase, the enzyme encoded by FDFT1, in prostate cancer was studied.Methods:The association among common variants of FDFT1 with prostate cancer risk, the promoter activities of FDFT1 with different genotypes and the effects of inhibition of squalene synthase were studied, and the FDFT1 transcript levels of human prostate samples were quantified.Results:The A allele of rs2645429 was significantly associated with prostate cancer risk in a Japanese familial prostate cancer population. Rs2645429 was located in the promoter region of FDFT1, and the AA genotype showed significantly increased promoter activity. The knockdown of FDFT1 mRNA expression or squalene synthase inhibition led to a significant decrease in prostate cancer cell proliferation. Additionally, human prostate cancer specimens expressed significantly higher levels of FDFT1 mRNA compared with noncancerous specimens. Finally, aggressive cancers showed higher transcript levels.Conclusions:FDFT1 and its encoded enzyme, squalene synthase, may play an important role in prostate cancer development and its aggressive phenotypes.Prostate Cancer and Prostatic Diseases advance online publication, 1 May 2012; doi:10.1038/pcan.2012.14.
    Prostate cancer and prostatic diseases 05/2012; · 2.10 Impact Factor
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    ABSTRACT: Objectives: Recently, adrenal androgens have been targeted as key hormones for the development of castration-resistant prostate cancer therapeutics. While circulating adrenal androgens originate mainly from the adrenal glands, the testes also supply about 10%. Although widely used in androgen deprivation medical castration therapy, the effect of luteinizing-hormone (LH)-releasing hormone (RH) agonist on adrenal androgens has not been fully studied. In this study, changes in testicular and adrenal androgen levels were measured and compared to adrenocorticotropic hormone (ACTH) levels. To assess the possible role of LH in the adrenal glands, immunohistochemical studies of the LH receptor in normal adrenal glands were performed. Findings: Forty-seven patients with localized or locally progressive prostate cancer were treated with LH-RH agonist with radiotherapy. Six months after initiation of treatment, testosterone, dihydrotestosterone and estradiol levels were decreased by 90-95%, and dehydroepiandrosterone-sulfate (DHEA-S), DHEA, and androstendione levels were significantly decreased by 26-40%. The suppressive effect of LH-RH agonist at 12 months was maintained. ACTH levels showed an increasing trend at 6 months and a significant increase at 12 months. LH receptors were positively stained in the cortex cells of the reticular layer of the adrenal glands. Conclusions: The long-term LH-RH agonist treatment reduced adrenal-originated adrenal androgens. LH receptors in the adrenal cortex cells of the reticular layer might account for the underlying mechanism of reduced adrenal androgens.
    Journal of Andrology 04/2012; · 3.37 Impact Factor
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    ABSTRACT: Docetaxel is a first-line treatment choice in castration-resistant prostate cancer (CRPC). However, the management of CRPC remains an important challenge in oncology. There have been many reports on the effects of rapamycin, which is an inhibitor of the mammalian target of rapamycin (mTOR), in the treatment of carcinogenesis. We assessed the cytotoxic effects of the combination treatment of docetaxel and rapamycin in prostate cancer cells. Furthermore, we examined the relationship between these treatments and survivin, which is a member of the inhibitory apoptosis family. Prostate cancer cells were cultured and treated with docetaxel and rapamycin. The effects on proliferation were evaluated with the MTS assay. In addition, we evaluated the effect on proliferation of the combination treatment induced knockdown of survivin expression by small interfering RNA transfection and docetaxel. Protein expression levels were assayed using western blotting. PC3 cells and xenograft growth in nude mice were used to evaluate the in vivo efficacy of docetaxel and its combination with rapamycin. In vitro and in vivo, the combination of rapamycin with docetaxel resulted in a greater inhibition of proliferation than treatment with rapamycin or docetaxel alone. In addition, in vitro and in vivo, rapamycin decreased basal surviving levels, and cotreatment with docetaxel further decreased these levels. Transfection siRNA against survivin enhanced the cytotoxicity of docetaxel in PC3 cells. The rapamycin-dependent enhancement of the cytotoxic effects of docetaxel was associated with the downregulation of survivin expression. Our results suggest that the combination of docetaxel and rapamycin is a candidate for the improved treatment of advanced prostate cancer.
    Biochemical and Biophysical Research Communications 02/2012; 419(3):584-9. · 2.41 Impact Factor
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    ABSTRACT: A 58-year-old woman was referred to our outpatient clinic for further examination of a mass detected in the right kidney on follow-up ultrasonography performed for active surveillance of right ovarian cancer. Ultrasonography and computed tomography showed a cyst (diameter, 30 mm) with an irregular wall in the middle of the right kidney. Right nephrectomy was performed since malignancy was suspected. Histological findings of the mass indicated cholesterol granuloma. Although cholesterol granulomas in the middle ear have been frequently reported, those in other organs have been reported in few studies. In this patient, the cholesterol granuloma could be barely distinguished from the cancer by using imaging techniques.
    Nippon Hinyōkika Gakkai zasshi. The japanese journal of urology 05/2011; 102(3):586-90.
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    ABSTRACT: Prostate cancer cell proliferation is inhibited by 1a,25-dihydroxyvitamin D(3). Survivin is a member of the inhibitors of apoptosis protein family. Several studies indicate that survivin down-regulation sensitizes human tumor cells of different histological origins to conventional chemotherapeutic drugs. We assessed the effect of survivin gene expression on the proliferation of prostate cancer cells in vitro and in vivo. We also examined the antitumor sensitization effect of survivin inhibition in 1a,25-dihydroxyvitamin D(3) treatment for prostate cancer cells. We knocked down gene expression levels of survivin using siRNA against survivin in vitro and in vivo. We then assessed survivin expression in 1a,25-dihydroxyvitamin D(3) treatment and examined the antitumor sensitization effect of survivin inhibition using siRNA in 1a,25-dihydroxyvitamin D(3) treatment of hormone resistant prostate cancer cells. In vitro and in vivo siRNA against survivin significantly inhibited cell and tumor growth compared with control siRNA. In LNCaP and PC3 cells 1a,25-dihydroxyvitamin D(3) decreased survivin gene expression and inhibited cell proliferation. However, survivin gene expression and cell proliferation were not inhibited in DU145 cells but after siRNA transfection against survivin DU145 cell proliferation was inhibited by 1a,25-dihydroxyvitamin D(3). Findings suggest that survivin has a significant association with prostate cancer cell proliferation and an essential role in 1a,25-dihydroxyvitamin D(3) induced prostate cancer cell growth inhibition. It seems that the eliminating survivin in 1a,25-dihydroxyvitamin D(3) therapy for hormone refractory prostate cancer is a potential therapeutic option.
    The Journal of urology 02/2011; 185(4):1497-503. · 4.02 Impact Factor
  • Journal of Urology - J UROL. 01/2011; 185(4).
  • Journal of Urology - J UROL. 01/2011; 185(4).
  • European Urology Supplements - EUR UROL SUPPL. 01/2011; 10(2):264-264.
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    ABSTRACT: Several prior studies show a relationship between genetic markers at chromosome 8q24 and an increased prostate cancer risk. We confirmed the association of 8q24 markers with prostate cancer in the Japanese population and the association of these genetic variants with clinical characteristics. Included in this study were 134 patients with familial prostate cancer, 158 with sporadic prostate cancer and 119 controls. All were Japanese. We genotyped the 2, 8q24 markers SNP rs1447295 and microsatellite marker DG8S737 using real-time polymerase chain reaction and polymerase chain reaction based assay with fluorescence labeled primers. There was a significant positive association between the DG8S737 -12 allele and familial prostate cancer risk (OR 1.86, 95% CI 1.11-3.00, p = 0.02) and a significant association of risk with the rs1447295 A allele (OR 2.36, 95% CI 1.41-3.94, p = 0.002). Significant associations were noted for each marker in men with a high Gleason score. Two alleles at 8q24 are genetic risk factors for familial prostate cancer and high grade disease.
    The Journal of urology 08/2010; 184(2):738-42. · 4.02 Impact Factor
  • Journal of Urology - J UROL. 01/2010; 183(4).
  • European Urology Supplements - EUR UROL SUPPL. 01/2010; 9(2):273-273.
  • European Urology Supplements - EUR UROL SUPPL. 01/2010; 9(2):75-75.
  • Journal of Urology - J UROL. 01/2010; 183(4).