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Katsusuke Naito

Publications and source records attributed to Katsusuke Naito.

At least 55 records · Page 3Linked to original sources

Clinical significance of chromosome 8p, 10q, and 16q deletions in prostate cancer.

BACKGROUND: We lack simple and reliable diagnostic tools to predict pathological staging as well as further progression of prostate cancer in individual cases. METHODS: We studied deletions on 8p (8p22 and 8p23-pter), 10q (10q24-qter), and 16q (16q24) by fluorescence in situ hybridization in 53 specimens from patients with prostate cancer, and compared the status of these deletions with various clinical parameters. Forty-five cases were further evaluated regarding disease progression with a median follow-up period of 62 months. RESULTS: The overall frequencies of deletions for 8p, 10q, and 16q were 74, 55, and 55%, respectively. The frequency of 8p and 16q deletions increased significantly in parallel with tumor grade (P < 0.01 and < 0.05, respectively), while that of 10q deletions did not. Patients whose tumors showed 8p22 deletions had a significantly higher frequency in pT3 or metastatic tumors than in pT2 tumors. Patients whose tumors showed both 8p22 and 16q24 deletions had a significantly higher frequency of nodal metastases than non-metastases. A Cox hazard proportional model revealed 8p22 deletion to be the strongest parameter predictive of disease progression (hazard ratio = 6.624; P = 0.0001). CONCLUSION: Estimation of 8p22 and 16q24 deletions may serve as a genetic diagnosis for predicting pathological staging as well as disease progression in prostate cancer.

Aged↗

Granulocyte colony-stimulating factor may promote proliferation of human bladder cancer cells mediated by basic fibroblast growth factor.

OBJECTIVES: To investigate whether granulocyte colony-stimulating factor (G-CSF) promotes the proliferation of two bladder cancer cell lines, and to assess the mechanism of tumor proliferation in terms of cytokine expression. MATERIAL AND METHODS: The proliferation of two bladder cancer cell lines derived from transitional cell carcinoma (KK-47 and T-24) was assessed by using the double-layer soft agarose colony assay in combination with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Seven cytokines were measured in the culture supernatant. Expression of granulocyte colony-stimulating factor (G-CSF) receptor and fibroblast growth factor (FGF) receptor mRNA was studied by means of reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: Recombinant human G-CSF (rhG-CSF) caused greater induction of the proliferation of KK-47 cells in the presence than in the absence of peripheral blood mononuclear cells (PBMCs) and its effect was dose-dependent. In contrast, rhG-CSF did not stimulate the proliferation of T-24 cells. Among several cytokines measured, only basic FGF was elevated in cultures of KK-47 cells with or without PBMCs. The basic FGF level was significantly increased by rhG-CSF stimulation in a dose-dependent manner. Specific PCR products for the G-CSF and FGF receptors were observed in KK-47 cells as well as PBMC, while no G-CSF receptor was detected in T-24 cells. CONCLUSION: rhG-CSF may promote the proliferation of KK-47 cells, probably via an increase in basic FGF production.

Carcinoma, Transitional Cell↗

Transforming growth factor-beta1 and renal cell cancer: cell growth, mRNA expression and protein production of cytokines.

PURPOSE: We evaluated the effects of transforming growth factor-beta1 (TGF-beta1) on growth activity, cytokine mRNA expression and cytokine protein production by renal cancer cells. MATERIALS AND METHODS: Exogenous continuous exposure of biologically active TGF-beta1 was performed on ACHN cells at various concentrations of 0.1 to 30 ng./ml. and the number of cells was counted each culture day. To determine the index of S-phase cells the bromodeoxyuridine pulse labeling method was used. Reverse transcriptase-polymerase chain reaction (PCR) was done and PCR products were quantified. Each supernatant cytokine level was measured using an enzyme-linked immunosorbent assay. RESULTS: TGF-beta1 significantly inhibited the growth activities of ACHN cells compared with controls. Bromodeoxyuridine labeling indexes after treating ACHN cells with TGF-beta1 (10 ng./ml.) showed that it began to decrease gradually after 24 hours and after 72 hours it was inhibited to approximately 40% compared with controls. The mRNA of TGF-beta1, TGF-beta types 1 and 2 receptors, interleukin-6 (IL-6) and granulocyte-macrophage colony-stimulating factor (GM-CSF) from ACHN cells was detected by reverse transcriptase-PCR assay. IL-6 and GM-CSF proteins were produced constitutively from ACHN cells but other cytokines were not. Adding TGF-beta1 to the cell culture medium did not influence mRNA expression, or the protein production of IL-6 or GM-CSF. CONCLUSIONS: The inhibition of growth activities of ACHN cells by TGF-beta1 are mediated by its direct binding to specific receptors on ACHN cells followed by cell cycle inhibition, while TGF-beta1 seems to have no effect on the production of the cytokines studied.

Carcinoma, Renal Cell↗

Angiotensin II dependent testicular fibrosis and effects on spermatogenesis after vasectomy in the rat.

PURPOSE: Vasectomy induces testicular interstitial fibrosis in time dependent fashion and inhibits spermatogenesis. We investigated the contribution of angiotensin II (Ang II) to the development of interstitial fibrosis after vasectomy. MATERIALS AND METHODS: Bilateral vasectomy was performed in 8-week-old Wistar rats and the testes were harvested 1 to 24 weeks after vasectomy. Interstitial fibrosis was evaluated by Masson's trichrome staining. Western blotting and immunohistochemistry were done to examine the expressions of heat shock protein 47 (HSP47), HNE (4-hydroxy-2,3-nonenal) and transforming growth factor-beta1 (TGF-beta1). The antioxidative agent N-acetylcysteine (NAC), the Ang II type 1 receptor antagonist losartan or the Ang converting enzyme inhibitor enalapril was given orally for 24 weeks to vasectomized rats. Spermatogenesis was evaluated by testicular weight and the percent of haploid cells was analyzed by flow cytometry. RESULTS: Vasectomy significantly increased interstitial fibrosis (more than 8 weeks) and induced the expression of HSP47, HNE modified protein and TGF-beta1. TGF-beta1 and HSP47 immunoreactivity was localized to Leydig cells and fibroblasts. NAC or losartan but not enalapril inhibited the expression of these molecules induced by vasectomy. Increased interstitial fibrosis and impaired spermatogenesis were partially abrogated by NAC or losartan administration. CONCLUSIONS: There is Ang II type 1 receptor dependent fibrosis after vasectomy. Oxidative condition is considered to trigger and promote these fibrogenic processes. Ang II contributes to the regulation of intratesticular autocrine or paracrine functions after vasectomy.

Acetylcysteine↗

Fertile eunuch syndrome with the mutations (Trp8Arg and Ile15Thr) in the beta subunit of luteinizing hormone.

Fertile eunuch syndrome is caused by isolated LH deficiency, but its pathophysiology still remains controversial. We report a case of fertile eunuch syndrome with homozygous Trp8Arg and Ile15Thr mutations in the LH beta subunit gene. An 18-year-old man was admitted to our hospital for hypogonadism. Examination of genitalia revealed Tanner G1PH1, whereas both testes were elastically palpated and developed up to 18 ml. Endocrinological evaluations revealed normogonadotropic hypogonadism and there were normal responses after GnRH and hCG stimulation. Intratesticular testosterone concentration was almost normal (1.34 x 10(3) ng/g). By PCR direct sequencing, homozygous Trp (8) Arg and Ile (15) Thr mutations in exon 2 of LH beta were detected. Normal virilization and improved semen parameters were achieved after hCG supplementation. To our knowledge, this is the first case of fertile eunuch syndrome with homozygous Trp (8) Arg and Ile (15) Thr mutations in beta subunit of LH gene.

Adolescent↗

Difference between Swedish and Japanese men in the association between AR CAG repeats and prostate cancer suggesting a susceptibility-modifying locus overlapping the androgen receptor gene.

Previous studies have shown that short CAG repeats in the androgen receptor (AR) gene are associated with increased risk of prostate cancer. It is unclear if this association is due to linkage disequilibrium with a susceptibility locus or directly linked to the possible functional impact of the length of the CAG repeats. In this study, the number of the AR CAG repeats was determined in prostate cancer patients, benign prostatic hyperplasia (BPH) patients, and controls in both Swedish and Japanese men. Prostate cancer patients included 59 Swedish hereditary, 59 Swedish sporadic and 33 Japanese sporadic cases. BPH patients included 38 Swedish and 33 Japanese cases. Controls included 98 Swedish healthy men and 43 Japanese men without either prostate cancer or BPH. No significant difference in AR CAG repeats was found in comparison between BPH patients and controls. In contrast, both Swedish hereditary and sporadic prostate cancer patients had shorter AR CAG repeats than Swedish controls, but Japanese prostate cancer patients had longer repeats than controls. These differences between the two populations in the association of prostate cancer and the AR CAG repeats may suggest that the AR CAG repeats are in linkage disequilibrium with a prostate cancer susceptibility locus localized in a small region flanking or overlapping the AR gene at Xq12.1.

Adolescent↗

[Signet ring cell carcinoma of the prostate successfully treated with endocrine therapy: a case report].

A 67-year-old man complained of dysuria. The prostate was enlarged and stony hard. The serum level of prostate specific antigen was abnormally high (46.2 ng/ml). Prostatic biopsy showed signet ring cells which were stained positive for prostate specific antigen and poorly differentiated adenocarcinoma. Computed tomographic scan revealed the enlargement of the para-aortic lymph nodes. Endocrine therapy with luteinizing hormone-releasing hormone agonist was started. After two months, the serum level of prostate specific antigen decreased to the normal range. The pathological findings and the good response to endocrine therapy in our case suggest that signet ring cell carcinoma of the prostate is only a morphologic variant of ordinary prostatic adenocarcinoma.

Aged↗

[Tuberculous epididymitis caused by intravesical BCG therapy: a case report].

We describe a case of tuberculous epididymitis that occurred 35 months after completion of a course of intravesical Bacillus Calmette-Guerin (BCG). A 67-year-old man had received trasuretheral resection for bladder cancer in February 1997. Two weeks after the operation, a course of 8 weekly intravesical instillations of BCG (Tokyo 172 strain) was carried out between March and April, 1997. Under the diagnosis of benign prostatic hypertrophy, transuretheral resection of the prostate was performed in March 1998. Multiple tuberculous nodules were histopathologically detected in resected prostatic tissues. The patient complained of a small nodule in the right epididymal tail in August 2001. The nodule developed during 6 weeks, with spontaneous perforation of the scrotal skin and discharge of pus. The pus contained acid-fast bacilli, which were shown to be tubercle bacilli by polymerase chain reaction (PCR) with pan-mycobacterium primer. MPB64-T2, T6 and pncA-7, 11C were positive, while PT-1, 2 and pncA-7, 10 were negative by PCR. These results revealed that Mycobacterium bovis (BCG Organism) was the cause of the epididymitis. Drug therapy for 3 months with rifampicin, isoniazid and ethambutol was initiated in September 2001, and right orchiectomy was performed in October. Histopathological examination showed tuberculous epididymitis. In this case, persistent BCG organisms may have reached the epididymis from the prostate, and may have been activated by immunosuppression associated with aging. In addition, PCR with species-specific primers was useful in differentiating Mycobacterium bovis from Mycobacterium tuberculosis.

Administration, Intravesical↗

[Transitional cell carcinoma of the ureter with inverted proliferation: a difficult case to make a differential diagnosis with ureteral polyp].

A 59-year-old man was admitted to our hospital in June 2001 for evaluation of an asymptomatic microscopic hematuria. One year prior to presentation, he had a spontaneous discharge of a left ureteral stone. Excretory urography and retrograde pyelography showed a filling defect in the middle portion of the left ureter. Cystoscopic examination did not reveal any abnormality, and urinary cytology was class I. Cold cup biopsy was performed under ureteroscopy, and pathology revealed inflammatory fibrovascular tissue but with no malignancy. Selective washing cytology was class III, whereas selective washing cytology done at the referring hospital was reported to be class V. Under a preoperative diagnosis of a left fibroepithelial ureteral polyp or a transitional cell carcinoma, left segmental ureterectomy was performed. The tumor was 5 x 5 x 5 mm in size, pedunculated, and smooth-surfaced. Intraoperative pathological examination of a frozen section showed an inverted type transitional cell carcinoma. Therefore, a left nephroureterectomy was performed, and the final histopathological examination confirmed an inverted type transitional cell carcinoma of grade 2. The patient is healthy and free of disease 15 months after operation. We also reviewed the current literature relating to transitional cell carcinomas of the ureter with inverted proliferation.

Carcinoma, Transitional Cell↗

Clinical significance of allelic loss of chromosome region 5q22.3 approximately q23.2 in nonpapillary renal cell carcinoma.

To analyze the clinical significance of copy number gain and loss at chromosome region 5q21 approximately q23, 105 nonpapillary renal cell carcinomas (RCC) were examined by interphase cytogenetic analysis using the dual-color fluorescence in situ hybridization (FISH) technique. DNA probes for D5S23 (5p15.2), cCI5-243 (5q21.2 approximately q21.3), and cCI5-215 (5q22.3 approximately q23.2) were used, and the signals for cCI5-243 and cCI5-215 were compared with those for D5S23 as the numerical control. Aneusomy (three or more copies) of chromosome 5 was found in 22 tumors (21.0%). Aneusomy was significantly correlated with loss at 5q21 approximately q23, while disomy with gain at 5q21 approximately q23 (P<0.05). Aneusomy was also significantly related to poor disease-specific survival (P<0.01). Gain and loss at cCI5-243 were seen in 34 (32.4%) and 59 (56.2%) tumors, respectively, while gain and loss at cCI5-215 occurred in 55 (52.4%) and 45 (42.9%) cases, respectively. The frequency of gain at cCI5-215 was significantly correlated with a smaller tumor diameter (7 cm or less, P<0.05), while loss with a larger one (>7 cm, P<0.05). Both loss at cCI5-215 and aneusomy of chromosome 5 were significantly related to poor disease-specific survival (P<0.05). In conclusion, alterations of chromosome 5 (including allelic loss of 5q22.3 approximately q23.2) could be a useful genetic marker for predicting the patient prognosis of RCC.

Adult↗

Numerical aberrations of chromosome 9 in bladder cancer. A possible prognostic marker for early tumor recurrence.

To investigate whether nonrandom aberrations of chromosomal numbers could predict tumor recurrence in patients with bladder cancer, archival urine cytology specimens (Giemsa-stained) from patients previously treated for transitional cell carcinoma of the urinary bladder were studied retrospectively by fluorescence in situ hybridization. A total of 48 patients (pTis, 6; pTa, 2: pT1, 32; and pT2-4, 8) were consecutively enrolled in this study, and numerical aberrations of chromosomes 9 and 17 were investigated. Cytology was diagnosed as negative for malignancy in 18 patients and positive in 30 patients. Twenty-seven of the 48 patients (56%) had one or more chromosomal aberrations. The frequency of numerical aberrations of chromosome 17 was correlated with increasing stage and grade, whereas loss of copies of chromosome 9 (monosomy) was frequently observed at a lower stage and grade. Chromosomal aberrations were detected in 9 (50%) of 18 patients with negative or equivocal cytology (class I, II, or III) by the Papanicolaou classification. Of eight patients with negative or equivocal cytology who developed tumor recurrence, four (50%) showed monosomy 9 and one (14%) showed a numerical aberration of chromosome 17. All six patients who showed monosomy of chromosome 9 developed tumor recurrence within 12 months, whereas four of the nine patients who did not show monosomy of this chromosome developed recurrence within 12 months (P<0.05, Fisher test). These results suggest that monosomy of chromosome 9 might be a prognostic marker for early tumor recurrence in patients with negative or equivocal cytology specimens.

Adult↗

Influence of interstitial fibrosis on spermatogenesis after vasectomy and vasovasostomy.

This study focused on the testicular interstitial fibrosis after vasectomy and the intraseminiferous status [i.e., Johnsen's score, proliferative cell nuclear antigen (PCNA) expression] following vasectomy reversal. Testicular biopsy specimens from 21 consecutive men were obtained at vasovasostomy. Percent of interstitial fibrosis was determined quantitatively by NIH-image after Masson Trichrome staining. PCNA-labeling index (LI) was calculated on each testis. The associations between the obstructive interval and each parameter were examined. These parameters were also analyzed on whether patency or pregnancy was achieved or not. Significant decrease in PCNA-LI and increase in interstitial fibrosis were observed along with the obstructive interval (p <0.0001, p = 0.0005, respectively). Interstitial fibrosis of the patients without patency/fertility was significantly greater than that of the patients with patency/fertility (47.5%/39.0% versus 33.4%/32.3%, p = 0.02/0.04, respectively). PCNA-LI and Johnsen's score did not predict the treatment outcome. Interstistial fibrosis, but not the extent of germ cell differentiation or DNA synthesis, reflects the treatment outcome after vasectomy reversal. Interstistial fibrosis contributes to the irreversible damage of vasectomized testes.

Adult↗

Activation of mitogen activated protein kinases and apoptosis of germ cells after vasectomy in the rat.

PURPOSE: Vasectomy induces a large amount of germ cell apoptosis. We examined the activation of mitogen activated protein kinases (MAPKs) in association with the apoptosis and proliferation of germ cells after vasectomy in the rat. MATERIALS AND METHODS: Eight-week-old Wistar rats underwent bilateral vasectomy and the testes were harvested 1 to 9 days after vasectomy. Germ cell apoptosis was evaluated by terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling and electrophoretic assay of DNA fragmentation. Western blotting and immunohistochemistry were used to examine the temporal and spatial activation of signal regulated kinases 1/2, c-Jun-terminal kinases 1/2 and p38. Phospho-specific MAPK antibodies were used to examine their activations. Proliferation of germ cells was evaluated by proliferative nuclear cell antigen expression. RESULTS: Germ cell apoptosis was detected predominantly in primary spermatocytes with a peak 7 days after vasectomy. Signal regulated kinases 1/2, c-Jun-terminal kinases 1/2 and p38 were constitutively expressed in the control testis. Western blotting and immunohistochemistry showed rapid activation of signal regulated kinases 1/2, followed by activation of c-Jun-terminal kinases 1/2 and p38. Immunohistochemical study demonstrated the temporal and spatial relationships of apoptosis and MAPK activation in primary spermatocytes. On the other hand, proliferating cell nuclear antigen expression was enhanced in tetraploid spermatocyte and spermatogonia maximally 5 days after vasectomy. CONCLUSIONS: MAPKs were rapidly activated after vasectomy and germ cell apoptosis was observed after vasectomy. In contrast to the delayed phase up to 24 weeks after vasectomy, we observed hyperdynamic cellular turnover, spermatocyte loss through apoptosis and enhanced germ cell proliferation transiently at the early phase after vasectomy.

Animals↗

Renal cell carcinoma: allelic loss at chromosome 9 using the fluorescent multiplex-polymerase chain reaction technique.

Loss of tumor-suppressor genes on both arms of chromosome 9 appears to be common in many types of cancer. Chromosome 9q is often partially deleted in bladder cancer, lung cancer, and basal cell carcinoma. However, little data are available on allelic loss on chromosome 9 in renal cell carcinoma (RCC). One hundred and nine nonpapillary RCCs were studied for loss of heterozygosity (LOH) at 13 loci on chromosome 9 by using the fluorescent multiplex-polymerase chain reaction method to compare DNA from tumor samples and peripheral blood lymphocytes. At the loci tested, LOH was found in from 2.3% (9q31, D9S938) to 17% (9q22, 1AJL) of informative cases, and 27 (24.8%) of the 109 RCCs had LOH at 1 or more loci of chromosome 9. LOH was more often detected at 9q22 within the PTCH gene (17%) when compared with LOH at the other 12 loci (P = 0.0172). Regarding the relationship with clinical parameters, however, there were no statistically significant associations between this LOH and tumor stage or grade. Among the 109 tumors, 6 (5.5%) showed replication errors. Our results suggest that LOH of the PTCH gene may be related to the development of nonpapillary RCC, although the clinical relevance has not been not clarified.

Adult↗

Renal metastasis from squamous cell carcinoma of the hypopharynx.

We present a rare case of metastatic renal tumor originating from squamous cell carcinoma of the hypopharynx. A 67-year-old man treated with irradiation for hypopharyngeal carcinoma was referred to our hospital with gross hematuria and a left renal mass, which was delineated as a heterogeneously enhanced mass by CT scan. Left nephrectomy was performed, and the non-encapsulated mass was gray in color macroscopically. Histological examination of the specimen revealed alveolar proliferation of small cancer cells, which was consistent with the original tumor of the hypopharynx. The left renal tumor was diagnosed as poorly differentiated squamous cell carcinoma metastasized from the hypopharynx. The patient remains alive, with no evidence of disease, 8 months following left nephrectomy. This case was thought to be the first report of a renal metastasis from a hypopharyngeal carcinoma that was diagnosed clinically and treated with nephrectomy.

Aged↗

[Small cell carcinoma of the prostate successfully treated with combined chemotherapy and radiotherapy: a case report].

A 49-year-old man complained of dysuria and pollakisuria. The prostate was enlarged, and the serum level of prostate specific antigen was within the normal range. Under the diagnosis of benign prostatic hypertrophy, transurethral resection of the prostate was performed. Unexpectedly, histopathological examination of the resected tissues revealed pure small cell carcinoma. The serum level of progastrin-releasing peptide (ProGRP) was slightly elevated. The cancer was clinically diagnosed as stage C. Pelvic radiotherapy combined with chemotherapy using cisplatin (CDDP) and etoposide (VP-16) was started according to the treatment for limited small cell cancer of the lung. After one month, the serum level of ProGRP decreased to the normal range. After four months, the prostate was reduced in size without any findings of metastases on computed tomography, and prostate biopsy revealed no viable cancer cells.

Carcinoma, Small Cell↗