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Shinsuke Kurokawa

Publications and source records attributed to Shinsuke Kurokawa.

4 recordsLinked to original sources
PubMed2005

Intraindividual variation in total and percent free prostate-specific antigen levels in prostate cancer suspects.

OBJECTIVES: To investigate intraindividual total and percent free serum prostate-specific antigen (PSA) in prostate cancer suspects and to understand the clinical implications. PATIENTS AND METHODS: Total and percent free PSA were measured using Tandem-R or chemiluminescent enzyme-linked immunoassay for a median of three times in 126 men. Prostate biopsies were performed in all patients; benign prostatic hyperplasia was diagnosed in 81 patients and prostate cancer in 45 patients. RESULTS: The overall mean coefficients of variation for total and percent free PSA were 16.10 +/- 11.94% and 15.45 +/- 15.91%, respectively. A significant correlation (p = 0.0056) was observed between the two variations. The variations in total and percent free PSA were related to none of such stratifications as baseline total PSA level, histology, age, or measurement interval, but for measurement interval on that for total PSA. CONCLUSION: Intraindividual variation in serum PSA should be considered in decision-making about performing prostate biopsies. Also, care should be taken in interpreting repeated percent free PSA measurements in order to enhance the specificity of total PSA, because it had a similar variation to total PSA variation.

Aged↗
PubMed2003

Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer.

BACKGROUND: The neuroendocrine (NE) pathway has been attracting attention as a mechanism for the androgen-independent progression because the neuropeptide provokes tumor growth and inhibits apoptosis under androgen-deprived milieu in prostate cancer cells. On the basis that serum progastrin-releasing peptide (ProGRP) is elevated in patients with advanced disease stage, we examined the prognostic value of the neuropeptide. METHODS: Serum ProGRP status was determined with an enzyme-linked immunosorbent assay (ELISA) in 460 men with benign and malignant prostatic diseases, chronic renal failure, and healthy controls. Seventy patients with metastatic prostate cancer including four patients (5.7%) with NE carcinoma who underwent hormonal therapy were enrolled in the prognostic analyses by Cox proportional hazards model. RESULTS: The serum status steadily shifted toward predominant expression of ProGRP with the progression of prostate cancer into metastatic and androgen-independent stages. Univariate analysis revealed that the deteriorated performance status (PS) and extent of bony disease (EOD), and high serum alkaline phosphatase (ALP), serum ProGRP, and nadir prostate-specific antigen (PSA) levels were associated with a lower progression-free survival (PFS) rate (P < 0.005). Multivariate analysis demonstrated that PS, serum ProGRP, and nadir PSA held an independent predictive value for PFS (P < 0.05), and all correlated with bone-related factors. Serum ProGRP was the most significant predictor among pre-treatment factors in this model (P = 0.0094). CONCLUSIONS: The neuropeptide precursor ProGRP is a distinct serum marker that is useful to know the NE milieu and provides prognostic information in patients with advanced prostate cancer. Standard therapy for metastatic prostate cancer may make progress when further studies will clarify the causative link between serum ProGRP level and androgen-independent disease progression.

Adult↗
PubMed2003

Forced expression of cytidine deaminase confers sensitivity to capecitabine.

OBJECTIVE: Cytidine deaminase (CDD) is involved in the metabolism of new pyrimidine analogues, capecitabine (N(4)-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine) and gemcitabine (2',2'-difluorodeoxycytidine). The purpose of the present study was to directly examine the role of CDD in tumor cells themselves in mediating the sensitivity to capecitabine compared with gemcitabine. METHODS: The human bladder cancer cell line T24 was transfected with human CDD2 cDNA by the lipofectin method. RESULTS: Transfection of CDD2 cDNA did not change the levels of thymidine phosphorylase, dihydropyrimidine dehydrogenase and thymidylate synthase (TS) but increased the CDD activity significantly (p < 0.01). Forced expression of CDD made T24 sensitive to 5'-deoxy-5-fluorocytidine (5'DFCR) in vitro and capecitabine in vivo, but resistant to gemcitabine both in vitro and in vivo. Tetrahydrouridine, a specific CDD inhibitor, abrogated the changes in the in vitro sensitivity to 5'DFCR and gemcitabine by transfection of CDD2 cDNA. Transfection of CDD2 cDNA resulted in a significant increase in cellular 5-fluorouracil level (p < 0.01) and inhibition of TS activity (p < 0.01) after treatment with 5'DFCR in vitro. CONCLUSIONS: The present study clearly showed direct evidence for the contribution of CDD in tumor cells themselves to the sensitivities to capecitabine and gemcitabine.

Animals↗