Kentaro Kuroiwa
Memorial Sloan Kettering Cancer Center
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Kentaro Kuroiwa.
BJUI | 2007
Amita Shukla-Dave; Hedvig Hricak; Michael W. Kattan; Darko Pucar; Kentaro Kuroiwa; Hui Ni Chen; Jessica Spector; Jason A. Koutcher; Kristen L. Zakian; Peter T. Scardino
To design new models that combine clinical variables and biopsy data with magnetic resonance imaging (MRI) and MR spectroscopic imaging (MRSI) data, and assess their value in predicting the probability of insignificant prostate cancer.
BJUI | 2006
Theresa M. Koppie; Fernando J. Bianco; Kentaro Kuroiwa; Victor E. Reuter; Bertrand Guillonneau; James A. Eastham; Peter T. Scardino
Authors from New York present their experience with exclusively anteriorly located prostate cancers and compare them to those located only in the posterior part of the prostate. In this very large series, they found that the former group had lower Gleason grades and lower rates of extraprostatic extension.
Molecular Endocrinology | 2010
Masaki Shiota; Akira Yokomizo; Yasuhiro Tada; Junichi Inokuchi; Katsunori Tatsugami; Kentaro Kuroiwa; Takeshi Uchiumi; Naohiro Fujimoto; Narihito Seki; Seiji Naito
There are currently few successful therapies for castration-resistant prostate cancer (CRPC). CRPC is thought to result from augmented activation of the androgen/androgen receptor (AR) signaling pathway, which could be enhanced by AR cofactors. In this study, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) was found to be an AR cofactor. PGC-1alpha interacted with the N-terminal domain of AR, was involved in the N- and C-terminal interaction of AR, and enhanced the DNA-binding ability of AR to androgen-responsive elements in the prostate-specific antigen enhancer and promoter regions to increase the transcription of AR target genes. Silencing of PGC-1alpha suppressed cell growth of AR-expressing prostate cancer (PCa) cells by inducing cell-cycle arrest at the G(1) phase, similar to inhibition of androgen/AR signaling. Furthermore, PGC-1alpha knock-down also suppressed cell growth in the castration-resistant LNCaP-derivatives. These findings indicate that PGC-1alpha is involved in the proliferation of AR-expressing PCa cells by acting as an AR coactivator. Modulation of PGC-1alpha expression or function may offer a useful strategy for developing novel therapeutics for PCa, including CRPC, which depends on AR signaling by overexpressing AR and its coactivators.
Journal of Clinical Pathology | 2009
Kentaro Kuroiwa; Hiroshi Uchino; Akira Yokomizo; Seiji Naito
Aims: To investigate how the biopsy Gleason score (GS) and the clinical risk classification have been changed by the reporting rules. Methods: 565 prostate biopsy specimens were reassessed. Each Gleason pattern, 1 to 5, was interpreted according to the modified Gleason grading system proposed by the International Society of Urological Pathology. The GS for each case was assigned by the previous reporting rules in the institute (OLD rules), applying the overall-scoring, and ignoring a pattern occupying less than 5% and the tertiary pattern. The GS was also assigned according to the NEW rules, applying the highest-core scoring and reflecting a pattern occupying less than 5% and the tertiary pattern. Results: GS upgrading by the NEW rules was observed in 195 (35%) patients. Of these, 179 (92%) patients were upgraded only by applying the highest-core scoring. Of 198 patients with GS 6 by the OLD rules, 22 (11%) were upgraded to GS 3+4. Of 172 patients with GS 3+4 by the OLD rules, 59 (34%) and 28 (16%), respectively, were upgraded to GS 4+3 and ⩾8. Of 108 patients with GS 4+3 by the OLD rules, 63 (58%) were upgraded to GS ⩾8. As a result, the distribution of D’Amico’s clinical risk classification (low, intermediate and high risk) was changed from 26%, 43% and 31% to 23%, 35% and 41%, respectively. Conclusions: Clinicians should be aware that the reporting rules, especially the highest-core scoring, contribute to a significant upward shift of the biopsy GS and risk classification.
BJUI | 2010
Liang Wang; Oguz Akin; Yousef Mazaheri; Nicole Ishill; Kentaro Kuroiwa; Jingbo Zhang; Hedvig Hricak
Study Type – Diagnosis (exploratory cohort) Level of Evidence
The Journal of Urology | 2017
Junichi Inokuchi; Kentaro Kuroiwa; Yoshiyuki Kakehi; Mikio Sugimoto; Toshiki Tanikawa; Hiroyuki Fujimoto; Momokazu Gotoh; Naoya Masumori; Osamu Ogawa; Masatoshi Eto; Chikara Ohyama; Akito Yamaguchi; Hideyasu Matsuyama; Tomohiko Ichikawa; Tomohiko Asano; Atsushi Takenaka; Kiyohide Fujimoto; Raizo Yamaguchi; Tomonori Habuchi; Katsuyoshi Hashine; Yoichi Arai; Norihiko Tsuchiya; Hiroyuki Nishiyama; Nobuo Shinohara; Masashi Niwakawa; Shin Egawa; Seiichiro Ozono; Tomomi Kamba; Kazuo Nishimura; Tatsuo Tochigi
INTRODUCTION AND OBJECTIVES: Chronological age is an important factor in in determining the treatment option and clinical response of patients with upper-tract urothelial carcinoma (UTUC). Much evidence suggests that chronological age alone is an inadequate indicator to predict the clinical response to radical nephroureterecyomy (RNU). On the other hand, prognostic impact of biological age has not been reported previously. Defining the biological age consists of the determination of a number of biological age markers including telomeres, chromatin, and some blood sampling data which is commonly measured in clinical practice. Therefore, the aim of our study was the validation of the prognostic significance of biological age related factors in a large cohort of UTUC patients. METHODS: We retrospectively reviewed the data from 1349 patients with localized UTUC (Ta-4N0M0) treated by RNU. WBC, NLR, Hb, PLT, CRP, Alb, ALP, LDH, Cr, corrected Ca were tested by the Spearman correlation to indicate the direction of association to chronological age. The test yielded significant, negative associations of Hb (P<0.001) and WBC (P1⁄40.010) with chronological age. Hb (g/dl) and WBC (counts/ml) were analyzed to compare the 10-year cancer-specific survival (CSS) by Cox regression analysis as categorical variables (>14, 13-13.9, 12-12.9, 11-11.9, and <11), and (9200-8500, 84996000, 5999-4500, 4499-3200, <3200, and >9200), respectively. To establish the scoring system, we assigned points for these categories, and then correlated the total points to predicted probability of the surviving outcome as follows; point 00000 for Hb >14 (reference) and 13-13.9 (OR: 1.533), point 00100 for 12-12.9 (OR: 2.391), point 00200 for 11-11.9 (OR: 3.015), and point 00300 for <11 (OR: 3.584). For WBC, point 00100 was assigned for >9200 (OR: 2.541) and 00000 was assigned for the rest; 9200-8500 (reference), 8499-6000 (OR: 0.873), 5999-4500 (OR: 0.772), 4499-3200 (OR: 0.486), and <3200 (OR: 1.277). RESULTS: 10-year CSS in higher risk group with score 4 or larger in age<60 was worse than score-0, or 1 in age >80 (mean estimated survival 69.7 months, CI: 33.3-106 v.s. 103.5. CI: 91-115.9). Concordance index between biological age scoring and chronological age was 0.704 for CSS and 0.798 for recurrence-free survival. CONCLUSIONS: The biological age scoring developed for patients with UTUC undergoing RNU. It was applicable to those with localized disease, and performed well in diverse age populations
Radiology | 2006
Oguz Akin; Evis Sala; Chaya S. Moskowitz; Kentaro Kuroiwa; Nicole Ishill; Darko Pucar; Peter T. Scardino; Hedvig Hricak
The Journal of Urology | 2007
Peter T. Scardino; Peter R. Carroll; Michael J. Zelefsky; Oliver Sartor; Hedvig Hricak; Thomas M. Wheeler; Samson W. Fine; John Trachtenberg; Mark A. Rubin; Mak Ohori; Kentaro Kuroiwa; Michel Rossignol; Lucien Abenhaim
Radiology | 2006
Liang Wang; Hedvig Hricak; Michael W. Kattan; Hui Ni Chen; Peter T. Scardino; Kentaro Kuroiwa
Radiology | 2005
Darko Pucar; Amita Shukla-Dave; Hedvig Hricak; Chaya S. Moskowitz; Kentaro Kuroiwa; Semra Olgac; Lanie Ebora; Peter T. Scardino; Jason A. Koutcher; Kristen L. Zakian