Bladder Carcinogenesis - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Bladder Carcinogenesis

The Experts below are selected from a list of 3276 Experts worldwide ranked by ideXlab platform

Shoji Fukushima – One of the best experts on this subject based on the ideXlab platform.

  • Vascular endothelial growth factor mRNA levels as a biomarker for short‐term N‐butyl‐N‐(4‐hydroxybutyl) nitrosamine‐induced rat Bladder Carcinogenesis bioassay
    Journal of Applied Toxicology, 2014
    Co-Authors: Shin Wakui, Hideki Wanibuchi, Tomoko Mutou, Hiroyuki Takahashi, Masahiro Ikegami, Shoji Fukushima

    Abstract:

    Generically, carcinogenic effects of chemicals in Bladder Carcinogenesis are judged by induction of papillary or nodular (PN) hyperplasia in rats given N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) for 4 weeks and the test chemical for 22–28 weeks. However, upregulation of vascular endothelial growth factor (VEGF) begins early in rat BBN Bladder Carcinogenesis. To establish a short-term rat Bladder carcinogenic bioassay, we analyzed the correlations between VEGF, VEGF mRNA and Bladder lesions inductions at 10 and 26 weeks after BBN treatment. Six-week-old male Wistar (slc) rats were given 0.05% BBN for 4, 10 or 26 weeks. To avoid individual rat bias, the Bladders were investigated by partial cystectomy at 10 weeks and total cystectomy at 26 weeks. After induction, PN hyperplasia and carcinoma in rats increased with the length of BBN treatment and immunohistochemical VEGF expression also increased following Carcinogenesis, but the immunoreactivity of individual lesions was quite variable. Moreover, induction of PN hyperplasia at 10 weeks’ BBN treatment was not significantly correlated with that at 26 weeks’ treatment; thus, it was not possible to predict the carcinogenic effect due to the induction of PN hyperplasia at 26 weeks’ BBN treatment by that at 10 weeks’ treatment. However, VEGF mRNA levels of rat Bladders at 10 weeks’ BBN treatment revealed a strong significant correlation with the incidence of Bladder lesions at 26 weeks’ treatment. Here, we suggest that quantitative VEGF mRNA levels are a good biomarker for a short-term BBN-induced bioassay for rat Bladder Carcinogenesis. Copyright © 2014 John Wiley & Sons, Ltd.

  • Inhibition of rat urinary Bladder Carcinogenesis by the antiangiogenic drug TNP-470.
    Asian Pacific Journal of Cancer Prevention, 2006
    Co-Authors: Hideki Wanibuchi, Elsayed I Salim, Min Wei, Anna Kinoshita, Keiichirou Morimura, Katsuichi Sudo, Shoji Fukushima

    Abstract:

    Potential inhibitory effects of the antiangiogenic drug TNP-470 on rat urinary Bladder Carcinogenesis were investigated in F344 male rats initiated with 0.05% BBN in the drinking water for 8 weeks. Group 1 was then continuously treated with TNP-470 by subcutaneous injection using osmotic minipump until the end of the experiment; group 2 served as the control with only initiation. The incidences and multiplicities of papillomas and carcinomas in the TNP-470-treated group were significantly decreased compared to the control group values along with the tumor vascular density. In conclusion, TNP-470 can inhibit rat urinary Bladder Carcinogenesis, presumably through its effects on angiogenesis.

  • Assessment of L-ascorbic acid requirement for prolonged survival in ODS rats and their susceptibility to urinary Bladder Carcinogenesis by N-butyl-N-(4-hydroxybutyl)nitrosamine.
    Cancer Letters, 2004
    Co-Authors: Satoru Mori, Susumu Makino, Yasushi Kurata, Yasuyoshi Takeuchi, Motoko Toyama, Toshio Harauchi, Shoji Fukushima

    Abstract:

    Assessment of l-ascorbic acid requirement for prolonged survival in ODS (genotype: od/od) rats and their susceptibility to urinary Bladder Carcinogenesis by N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) were examined. In ODS rats without l-ascorbic acid synthesizing ability, the 50 ppm dietary total ascorbic acid (TAA) was insufficient to survive for 4 weeks, the 250 ppm dietary TAA was sufficient to survive for 36 weeks. In examination of BBN treatment, ODS rats – although showing a lower availability of TAA than the heterozygotes (+/od) and normal (++) rats with l-ascorbic acid synthesizing ability-were equally susceptible to Bladder Carcinogenesis.

Hideki Wanibuchi – One of the best experts on this subject based on the ideXlab platform.

  • Isoleucine, Leucine and Their Role in Experimental Models of Bladder Carcinogenesis
    Branched Chain Amino Acids in Clinical Nutrition, 2015
    Co-Authors: Min Wei, Xiao-li Xie, Shotaro Yamano, Anna Kakehashi, Hideki Wanibuchi

    Abstract:

    Branched chain amino acids (BCAA) may facilitate tumor growth; consequently, it is reasonable to assume that the dietary intake of BCAA may play a role in Bladder Carcinogenesis. To date, however, there is no epidemiological data relevant to a relationship of dietary BCAA with the risk of Bladder cancer. On the other hand, there are a few experimental studies reported in the literature. This chapter focuses on the studies evaluating the effects of l-isoleucine and l-leucine on Bladder Carcinogenesis in experimental animals. These three studies employed a two-stage (initiation–promotion) Carcinogenesis protocol with male F344 rats. The results show that the effects of dietary BCAA on rat Bladder Carcinogenesis is dependent on the type of basal diet used.

  • Ethanol-extracted propolis enhances BBN-initiated urinary Bladder Carcinogenesis via non-mutagenic mechanisms in rats
    Food and Chemical Toxicology, 2015
    Co-Authors: Xiao-li Xie, Shotaro Yamano, Anna Kakehashi, Masaki Fujioka, Kenichiro Doi, Hirokazu Tachibana, He Fang, Hideki Wanibuchi

    Abstract:

    Abstract Ethanol-extracted propolis (EEP) is used for medical, dietetic and cosmetic purposes. In this study, the effects of EEP on urinary Bladder Carcinogenesis, its underlying mechanism and in vivo genotoxicity were investigated. In experiment 1, rats were treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 2 or 4 weeks followed by dietary administration of 0.125, 0.25, 0.5 or 1% EEP for 4 or 32 weeks, respectively. At week 6, the mRNA levels of top2a, cyclin D1 and survivin were significantly elevated in the 0.5 and 1% EEP groups. At week 36, the incidence and multiplicity of urothelial carcinomas and total tumors were markedly elevated in all EEP groups. In experiment 2, rats were fed basal diet or the 1% EEP diet for 13 weeks without carcinogen initiation. Increases in urinary precipitate, cell proliferation and incidence of simple hyperplasia were observed in the 1% EEP group. In experiment 3, dietary administration of 2.5% EEP to gpt delta rats for 13 weeks did not induce any obvious mutagenicity in the urinary Bladder urothelium. Taken together, EEP enhanced BBN-initiated rat urinary Bladder Carcinogenesis in a non-genotoxic manner through increasing formation of urinary precipitate, enhancing cell proliferation and inhibiting apoptosis during the early stages of Carcinogenesis.

  • Vascular endothelial growth factor mRNA levels as a biomarker for short‐term N‐butyl‐N‐(4‐hydroxybutyl) nitrosamine‐induced rat Bladder Carcinogenesis bioassay
    Journal of Applied Toxicology, 2014
    Co-Authors: Shin Wakui, Hideki Wanibuchi, Tomoko Mutou, Hiroyuki Takahashi, Masahiro Ikegami, Shoji Fukushima

    Abstract:

    Generically, carcinogenic effects of chemicals in Bladder Carcinogenesis are judged by induction of papillary or nodular (PN) hyperplasia in rats given N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) for 4 weeks and the test chemical for 22–28 weeks. However, upregulation of vascular endothelial growth factor (VEGF) begins early in rat BBN Bladder Carcinogenesis. To establish a short-term rat Bladder carcinogenic bioassay, we analyzed the correlations between VEGF, VEGF mRNA and Bladder lesions inductions at 10 and 26 weeks after BBN treatment. Six-week-old male Wistar (slc) rats were given 0.05% BBN for 4, 10 or 26 weeks. To avoid individual rat bias, the Bladders were investigated by partial cystectomy at 10 weeks and total cystectomy at 26 weeks. After induction, PN hyperplasia and carcinoma in rats increased with the length of BBN treatment and immunohistochemical VEGF expression also increased following Carcinogenesis, but the immunoreactivity of individual lesions was quite variable. Moreover, induction of PN hyperplasia at 10 weeks’ BBN treatment was not significantly correlated with that at 26 weeks’ treatment; thus, it was not possible to predict the carcinogenic effect due to the induction of PN hyperplasia at 26 weeks’ BBN treatment by that at 10 weeks’ treatment. However, VEGF mRNA levels of rat Bladders at 10 weeks’ BBN treatment revealed a strong significant correlation with the incidence of Bladder lesions at 26 weeks’ treatment. Here, we suggest that quantitative VEGF mRNA levels are a good biomarker for a short-term BBN-induced bioassay for rat Bladder Carcinogenesis. Copyright © 2014 John Wiley & Sons, Ltd.

Samuel M. Cohen – One of the best experts on this subject based on the ideXlab platform.

  • Urinary Bladder Carcinogenesis
    Toxicologic Pathology, 2016
    Co-Authors: Samuel M. Cohen

    Abstract:

    Urinary Bladder Carcinogenesis in rodents bears numerous similarities to the diseases in humans. In rats, the process progresses through the morphologic stages of simple hyperplasia, papillary and nodular hyperplasia, papilloma, noninvasive, and invasive carcinoma. In mice, the pathogenesis can be similar or can follow a sequence of marked dysplasia with or without hyperplasia, leading to carcinoma in situ and ultimately to high-grade invasive carcinoma. Although the papillary and nonpapillary diseases appear to be related in rodents and in humans, they are distinct morphologically, biologically, and molecularly. Numerous classes of genotoxic chemicals have been identified as Bladder carcinogens in rodents, and some of these have also been identified as carcinogenic in humans, most notably, aromatic amines, nitrosamines, and cyclophosphamide. In contrast, nongenotoxic chemicals appear to be highly specific with respect to species, strain, diet, agent, dose, and mechanism. For some, it is unclear whether t…

  • Effects of Diet on Urinary Bladder Carcinogenesis and Cancer Prevention
    Journal of Nutrition, 1997
    Co-Authors: Samuel M. Cohen, Tsuneo Masui, Emily M. Garland, Lora L. Arnold

    Abstract:

    Urine plays a major role in Bladder Carcinogenesis, acting as a transport mechanism for carcinogens, containing several growth factors stimulating cell proliferation, and indirectly affecting chemicals by alterations in concentrations of normal urinary components such as electrolytes, water and proteins. These latter effects are greatly modified by diet composition and consumption and also by water consumption. Several examples of these effects are presented.

  • Effects of diet on urinary Bladder Carcinogenesis and cancer prevention : Symposium: Animal diets for nutritional and toxicological research
    Journal of Nutrition, 1997
    Co-Authors: Samuel M. Cohen, Tsuneo Masui, Emily M. Garland, Lora L. Arnold

    Abstract:

    Urine plays a major role in Bladder Carcinogenesis, acting as a transport mechanism for carcinogens, containing several growth factors stimulating cell proliferation, and indirectly affecting chemicals by alterations in concentrations of normal urinary components such as electrolytes, water and proteins. These latter effects are greatly modified by diet composition and consumption and also by water consumption. Several examples of these effects are presented.