Effects of stones and other physical factors on the induction of rodent bladder cancer

Overexpression of annexin a1 induced by terephthalic acid calculi in rat bladder cancer

“…ANNA1 can be transcriptionally activated by various endogenous and exogenous stresses, including lipopolysaccharide [17], phorbol ester [18], inflammatory mediators, heat, H 2 O 2 , and arsenite [19]. Inflammatory mediators are thought to play an important role in bladder carcinogenesis induced by calculi [4]. Therefore, the overexpression of ANNA1 we identified in our animal model is consistent with this concept.…”

Overexpression of annexin a1 induced by terephthalic acid calculi in rat bladder cancer

“…ANNA1 can be transcriptionally activated by various endogenous and exogenous stresses, including lipopolysaccharide [17], phorbol ester [18], inflammatory mediators, heat, H 2 O 2 , and arsenite [19]. Inflammatory mediators are thought to play an important role in bladder carcinogenesis induced by calculi [4]. Therefore, the overexpression of ANNA1 we identified in our animal model is consistent with this concept.…”

Cell Proliferation and DNA Content in Rat Urothelial Lesions after Repeat Intravesical Instillations of Mitomycin C and Bacillus Calmette-Guérin

“…Cell proliferation is regarded as an important factor in allowing bladder carcinogenesis to alter gene in- formation and promote tumor development. Although the mitotic index in rat urothelium is normally very low [28,29] , our results showed that Ki-67-positive cells were present at each layer of the proliferative urothelium. As the urothelium changed from simple hyperplasia to dysplasia and to CIS, the LI value increased.…”

Urothelial Carcinogenesis in the Urinary Bladder of Rats Treated with Naveglitazar, a γ-dominant PPAR α/γ Agonist: Lack of Evidence for Urolithiasis as an Inciting Event

“…However, survival of the males was sufficient through week 80 to detect a strong carcinogenic effect in the bladder, had it been present. In the rat, the most commonly identified indirect (noncompound specific) mechanism of carcinogenicity of the lower urinary tract is increased formation of urinary solids, which leads to chronic irritation, cell proliferation, and eventually, neoplasia (Clayson et al, 1995;Cohen et al, 2002;Cohen, 2005). Because of the previously described association of PPAR α/γ dual agonists with neoplasms of the urothelium, we investigated the potential for naveglitazar to cause changes in urinary composition, inflammation, and cell proliferation.…”

Overexpression of annexin a1 induced by terephthalic acid calculi in rat bladder cancer

“…ANNA1 can be transcriptionally activated by various endogenous and exogenous stresses, including lipopolysaccharide [17], phorbol ester [18], inflammatory mediators, heat, H 2 O 2 , and arsenite [19]. Inflammatory mediators are thought to play an important role in bladder carcinogenesis induced by calculi [4]. Therefore, the overexpression of ANNA1 we identified in our animal model is consistent with this concept.…”

Cell Proliferation and DNA Content in Rat Urothelial Lesions after Repeat Intravesical Instillations of Mitomycin C and Bacillus Calmette-Guérin

“…Cell proliferation is regarded as an important factor in allowing bladder carcinogenesis to alter gene in- formation and promote tumor development. Although the mitotic index in rat urothelium is normally very low [28,29] , our results showed that Ki-67-positive cells were present at each layer of the proliferative urothelium. As the urothelium changed from simple hyperplasia to dysplasia and to CIS, the LI value increased.…”

Urothelial Carcinogenesis in the Urinary Bladder of Rats Treated with Naveglitazar, a γ-dominant PPAR α/γ Agonist: Lack of Evidence for Urolithiasis as an Inciting Event

“…However, survival of the males was sufficient through week 80 to detect a strong carcinogenic effect in the bladder, had it been present. In the rat, the most commonly identified indirect (noncompound specific) mechanism of carcinogenicity of the lower urinary tract is increased formation of urinary solids, which leads to chronic irritation, cell proliferation, and eventually, neoplasia (Clayson et al, 1995;Cohen et al, 2002;Cohen, 2005). Because of the previously described association of PPAR α/γ dual agonists with neoplasms of the urothelium, we investigated the potential for naveglitazar to cause changes in urinary composition, inflammation, and cell proliferation.…”

Overexpression of annexin a1 induced by terephthalic acid calculi in rat bladder cancer

“…ANNA1 can be transcriptionally activated by various endogenous and exogenous stresses, including lipopolysaccharide [17], phorbol ester [18], inflammatory mediators, heat, H 2 O 2 , and arsenite [19]. Inflammatory mediators are thought to play an important role in bladder carcinogenesis induced by calculi [4]. Therefore, the overexpression of ANNA1 we identified in our animal model is consistent with this concept.…”

Cell Proliferation and DNA Content in Rat Urothelial Lesions after Repeat Intravesical Instillations of Mitomycin C and Bacillus Calmette-Guérin

“…Cell proliferation is regarded as an important factor in allowing bladder carcinogenesis to alter gene in- formation and promote tumor development. Although the mitotic index in rat urothelium is normally very low [28,29] , our results showed that Ki-67-positive cells were present at each layer of the proliferative urothelium. As the urothelium changed from simple hyperplasia to dysplasia and to CIS, the LI value increased.…”

Urothelial Carcinogenesis in the Urinary Bladder of Rats Treated with Naveglitazar, a γ-dominant PPAR α/γ Agonist: Lack of Evidence for Urolithiasis as an Inciting Event

“…However, survival of the males was sufficient through week 80 to detect a strong carcinogenic effect in the bladder, had it been present. In the rat, the most commonly identified indirect (noncompound specific) mechanism of carcinogenicity of the lower urinary tract is increased formation of urinary solids, which leads to chronic irritation, cell proliferation, and eventually, neoplasia (Clayson et al, 1995;Cohen et al, 2002;Cohen, 2005). Because of the previously described association of PPAR α/γ dual agonists with neoplasms of the urothelium, we investigated the potential for naveglitazar to cause changes in urinary composition, inflammation, and cell proliferation.…”