Prevention of urinary bladder cancer in the FHIT knock-out mouse with Rofecoxib, a Cox-2 inhibitor

D’Arca, Domenico; LeNoir, James; Wildemore, Bernadette; Gottardo, Fedra; Bragantini, Emma; Shupp-Byrne, Dolores; Zanesi, Nicola; Fassan, Matteo; Croce, Carlo M.; Gomella, Leonard G.; Baffa, Raffaele

doi:10.1016/j.urolonc.2009.01.016

Cited by 14 publications

(10 citation statements)

References 26 publications

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“…Several studies have supported the involvement of cyclooxygenase-2 expression in carcinogenesis [9][10][11][12][13]. Indeed, increased expression of COX-2 and antiproliferative effects of COX-2 inhibitors were found in several types of cancer such as osteosarcoma [14], colorectal carcinomas [15,16], urinary bladder cancer [17], breast cancer [18], prostate cancer [19] and lung cancer [11,20]. Furthermore, preclinical studies in vivo have supported the benefit of COX-2 inhibition in cancer [21][22][23][24][25].…”

Section: Introductionmentioning

confidence: 94%

COX-2 Inhibitors, a Potential Synergistic Effect with Antineoplastic Drugs in Lung Cancer

Hohenforst-Schmidt¹,

Petanidis²,

Zogas³

et al. 2017

Oncomedicine

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Background: Lung cancer represents the leading cause of cancer-related deaths worldwide and novel therapeutic approaches targeting crucial pathways are urgently needed to improve its treatment. Inflammation plays a critical role in multistage tumor development and increased evidence has supported the involvement of cyclooxygenase-2 expression in carcinogenesis. We investigated the potential use of COX-2 inhibitors in cancer proliferation and apoptosis. Methods: Celecoxib, rofecoxib, etoricoxib, meloxicam, ibufrofen and indomethacin are the COX-2 inhibitors included in this study. Docetaxel and Cisplatin are the chemotherapeutic agents that we combined with COX-2 inhibitors. Lung cancer cell lines (NCI-H1048-Small cell lung cancer, A549-Non-small cell lung cancer) were purchased from ATCC LGC Standards. At indicated time-point, following 24h and 48h incubation, cell viability and apoptosis were measured with Annexin V staining by flow cytometry. Statistical analysis was performed by GraphPad Prism. Results: In Small cell lung cancer cells, following 24h incubation, combinations of docetaxel and meloxicam, docetaxel and ibuprofen, docetaxel and indomethacin, showed increased apoptosis when compared to docetaxel alone (p<0.0001). In Non-small cell lung cancer cells, the 24h incubation was not enough to induce satisfactory apoptosis, but following 48h incubation, docetaxel plus indomethacin showed more cytotoxicity when compared to docetaxel alone (p<0.0001). In addition, the combination of cisplatin plus indomethacin was the only combination to be found with higher cytotoxicity when compared to cisplatin alone after 48h treatment (p<0.0001). Conclusion: Depending on the drug, the synergistic effect of COX-2 inhibitors plus chemotherapeutic agents has been demonstrated in lung cancer. Our suggestion is that COX-2 inhibitors could be used as additive and maintenance treatment in combination to antineoplastic agents in lung cancer patients.

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Section: Introductionmentioning

confidence: 94%

COX-2 Inhibitors, a Potential Synergistic Effect with Antineoplastic Drugs in Lung Cancer

Hohenforst-Schmidt¹,

Petanidis²,

Zogas³

et al. 2017

Oncomedicine

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“…A particularly significant risk reduction (43%) was observed for non-smokers [61]. Experiments on mice with bladder cancer induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BNN) demonstrated that rofecoxib (a selective COX-2 inhibitor) caused a considerable decrease in the incidence of precancerous lesions and tumors [62]. The effects for meloxicam were not statistically significant [63].…”

Section: Non-steroidal Anti-inflammatory Drugsmentioning

confidence: 99%

Bladder cancer prevention

Długosz

Królik²

2017

Nowotwory. Journal of Oncology

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“…Similar reports later confirmed this finding, and the chemoprevention effect covered urinary bladder cancer (83). The effect of NSAIDs, including aspirin, celecoxib, rofecoxib, naproxen and indomethacin, was evidenced by results in the BBN-induced models (84–89). Other agents, including histone deacetylase inhibitor (90), sulforaphone (91), sirolimus (92), atorvastatin (93), and natural extracts or compounds including green tea polyphenol (94), cranberry juice concentrate (95), aqueous extract of sclerotia of Polyporus umbellatus Fries (96) and isothiocyanates (97) have also been demonstrated to possess efficacy in the prevention of bladder tumor development, although some herbal extracts were revealed not to be as effective as previously thought (98).…”

Section: Carcinogen-induced Modelsmentioning

confidence: 99%

“…P27 knock-out mice are more sensitive to MNU, while Stat3-transgenic mice, Fez1/Lzts1-deficient, Keap1 knock-out and FHIT knock-out mice are more susceptible to BBN (89,124–127). As the inducing period was curtailed, studies using carcinogen-induced GEM models could save time, which combines the advantages of the two types of model.…”

Section: Transgenic Modelsmentioning

confidence: 99%

Current animal models of bladder cancer: Awareness of translatability (Review)

Ding

Pan

et al. 2014

Experimental and Therapeutic Medicine

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Experimental animal models are crucial in the study of biological behavior and pathological development of cancer, and evaluation of the efficacy of novel therapeutic or preventive agents. A variety of animal models that recapitulate human urothelial cell carcinoma have thus far been established and described, while models generated by novel techniques are emerging. At present a number of reviews on animal models of bladder cancer comprise the introduction of one type of method, as opposed to commenting on and comparing all classifications, with the merits of a certain method being explicit but the shortcomings not fully clarified. Thus the aim of the present study was to provide a summary of the currently available animal models of bladder cancer including transplantable (which could be divided into xenogeneic or syngeneic, heterotopic or orthotopic), carcinogen-induced and genetically engineered models in order to introduce their materials and methods and compare their merits as well as focus on the weaknesses, difficulties in operation, associated problems and translational potential of the respective models. Findings of these models would provide information for authors and clinicians to select an appropriate model or to judge relevant preclinical study findings. Pertinent detection methods are therefore briefly introduced and compared.

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Prevention of urinary bladder cancer in the FHIT knock-out mouse with Rofecoxib, a Cox-2 inhibitor

Cited by 14 publications

References 26 publications

COX-2 Inhibitors, a Potential Synergistic Effect with Antineoplastic Drugs in Lung Cancer

COX-2 Inhibitors, a Potential Synergistic Effect with Antineoplastic Drugs in Lung Cancer

Bladder cancer prevention

Current animal models of bladder cancer: Awareness of translatability (Review)

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