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Celecoxib - A Selective Cyclooxygenase-2 Inhibitor Exhibits Dose - Dependent Chemopreventive Activity on an Animal Model of Colorectal Cancer*

100%
Spychalski M., Dziki Ł., Buczyński J., Kulig A., Sporny S., Dziki A.
Polish Journal of Surgery
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2008
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vol. 80
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issue 5
248-255
EN
Colorectal cancer (CRC) is still one of the unresolved issues in medicine. Despite constant improvements in diagnosis and treatment, the prognosis for CRC is unsatisfactory. In recent years, much attention has been paid to experiments concerning chemoprevention of CRC.The aim of the study was evaluation of the effectiveness of celecoxib, a selective Cyclooxygenase-2 (COX-2) inhibitor of chemically-induced CRC carcinogenesis in Fisher F344 rats.Material and methods. Forty-five four-week old male F344 rats were randomized into four groups. In Groups 1, 2, and 3, we induced the CRC carcinogenesis through two subcutaneous injections of Azoxymethane in doses of 20 mg/kg. Rats from groups 1 and 2 were treated with celecoxib in doses of 10 and 30 mg/kg from the start of the experiment. Group 4 was a negative control. The experiment ended in the 26th week. We assessed the following parameters: the number of Aberrant Crypt Foci (premalignant lesions in colons) and the immunoexpression indexes: COX-2, Vascular Endothelial Growth Factor (VEGF), and c-myc.Results. Celecoxib reduced the ACF number. The ACF reduction was dose-dependent. The median ACF number per field of vision was as follows for each of the groups: 1.7, 0.75, 3.2, and 0.2. Celecoxib, irrespective of the dose, reduced the VEGF immunoexpression index. We did not observe a reduction of COX-2 or c-myc immunoexpression in the celecoxib groups.Conclusions. In this experiment, we proved that celecoxib possessed chemopreventive activity. Carcinogenesis inhibition by selective COX-2 inhibitor was dose-dependent. We demonstrated that celecoxib hidners angiogenesis, expressed as VEGF immunoexpression. We indirectly confirmed the hypothesis of a celecoxib COX-2 independent pathway mechanism of action.
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Synthesis, COX-1/2 inhibition and antioxidant activities of new oxicam analogues designed as potential chemopreventive agents

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Szczęśniak-Sięga B., Gębczak K., Gębarowski T., Maniewska J.
Acta Biochimica Polonica
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2018
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vol. 65
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issue 2
199-207
EN
Oxicams (e.g. piroxicam, meloxicam) are widely used nonsteroidal anti-inflammatory drugs (NSAIDs). A large body of evidence from epidemiological and preclinical studies has shown that NSAIDs have a chemopreventive effect on different types of cancer, especially in colorectal cancer. Moreover, mounting evidence from preclinical and clinical studies suggests that persistent inflammation functions as a driving force in the journey to cancer. What is more, inflammation induces reactive oxygen and nitrogen species, which cause damage to important cellular components (e.g., DNA, proteins and lipids), which can directly or indirectly contribute to malignant cell transformation. In this study, we discuss the synthesis and the resultant newly synthesized oxicam derivatives which are potentially chemopreventive, and at the same time antioxidant. Compound 9c, with the highest therapeutic index in the LoVo cancer cell line, was found to be the most efficient in ROS scavenging activity under conditions of oxidative stress.
3
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COMBINATIONS OF ISOTHIOCYANATES WITH DRUGS – A CHANCE OR THREAT TO CHEMOPREVENTION AND CANCER TREATMENT?

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Mielczarek L., Chilmonczyk Z., Suchocki P., Wroczyński P., Wiktorska K.
Acta Poloniae Pharmaceutica - Drug Research
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2018
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vol. 75
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issue 4
829-841
EN
Isothiocyanates (ITCs) are a group of compounds of natural origin which exhibit anticancer properties. In addition to the cytotoxic impact on cancer cells, confirmed in the multiple cell lines and the in vivo models, ITCs exhibit the cytoprotective effect in normal cells by regulating the activity of enzymes involved in xenobiotic metabolism. These properties of ITCs have led to a continuing increase in the number of studies which have shown that ITCs can sensitize cancer cells to cytostatic drugs used as standard in cancer therapies. On the other hand these compounds may decrease the effectiveness of drugs by deregulating the metabolising system of the cell. This paper discusses the results of preclinical study on ITCs applications in combination therapy as well as their role in drug metabolism.
4
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Rola mesalazyny w chemoprewencji raka jelita grubego

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Wasilewski A., Cygankiewicz A.
Folia Medica Lodziensia
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2014
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vol. 41
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issue 2
121-137
EN
Colorectal cancer (CRC) is the fourth most commonly diagnosed cancer in females and the third in males. Every year there are more than a million new cases of colorectal cancer and more than six hundred thousand patients die. The risk factors of colorectal cancer include unhealthy lifestyle, genetic predisposition (found in about 25% of cases) and chronic colon inflammation i.e., ulcerative colitis and Crohn's disease. Many studies suggested the protective effect of nonsteroidal anti-inflammatory drugs, including mesalazine, on the chemoprevention of colorectal cancer. Studies have shown that the regular intake of mesalazine reduces the risk of developing colorectal polyps and cancer by its multidirectional action. Anti-inflammatory mechanisms include the modulation of inflammatory cytokine production, COX inhibition and impact on NF-κB and PPARδ pathways. Consequently, mesalazine inhibits, or at least delays, the processes of carcinogenesis.
PL
Rak jelita grubego (RJG) jest czwartym najczęściej rozpoznawanym rakiem u kobiet i trzecim u mężczyzn. Każdego roku stwierdza się ponad milion nowych zachorowań i ponad sześćset tysięcy zgonów z powodu RJG. Do czynników ryzyka RJG zalicza się niezdrowy styl życia, predyspozycje genetyczne (stwierdzane w około 25% przypadków zachorowań) oraz choroby zapalne jelit. Wśród pacjentów z wrzodziejącym zapaleniem jelita grubego i chorobą Leśniowskiego-Crohna występuje podwyższone ryzyko zachorowania na RJG. Wiele badań wykazało ochronne działanie niesteroidowych leków przeciwzapalnych, w tym mesalazyny, w chemoprewencji raka jelita grubego. Badania wykazały, że regularne przyjmowanie mesalazyny - dzięki jej wielokierunkowemu działaniu - powodowało redukcję rozwoju polipów jelita grubego i transformacji nowotworowej komórek jelita grubego. Przeciwzapalne mechanizmy działania mesalazyny polegają na modulowaniu produkcji cytokin zapalnych, hamowaniu cyklooksygenazy oraz odziaływaniu na szlaki sygnałowe z udziałem czynnika transkrypcyjnego NF-κB i receptorów PPARδ. W konsekwencji mesalazyna hamuje, bądź przynajmniej opóźnia, procesy nowotworzenia.
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