Increased expression of cyclooxygenase (COX)‐2 in DMBA‐induced hamster cheek pouch carcinogenesis and chemopreventive effect of a selective COX‐2 inhibitor celecoxib

Nishimura, Norihiko; Urade, Masahiro; Hashitani, Susumu; Noguchi, Kazuma; Manno, Yukiyo; Takaoka, Kazuki; Sakurai, Kazuo

doi:10.1111/j.1600-0714.2004.00254.x

Cited by 31 publications

(27 citation statements)

References 32 publications

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“…The duration of DMBA application and time of sacrifice were carefully planned according to the literature (27,29) at 9 weeks for the animals of the control group C 1 in order to achieve development of epithelial dysplasia, but not invasive SCC, at a rate of 100%; and at 14 weeks for the animals of the control group C 2 in order to achieve development of invasive SCC at a rate of 100% (27,29). Furthermore, the time of sulindac treatment in group B was carefully planned in order to initiate sulindac treatment at the beginning of the 10th week of the carcinogenesis at a point when all animals of group B develop epithelial dysplasia but not invasive SCC (27,29).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the time of sulindac treatment in group B was carefully planned in order to initiate sulindac treatment at the beginning of the 10th week of the carcinogenesis at a point when all animals of group B develop epithelial dysplasia but not invasive SCC (27,29). As a matter of fact, groups A 1 and C 1 had the same possibility for epithelia dysplasia development and groups A 2 , B, and C 2 had the same possibility for SCC development, so that any differences between these groups could be attributed only to sulindac administration.…”

Section: Discussionmentioning

confidence: 99%

“…Celecoxib, a selective COX-2 inhibitor, has also been shown to exert chemopreventive effects in the HOCM (29). The administration of celecoxib in the animals' diet delayed the onset of carcinoma formation that started at 10.0 and 11.2 weeks in the 500 and 1,500 ppm celecoxib group, instead of 8.7 weeks in the control group.…”

Section: Discussionmentioning

confidence: 99%

“…In the HOCM, development of epithelial dysplasia occurs at weeks 6 to 9 and development of invasive SCC at weeks 10 to 14 of the carcinogenesis process (27,29).…”

Section: Introductionmentioning

confidence: 99%

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In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Katoumas

Nikitakis

Perrea

et al. 2015

Cancer Prevention Research

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The antineoplastic properties of the NSAID sulindac have long been studied. The purpose of this study was to explore sulindac's in vivo effects on oral squamous cell carcinoma (SCC) oncogenesis using the hamster cheek pouch oral carcinogenesis model (HOCM). Thirty Syrian golden hamsters were divided into three experimental and two control groups (n ¼ 6 each). The animals' right buccal pouches were treated with carcinogen for 9 weeks in one experimental and one control group and for 14 weeks in all other three groups. The animals of two experimental groups received sulindac from the 1st week and those of the third experimental group from the 10th week. After the end of carcinogenesis, treated buccal pouches were removed and examined. In animals treated with carcinogen for 14 weeks, development of oral SCC and tumor volume were significantly lower in animals that received sulindac from the first week of the experiment. Oral SCC developing in animals that received sulindac were more frequently well differentiated compared with the control group. In animals treated with carcinogen for 9 weeks, the animals that received sulindac developed lower grade of epithelial dysplasia. Proliferation index Ki-67 and positivity for the antiapoptotic molecule survivin were lower in the animals that received sulindac. Treatment with sulindac appears to delays the progression of oral premalignant lesions to oral SCC in the HOCM, also resulting in smaller and better differentiated tumors. These in vivo antineoplastic effects may be related to sulindac's ability to decrease cell proliferation and to prevent survivin expression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…In the HOCM, development of epithelial dysplasia occurs at weeks 6 to 9 and development of invasive SCC at weeks 10 to 14 of the carcinogenesis process (27,29).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Katoumas

Nikitakis

Perrea

et al. 2015

Cancer Prevention Research

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“…The GcMAF dose of 100 pg/hamster was employed according to the study reported previously in mice bearing Ehlich ascites tumor (10). These hamsters were treated under ether anesthesia by painting a cheek pouch three times a week with 1% solution of DMBA (Wako Pure Chemical Industries, Ltd., Osaka, Japan) dissolved in acetone, as previously described (18,19). DMBA application was continued until the 13th week.…”

Section: Animals Carcinogen Treatment and Gcmaf Administrationmentioning

confidence: 99%

Inhibitory effect of vitamin D-binding protein-derived macrophage activating factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived carcinoma cell line

et al. 2011

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Abstract. This study investigated the inhibitory effect of vitamin D-binding protein-derived macrophage-activating factor (GcMAF) on carcinogenesis and tumor growth, using a 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced hamster cheek pouch carcinogenesis model, as well as the cytocidal effect of activated macrophages against HCPC-1, a cell line established from DMBA-induced cheek pouch carcinoma. DMBA application induced squamous cell carcinoma in all 15 hamsters of the control group at approximately 10 weeks, and all 15 hamsters died of tumor burden within 20 weeks. By contrast, 2 out of the 14 hamsters with GcMAF administration did not develop tumors and the remaining 12 hamsters showed a significant delay of tumor development for approximately 3.5 weeks. The growth of tumors formed was significantly suppressed and none of the hamsters died within the 20 weeks during which they were observed. When GcMAF administration was stopped at the 13th week of the experiment in 4 out of the 14 hamsters in the GcMAF-treated group, tumor growth was promoted, but none of the mice died within the 20-week period. On the other hand, when GcMAF administration was commenced after the 13th week in 5 out of the 15 hamsters in the control group, tumor growth was slightly suppressed and all 15 hamsters died of tumor burden. However, the mean survival time was significantly extended. GcMAF treatment activated peritoneal macrophages in vitro and in vivo, and these activated macrophages exhibited a marked cytocidal effect on HCPC-1 cells. Furthermore, the cytocidal effect of activated macrophages was enhanced by the addition of tumor-bearing hamster serum. These findings indicated that GcMAF possesses an inhibitory effect on tumor development and growth in a DMBA-induced hamster cheek pouch carcinogenesis model.

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Prognostic significance of cyclooxygenase‐2 and DNA topoisomerase IIα expression in oral carcinoma

et al. 2007

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Increased expression of cyclooxygenase (COX)‐2 in DMBA‐induced hamster cheek pouch carcinogenesis and chemopreventive effect of a selective COX‐2 inhibitor celecoxib

Abstract: The COX-2 expression was increased during hamster cheek pouch chemical carcinogenesis. Administration of celecoxib demonstrated the chemopreventive potential against the carcinogenesis.

Cited by 31 publications

References 32 publications

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Inhibitory effect of vitamin D-binding protein-derived macrophage activating factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived carcinoma cell line

Prognostic significance of cyclooxygenase‐2 and DNA topoisomerase IIα expression in oral carcinoma

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