Chemoprevention of intestinal adenomas in the ApcMin mouse by piroxicam: kinetics, strain effects and resistance to chemosuppression

Ritland, S; Gendler, Sandra J.

doi:10.1093/carcin/20.1.51

Cited by 87 publications

(61 citation statements)

References 27 publications

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“…This result is consistent with the notion that the majority of adenomas in Apc Min/+ mice are fixed already either in utero or perinatally just after birth (Shoemaker et al, 1995;Ritland and Gendler, 1999) It suggests, for the first time, that interference with tumour initiation and/or early promotion in Apc Min/+ mice can have a long-term beneficial consequence, even if the chemopreventive stimulus is discontinued postweaning. A similar reduction was observed in the colon, however overall colonic adenoma burden was so low that the difference between exposed and unexposed mice was not significant (result not shown).…”

Section: Resultssupporting

confidence: 89%

“…et al, 2002). In contrast, there are reports that document convincingly the ability of two NSAIDs other than aspirin, piroxicam (Ritland and Gendler, 1999) and celecoxib (Jacoby et al, 2000b), to decrease the number of established polyps and to prevent the development of nascent ones, when they are administered at a late stage during the lifetime of Apc Min/+ mice.…”

Section: Resultsmentioning

confidence: 99%

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Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

et al. 2003

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The nonsteroidal anti-inflammatory drug aspirin and the spice curcumin retard adenoma formation when administered long-term to Apc Min/+ mice, a model of human familial adenomatous polyposis coli. Both agents interfere with cyclooxygenase activity. When aspirin is administered to Apc Min/+ mice only postweaning, but not before, it is inefficacious, while curcumin given postweaning is active. Here the hypothesis was tested that dietary aspirin (0.05%) or curcumin (0.2%) prevent or delay adenoma formation in offsprings when administered to Apc Min/+ mothers and up to the end of weaning, but not afterwards. Whereas curcumin was without effect when administered in this way, aspirin reduced numbers of intestinal adenomas by 21%. When aspirin given up to the end of weaning was combined with curcumin administered from the end of weaning for the rest of the animals' lifetime, intestinal adenoma numbers were reduced by 38%. The combination was not superior to intervention postweaning with curcumin alone. These results show that aspirin exerts chemopreventive activity in the Apc Min/+ mouse during tumour initiation/early promotion, while curcumin is efficacious when given at a later stage of carcinogenic progression. Thus, the results suggest that in this mouse model aspirin and curcumin act during different 'windows' of neoplastic development.

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Section: Resultssupporting

confidence: 89%

Section: Resultsmentioning

confidence: 99%

Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

et al. 2003

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“…Many of these studies report a significant decrease in tumor number. Nonsteroidal antiinflammatory drugs such as piroxicam and sulindac, which target both COX-1 and COX-2, have been among the most potent agents in suppressing tumor formation in Apc ϩ/min mice (25)(26)(27)(28). More specifically, the important role of COX-2 in intestinal polyposis was demonstrated by using different selective COX-2 inhibitors (29-31).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc ^+/min mice

Korsisaari¹,

Kasman²,

Forrest³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Regional differences have also been observed with respect to the efficacy of NSAID treatment. Whereas treatment of Apc Min/ϩ with piroxicam results in a 95% reduction in tumor number, the distribution of residual tumors suggests that tumors of the duodenum and the colon are more resistant to chemosuppression (25). In addition, Apc Min/ϩ tumors derived from the colon are resistant to the effects of sulindac treatment, which rapidly induces the regression of 70-80% of Apc Min/ϩ tumors in the small intestine (26).…”

Section: Discussionmentioning

confidence: 99%

Deletion of cytosolic phospholipase A ₂ suppresses Apc ^Min -induced tumorigenesis

Hong

Bonventre

O’Leary

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

118

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Although nonsteroidal antiinflammatory drugs (NSAIDs) show great promise as therapies for colon cancer, a dispute remains regarding their mechanism of action. NSAIDs are known to inhibit cyclooxygenase (COX) enzymes, which convert arachidonic acid (AA) to prostaglandins (PGs). Therefore, NSAIDs may suppress tumorigenesis by inhibiting PG synthesis. However, various experimental studies have suggested the possibility of PG-independent mechanisms. Notably, disruption of the mouse group IIA secretory phospholipase A 2 locus (Pla2g2a), a potential source of AA for COX-2, increases tumor number despite the fact that the mutation has been predicted to decrease PG production. Some authors have attempted to reconcile the results by suggesting that the level of the precursor (AA), not the products (PGs), is the critical factor. To clarify the role of AA in tumorigenesis, we have examined the effect of deleting the group IV cytosolic phospholipase A2 (cPLA2) locus (Pla2g4). We report that Apc Min/؉ , cPLA2 ؊/؊ mice show an 83% reduction in tumor number in the small intestine compared with littermates with genotypes Apc Min/؉ , cPLA2 ؉/؊ and Apc Min/؉ , cPLA2 ؉/؉ . This tumor phenotype parallels that of COX-2 knockout mice, suggesting that cPLA 2 is the predominant source of AA for COX-2 in the intestine. The protective effect of cPLA2 deletion is thus most likely attributed to a decrease in the AA supply to COX-2 and a resultant decrease in PG synthesis. The tumorigenic effect of sPLA2 mutations is likely to be through a completely different pathway.

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Chemoprevention of intestinal adenomas in the ApcMin mouse by piroxicam: kinetics, strain effects and resistance to chemosuppression

Cited by 87 publications

References 27 publications

Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc ^+/min mice

Deletion of cytosolic phospholipase A ₂ suppresses Apc ^Min -induced tumorigenesis

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Chemoprevention of intestinal adenomas in the ApcMin mouse by piroxicam: kinetics, strain effects and resistance to chemosuppression

Cited by 87 publications

References 27 publications

Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

Age-related difference in susceptibility of ApcMin/+ mice towards the chemopreventive efficacy of dietary aspirin and curcumin

Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc +/min mice

Deletion of cytosolic phospholipase A 2 suppresses Apc Min -induced tumorigenesis

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Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc ^+/min mice

Deletion of cytosolic phospholipase A ₂ suppresses Apc ^Min -induced tumorigenesis