Abstract
The study was devised to investigate the effect of retinoic acid trifloromethyl chalcone (RAFC) on mammary carcinogenesis in female rats. The data revealed a significant decrease in number of rats with mammary tumor, number of tumors per rat and tumor volume by 54, 72 and 75% respectively in RAFC group compared to control group. The ibuprofen treated rats also showed a significant decrease in number of rats with tumor, number of tumors per rat and tumor volumes by 43%, 55%, and 59%, respectively. Treatment of rats with RAFC also increased the latency period of tumor induction significantly. Median detection period (50% of tumors) was 92, 83 and 56 days respectively in the rats from RAFC, ibuprofen and control groups respectively after DMBA induction. These results demonstrate that RAFC possesses strong chemopreventive activity against mammary carcinogenesis.
Highlights
In Western countries breast cancer is a most frequent malignant neoplasm among women
There was no significant difference in the initial and final average body weight of animals of control, ibuprofen and retinoic acid trifloromethyl chalcone (RAFC) groups (Table I)
The histopathological evaluation of the tumors excised from the rats of control, ibuprofen and RAFC group showed that all the 150 tumors from control and 72 tumors from ibuprofen groups were adenocarcinomas
Summary
In Western countries breast cancer is a most frequent malignant neoplasm among women. Despite intensive cancer control efforts, it remains the second leading cause of cancer deaths among American women (Singletary et al, 1998). Recent epidemiological studies suggested the presence of an inverse association between regular intake of NSAIDs and the relative risk of breast cancer (Harris et al, 2005; Harris et al, 1995; Harris et al, 1996). Animal studies have demonstrated the effects of NSAIDs against mammary carcinogenesis (Lee et al, 1992; McCormick et al, 1995), and in our laboratories, the common over-the-counter compound ibuprofen produced highly significant reductions in tumor size and tumor burden associated with inhibition of the genetic expression of COX isoforms (Joarder et al, 1997; Robertson et al, 1998; Alshafie et al, 1999)
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