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Moreover, serum DKK could be a safe and less invasive biomarker for the selection of patients who should receive antiDKK therapy.Putative mechanisms of antibodybased cancer therapy can be classified into two categories blocking function, targeting function.In blocking function, therapeutic antibody blocks the function of targetsignaling molecu les or receptors, by blocking ligand Bicalutamide binding, inhibiting cell cycle progression or DNA repair, inducing the regression of angiogenesis, increasing the internalization of receptors, or reducing proteolytic cleavage of receptors. The other mechanism of antibody therapy is the indirect action mediated by the immune system, including complementdependent cytotoxicity and antibodydependent cytotoxicity. Our data showed that the treatment of lung cancer cells with antiDKK antibody a lone induced apoptosis through the caspasedependent pathway.Another possibility of the anti tumoreffectofanti DKK antibody is thata ligandantibody complex comprising DKK and antiDKK antibody may overdrive the receptor ligand signals and change the balance of cell signals, which can induce cell death.The data implied that the induction of apoptosis of lung cancer cells by antiDKK antibody islike ly to be th rough the undefinedsignaling pa thway. Because DKK receptors relevant to cancer growth and invasion still remains unclear, further investigation of this pathway is required to answer the questions about the mechanism of antiDKK antibody efficacy.The early embryologic activity of DKK indeed requires a novel activity that resides within the N domain. The function of N may be associated with enhanced invasive activity and antiapoptotic signaling pathway that could be neutralized by antiDKK antibody.In summary, we have shown DKK as a biomarker for various kinds of common cancers and as a potential target for therapeutic antibodies.AntiDKK antibody would be a promising tool for cancer immunotherapy.The costs of publication of this article were defrayed in part by the payment of page charges.Supplementary Material Access the most recent version of this article at: doi. Click on Request Permissions which will take you to the Copyright Clearance Centers Downloaded from cancerres.aacrjournals.org on April. American Association for Cancer Research. The costs of publication of this article were defrayed in part by the payment of page charges.For this experiment, we selected a mouse strain in which wildtype neu is overexpressed in the mammary gland under the Riboflavin control of the MMTV long terminal repeat.Mice overexpressing wildtype neu develop focal mammary tumors after a long latency period. The diet of mice in the treatment group was supplemented with ppm celecoxib.Mice were palpated twice weekly for mammary gland tumor nodules, and the time of appearance of the first tumor was recorded.At the time of sacrifice, body weights were similar in the control. Mammary tissues were harvested from sacrificed animals, snapfrozen in liquid nitrogen and stored at C.PGE was assayed using an enzymelinked immunosorbent assay kit. PCR primers for individual EP receptors have been described previously. The identity of each PCR product was confirmed by DNA sequencing.All other data sets were evaluated for statistical significance using attest.Treatment with celecoxib inhibited the development of mammary tumors. All four receptor subtypes were detected in each of the three mammary glands tested or when reverse transcriptase enzyme was not included in the reverse transcriptase reaction.

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