![]() contributed equally to the design of the experiments, performance of the animal experiments and histology, the in vitro experiments, flow cytometry, and qRT-PCRs and contributed collection and analysis of the data. is supported by the German Research Foundation. are supported by the Max Eder Program of the Deutsche Krebshilfe. fellowships from the FUGE of RCN, the European Union Seventh Framework Programme (FP7/2007-2013, no. NIH (grants 1U54CA126513, RO1CA093405, and RO1CA120979) (T.C.W.), Clyde Wu Family Foundation (T.C.W.), Mitsukoshi Health and Welfare Foundation (Y.H.), Japan Society for the Promotion of Science Postdoctoral Fellowships for Research Abroad (Y.H.), and Uehara Memorial Foundation (Y.H.). Olavs University Hospital, Liaison Committee between the Central Norway Regional Health Authority and NTNU (C.-M.Z.), U.S. Funding: Supported by the RCN (D.C.), Joint Programme of the Medical Faculty of NTNU and St. The microarray and part of the bioinformatics work were provided by Norwegian Microarray Consortium–NTNU, a national technology platform supported by Functional Genomics Programme (FUGE) of Research Council of Norway (RCN) and NTNU. Takeuchi at Kyoto Pharmaceutical University for providing M 3KO mice. ![]() Diacou at Columbia University for extraction of enteric nervous system and K. Gronbech at Norwegian University of Science and Technology (NTNU) for valuable assistance and discussions A. Together, our findings suggest that vagal innervation contributes to gastric tumorigenesis via M 3 receptor–mediated Wnt signaling in the stem cells, and that denervation might represent a feasible strategy for the control of gastric cancer. In gastric cancer patients, tumor stage correlated with neural density and activated Wnt signaling, whereas vagotomy reduced the risk of gastric cancer. Furthermore, pharmacological inhibition or genetic knockout of the muscarinic acetylcholine M 3 receptor suppressed gastric tumorigenesis. In gastric organoid cultures, neurons stimulated growth in a Wnt-mediated fashion through cholinergic signaling. Denervation-induced suppression of tumorigenesis was associated with inhibition of Wnt signaling and suppression of stem cell expansion. Vagotomy or botulinum toxin type A treatment also enhanced the therapeutic effects of systemic chemotherapy and prolonged survival. In three separate mouse models of gastric cancer, surgical or pharmacological denervation of the stomach (bilateral or unilateral truncal vagotomy, or local injection of botulinum toxin type A) markedly reduced tumor incidence and progression, but only in the denervated portion of the stomach. We provide evidence that proper innervation is critical at all stages of gastric tumorigenesis. If you have previously requested that we remove your email address(es) completely from the Registry, then you will not be able to reactivate the deactivated account.The nervous system plays an important role in the regulation of epithelial homeostasis and has also been postulated to play a role in tumorigenesis. You will need to add any data previously on your record, as it will have all been deleted during the deactivation process. You will be redirected to your now reactivated ORCID record. Click the reactivate button to complete the process. As all identifying information on your account and account preferences have been deleted, you must fill in the reactivation form with your name, password, and preferred default visibility setting, and confirm your consent to the ORCID privacy policy and terms and conditions of use. If you do not receive the email, please contact us for assistance.Ĭlick the link in the account reactivation message to reactivate your account. The account reactivation message will be sent from You must click the link in the email to confirm your account reactivation. You will be prompted to either contact us (if you no longer have access to the email address(es) associated with your iD), or to submit, where a message will then display confirming that an account reactivation message has been sent to your registered email address. You can reactivate your account any time by entering an email address associated with your account into the email field of the reset password screen to start the process. Once you have deactivated your account, you will not be able to register for a new account using any of the email addresses associated with it.
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