| Chemopreventive efficacy of rapamycin on Peutz-Jeghers syndrome in a mouse model. | |
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MedLine Citation:
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PMID: 19147279 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Germline mutations in LKB1 cause Peutz-Jeghers syndrome (PJS), an autosomal dominant disorder with a predisposition to gastrointestinal polyposis and cancer. Hyperactivation of mTOR-signaling has been associated with PJS. We previously reported that rapamycin treatment of Lkb1(+/-) mice after the onset of polyposis reduced the polyp burden. Here we evaluated the preventive efficacy of rapamycin on Peutz-Jeghers polyposis. We found that rapamycin treatment of Lkb1(+/-) mice initiated before the onset of polyposis in Lkb1(+/-) mice led to a dramatic reduction in both polyp burden and polyp size and this reduction was associated with decreased phosphorylation levels of S6 and 4EBP1. Together, these findings support the use of rapamycin as an option for chemoprevention and treatment of PJS. |
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Authors:
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Chongjuan Wei; Christopher I Amos; Nianxiang Zhang; Jing Zhu; Xiaopei Wang; Marsha L Frazier |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-01-14 |
Journal Detail:
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Title: Cancer letters Volume: 277 ISSN: 1872-7980 ISO Abbreviation: Cancer Lett. Publication Date: 2009 May |
Date Detail:
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Created Date: 2009-03-30 Completed Date: 2009-05-07 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 7600053 Medline TA: Cancer Lett Country: Ireland |
Other Details:
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Languages: eng Pagination: 149-54 Citation Subset: IM |
Affiliation:
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Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, 1155 Pressler Boulevard, Houston, TX 77030, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibiotics, Antineoplastic / therapeutic use* Carrier Proteins / physiology Disease Models, Animal Germ-Line Mutation Intestinal Polyps / genetics, pathology, prevention & control* Mice Mice, Knockout Peutz-Jeghers Syndrome / genetics, pathology, prevention & control* Phosphorylation Phosphotransferases (Alcohol Group Acceptor) / physiology Protein-Serine-Threonine Kinases / genetics* Signal Transduction Sirolimus / therapeutic use* TOR Serine-Threonine Kinases |
| Grant Support | |
ID/Acronym/Agency:
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CA 123603/CA/NCI NIH HHS; CA 16672/CA/NCI NIH HHS; P30 CA016672-34S59033/CA/NCI NIH HHS; P30 ES 007784/ES/NIEHS NIH HHS; P30 ES007784-13/ES/NIEHS NIH HHS; P50 CA 70907/CA/NCI NIH HHS; P50 CA070907-09/CA/NCI NIH HHS; P50 CA070907-10/CA/NCI NIH HHS; R03 CA123603-02/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibiotics, Antineoplastic; 0/Carrier Proteins; 53123-88-9/Sirolimus; EC 2.7.1.-/Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.-/Stk11 protein, mouse; EC 2.7.1.1/TOR Serine-Threonine Kinases; EC 2.7.1.1/mTOR protein, mouse; EC 2.7.11.1/Protein-Serine-Threonine Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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