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"username": "knguyen15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "creatorSummary": "Baselga et al.", "numChildren": 2 }, "data": { "key": "X3DAGH2Z", "version": 106, "itemType": "journalArticle", "title": "Lapatinib with trastuzumab for HER2-positive early breast cancer (NeoALTTO): a randomised, open-label, multicentre, phase 3 trial", "creators": [ { "creatorType": "author", "firstName": "José", "lastName": "Baselga" }, { "creatorType": "author", "firstName": "Ian", "lastName": "Bradbury" }, { "creatorType": "author", "firstName": "Holger", "lastName": "Eidtmann" }, { "creatorType": "author", "firstName": "Serena", "lastName": "Di Cosimo" }, { "creatorType": "author", "firstName": "Evandro", "lastName": "de Azambuja" }, { "creatorType": "author", "firstName": "Claudia", "lastName": "Aura" }, { "creatorType": "author", "firstName": "Henry", "lastName": "Gómez" }, { "creatorType": "author", "firstName": "Phuong", "lastName": "Dinh" }, { "creatorType": "author", "firstName": "Karine", "lastName": "Fauria" }, { "creatorType": "author", "firstName": "Veerle", "lastName": "Van Dooren" }, { "creatorType": "author", "firstName": "Gursel", "lastName": "Aktan" }, { "creatorType": "author", "firstName": "Aron", "lastName": "Goldhirsch" }, { "creatorType": "author", "firstName": "Tsai-Wang", "lastName": "Chang" }, { "creatorType": "author", "firstName": "Zsolt", "lastName": "Horváth" }, { "creatorType": "author", "firstName": "Maria", "lastName": "Coccia-Portugal" }, { "creatorType": "author", "firstName": "Julien", "lastName": "Domont" }, { "creatorType": "author", "firstName": "Ling-Min", "lastName": "Tseng" }, { "creatorType": "author", "firstName": "Georg", "lastName": "Kunz" }, { "creatorType": "author", "firstName": "Joo Hyuk", "lastName": "Sohn" }, { "creatorType": "author", "firstName": "Vladimir", "lastName": "Semiglazov" }, { "creatorType": "author", "firstName": "Guillermo", "lastName": "Lerzo" }, { "creatorType": "author", "firstName": "Marketa", "lastName": "Palacova" }, { "creatorType": "author", "firstName": "Volodymyr", "lastName": "Probachai" }, { "creatorType": "author", "firstName": "Lajos", "lastName": "Pusztai" }, { "creatorType": "author", "firstName": "Michael", "lastName": "Untch" }, { "creatorType": "author", "firstName": "Richard D", "lastName": "Gelber" }, { "creatorType": "author", "firstName": "Martine", "lastName": "Piccart-Gebhart" } ], "abstractNote": "SummaryBackground\nThe anti-HER2 monoclonal antibody trastuzumab and the tyrosine kinase inhibitor lapatinib have complementary mechanisms of action and synergistic antitumour activity in models of HER2-overexpressing breast cancer. We argue that the two anti-HER2 agents given together would be better than single-agent therapy.\nMethods\nIn this parallel groups, randomised, open-label, phase 3 study undertaken between Jan 5, 2008, and May 27, 2010, women from 23 countries with HER2-positive primary breast cancer with tumours greater than 2 cm in diameter were randomly assigned to oral lapatinib (1500 mg), intravenous trastuzumab (loading dose 4 mg/m2, subsequent doses 2 mg/kg), or lapatinib (1000 mg) plus trastuzumab. Treatment allocation was by stratified, permuted blocks randomisation, with four stratification factors. Anti-HER2 therapy alone was given for the first 6 weeks; weekly paclitaxel (80 mg/m2) was then added to the regimen for a further 12 weeks, before definitive surgery was undertaken. After surgery, patients received adjuvant chemotherapy followed by the same targeted therapy as in the neoadjuvant phase to 52 weeks. The primary endpoint was the rate of pathological complete response (pCR), analysed by intention to treat. This trial is registered with ClinicalTrials.gov, NCT00553358.\nFindings\n154 patients received lapatinib, 149 trastuzumab, and 152 the combination. pCR rate was significantly higher in the group given lapatinib and trastuzumab (78 of 152 patients [51·3%; 95% CI 43·1–59·5]) than in the group given trastuzumab alone (44 of 149 patients [29·5%; 22·4–37·5]; difference 21·1%, 9·1–34·2, p=0·0001). We recorded no significant difference in pCR between the lapatinib (38 of 154 patients [24·7%, 18·1–32·3]) and the trastuzumab (difference −4·8%, −17·6 to 8·2, p=0·34) groups. No major cardiac dysfunctions occurred. Frequency of grade 3 diarrhoea was higher with lapatinib (36 patients [23·4%]) and lapatinib plus trastuzumab (32 [21·1%]) than with trastuzumab (three [2·0%]). Similarly, grade 3 liver-enzyme alterations were more frequent with lapatinib (27 [17·5%]) and lapatinib plus trastuzumab (15 [9·9%]) than with trastuzumab (11 [7·4%]).\nInterpretation\nDual inhibition of HER2 might be a valid approach to treatment of HER2-positive breast cancer in the neoadjuvant setting.\nFunding\nGlaxoSmithKline.", "publicationTitle": "The Lancet", "publisher": "", "place": "", "date": "18", "volume": "379", "issue": "9816", "section": "", "partNumber": "", "partTitle": "", "pages": "633-640", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "The Lancet", "DOI": "10.1016/S0140-6736(11)61847-3", "citationKey": "", "url": "http://www.sciencedirect.com/science/article/pii/S0140673611618473", "accessDate": "2016-11-16T01:19:32Z", "PMID": "", "PMCID": "", "ISSN": "0140-6736", "archive": "", "archiveLocation": "", "shortTitle": "Lapatinib with trastuzumab for HER2-positive early breast cancer (NeoALTTO)", "language": "", "libraryCatalog": "ScienceDirect", "callNumber": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2016-11-16T01:19:32Z", "dateModified": "2016-11-16T01:19:32Z" } }, { "key": "87XPGJKN", "version": 105, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/87XPGJKN", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/87XPGJKN", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/689058/items/9FXV3B9H", "type": "application/json" } }, "meta": { "createdByUser": { "id": 2607171, "username": "jlam15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jlam15", "type": "text/html" } } } }, "data": { "key": "87XPGJKN", "version": 105, "parentItem": "9FXV3B9H", "itemType": "attachment", "linkMode": "linked_url", "title": "PubMed entry", "accessDate": "2016-10-14T00:40:43Z", "url": "http://www.ncbi.nlm.nih.gov/pubmed/19136477", "note": "", "contentType": "text/html", "charset": "", "tags": [], "relations": {}, "dateAdded": "2016-10-14T00:40:43Z", "dateModified": "2016-10-14T00:40:43Z" } }, { "key": "DN4TD39C", "version": 105, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/DN4TD39C", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/DN4TD39C", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/689058/items/9FXV3B9H", "type": "application/json" } }, "meta": { "createdByUser": { "id": 2607171, "username": "jlam15", "name": "", "links": { "alternate": { "href": 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"type": "application/json" } }, "meta": { "createdByUser": { "id": 2607171, "username": "jlam15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jlam15", "type": "text/html" } } } }, "data": { "key": "RMT63SVV", "version": 105, "parentItem": "9FXV3B9H", "itemType": "attachment", "linkMode": "linked_url", "title": "Full Text PDF", "accessDate": "2016-10-14T00:40:43Z", "url": "http://carcin.oxfordjournals.org/content/30/3/377.full.pdf", "note": "", "contentType": "application/pdf", "charset": "", "tags": [], "relations": {}, "dateAdded": "2016-10-14T00:40:43Z", "dateModified": "2016-10-14T00:40:43Z" } }, { "key": "9FXV3B9H", "version": 105, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/9FXV3B9H", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/9FXV3B9H", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2607171, "username": "jlam15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jlam15", "type": "text/html" } } }, "creatorSummary": "Greenhough et al.", "parsedDate": "2009-03-01", "numChildren": 3 }, "data": { "key": "9FXV3B9H", "version": 105, "itemType": "journalArticle", "title": "The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment", "creators": [ { "creatorType": "author", "firstName": "Alexander", "lastName": "Greenhough" }, { "creatorType": "author", "firstName": "Helena J. M.", "lastName": "Smartt" }, { "creatorType": "author", "firstName": "Amy E.", "lastName": "Moore" }, { "creatorType": "author", "firstName": "Heather R.", "lastName": "Roberts" }, { "creatorType": "author", "firstName": "Ann C.", "lastName": "Williams" }, { "creatorType": "author", "firstName": "Christos", "lastName": "Paraskeva" }, { "creatorType": "author", "firstName": "Abderrahmane", "lastName": "Kaidi" } ], "abstractNote": "It is widely accepted that alterations to cyclooxygenase-2 (COX-2) expression and the abundance of its enzymatic product prostaglandin E2 (PGE2) have key roles in influencing the development of colorectal cancer. Deregulation of the COX-2/PGE2 pathway appears to affect colorectal tumorigenesis via a number of distinct mechanisms: promoting tumour maintenance and progression, encouraging metastatic spread, and perhaps even participating in tumour initiation. Here, we review the role of COX-2/PGE2 signalling in colorectal tumorigenesis and highlight its ability to influence the hallmarks of cancer—attributes defined by Hanahan and Weinberg as being requisite for tumorigenesis. In addition, we consider components of the COX–prostaglandin pathway emerging as important regulators of tumorigenesis; namely, the prostanoid (EP) receptors, 15-hydroxyprostaglandin dehydrogenase and the prostaglandin transporter. Finally, based on recent findings, we propose a model for the cellular adaptation to the hypoxic tumour microenvironment that encompasses the interplay between COX-2, hypoxia-inducible factor 1 and dynamic switches in β-catenin function that fine-tune signalling networks to meet the ever-changing demands of a tumour.", "publicationTitle": "Carcinogenesis", "publisher": "", "place": "", "date": "2009-03-01", "volume": "30", "issue": "3", "section": "", "partNumber": "", "partTitle": "", "pages": "377-386", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Carcinogenesis", "DOI": "10.1093/carcin/bgp014", "citationKey": "", "url": "http://carcin.oxfordjournals.org/content/30/3/377", "accessDate": "2016-10-14T00:40:43Z", "PMID": "", "PMCID": "", "ISSN": "0143-3334, 1460-2180", "archive": "", "archiveLocation": "", "shortTitle": "The COX-2/PGE2 pathway", "language": "en", "libraryCatalog": "carcin.oxfordjournals.org", "callNumber": "", "rights": "", "extra": "PMID: 19136477", "tags": [], "collections": [ "2SF4TMH6" ], "relations": {}, "dateAdded": "2016-10-14T00:40:43Z", "dateModified": "2016-10-14T00:40:43Z" } }, { "key": "96DB8X7U", "version": 103, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/96DB8X7U", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/96DB8X7U", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2639675, "username": "knguyen15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "96DB8X7U", "version": 103, "itemType": "webpage", "title": "GRAS Exemption Claim for DHA Algal Oil Derived from Schizochytrium sp", "creators": [], "abstractNote": "", "websiteTitle": "", "websiteType": "", "date": "", "publisher": "", "place": "", "DOI": "", "citationKey": "", "url": "http://www.fda.gov/downloads/Food/IngredientsPackagingLabeling/GRAS/NoticeInventory/ucm264032.pdf", "accessDate": "2016-10-08T04:39:24Z", "shortTitle": "", "language": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2016-10-08T04:39:24Z", "dateModified": "2016-10-08T04:39:45Z" } }, { "key": "MWM74EFK", "version": 101, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/MWM74EFK", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/MWM74EFK", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2639675, "username": "knguyen15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "MWM74EFK", "version": 101, "itemType": "webpage", "title": "", "creators": [], "abstractNote": "", "websiteTitle": "", "websiteType": "", "date": "", "publisher": "", "place": "", "DOI": "", "citationKey": "", "url": "http://www.fda.gov/downloads/Food/IngredientsPackagingLabeling/GRAS/NoticeInventory/ucm264032.pdf", "accessDate": "2016-10-08T04:38:43Z", "shortTitle": "", "language": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2016-10-08T04:38:43Z", "dateModified": "2016-10-08T04:38:43Z" } }, { "key": "ZPVMQ4X8", "version": 100, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/ZPVMQ4X8", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/ZPVMQ4X8", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2639675, "username": "knguyen15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "creatorSummary": "Coletta et al.", "parsedDate": "2010", "numChildren": 2 }, "data": { "key": "ZPVMQ4X8", "version": 100, "itemType": "journalArticle", "title": "Omega-3 Fatty Acids and Pregnancy", "creators": [ { "creatorType": "author", "firstName": "Jaclyn M", "lastName": "Coletta" }, { "creatorType": "author", "firstName": "Stacey J", "lastName": "Bell" }, { "creatorType": "author", "firstName": "Ashley S", "lastName": "Roman" } ], "abstractNote": "Omega-3 fatty acids are essential fatty acids that must be consumed in the diet. Adequate consumption of omega-3 fatty acids is vitally important during pregnancy as they are critical building blocks of fetal brain and retina. Omega-3 fatty acids may also play a role in determining the length of gestation and in preventing perinatal depression. The most biologically active forms of omega-3 fatty acids are docosahexaenoic acid and eicosapentaenoic acid, which are primarily derived from marine sources such as seafood and algae. Recent surveys, however, indicate that pregnant women in the United States and in other countries eat little fish and therefore do not consume enough omega-3 fatty acids, primarily due to concern about the adverse effects of mercury and other contaminants on the developing fetus. This review discusses the benefits of omega-3 fatty acid consumption during pregnancy and provides guidelines for obstetricians advising patients.", "publicationTitle": "Reviews in Obstetrics and Gynecology", "publisher": "", "place": "", "date": "2010", "volume": "3", "issue": "4", "section": "", "partNumber": "", "partTitle": "", "pages": "163-171", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Rev Obstet Gynecol", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046737/", "accessDate": "2016-10-08T04:38:08Z", "PMID": "", "PMCID": "", "ISSN": "1941-2797", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "PubMed Central", "callNumber": "", "rights": "", "extra": "PMID: 21364848\nPMCID: PMC3046737", "tags": [], "collections": [], "relations": {}, "dateAdded": "2016-10-08T04:38:08Z", "dateModified": "2016-10-08T04:38:08Z" } }, { "key": "IIHEQB45", "version": 100, "library": { "type": 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"", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "creatorSummary": "Gao et al.", "parsedDate": "2015", "numChildren": 1 }, "data": { "key": "9ZR8VJID", "version": 99, "itemType": "journalArticle", "title": "FAK/PYK2 promotes the Wnt/β-catenin pathway and intestinal tumorigenesis by phosphorylating GSK3β", "creators": [ { "creatorType": "author", "firstName": "Chenxi", "lastName": "Gao" }, { "creatorType": "author", "firstName": "Guangming", "lastName": "Chen" }, { "creatorType": "author", "firstName": "Shih-Fan", "lastName": "Kuan" }, { "creatorType": "author", "firstName": "Dennis Han", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "David D.", "lastName": "Schlaepfer" }, { "creatorType": "author", "firstName": "Jing", "lastName": "Hu" } ], "abstractNote": "Aberrant activation of Wnt/β-catenin signaling plays an unequivocal role in colorectal cancer, but identification of effective Wnt inhibitors for use in cancer remains a tremendous challenge. New insights into the regulation of this pathway could reveal new therapeutic point of intervention, therefore are greatly needed. Here we report a novel FAK/PYK2/GSK3β(Y216)/β-catenin regulation axis: FAK and PYK2, elevated in adenomas in APC(min/+) mice and in human colorectal cancer tissues, functioned redundantly to promote the Wnt/β-catenin pathway by phosphorylating GSK3β(Y216) to reinforce pathway output-β-catenin accumulation and intestinal tumorigenesis. We previously showed that Wnt-induced β-catenin accumulation requires Wnt-induced GSK3β/β-TrCP interaction; the current study revealed that phosphorylation of GSK3β(Y216) was a molecular determinant of GSK3β recruitment of β-TrCP. Pharmacological inhibition of FAK/PYK2 suppressed adenoma formation in APC(min/+) mice accompanied with reduced intestinal levels of phospho-GSK3β(Y216) and β-catenin, indicating that FAK/PYK2/GSK3β(Y216) axis is critical for the activation of Wnt/β-catenin signaling in APC driven intestinal tumorigenesis.", "publicationTitle": "eLife", "publisher": "", "place": "", "date": "2015", "volume": "4", "issue": "", "section": "", "partNumber": "", "partTitle": "", "pages": "", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Elife", "DOI": "10.7554/eLife.10072", "citationKey": "", "url": "", "accessDate": "", "PMID": "", "PMCID": "", "ISSN": "2050-084X", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "eng", "libraryCatalog": "PubMed", "callNumber": "", "rights": "", "extra": "PMID: 26274564\nPMCID: PMC4558782", "tags": [ { "tag": "Animals", "type": 1 }, { "tag": "Carcinogenesis", "type": 1 }, { "tag": "Colorectal Neoplasms", "type": 1 }, { "tag": "FAK", "type": 1 }, { "tag": "Female", "type": 1 }, { "tag": "Focal Adhesion Kinase 1", "type": 1 }, { "tag": "Focal Adhesion Kinase 2", "type": 1 }, { "tag": "GSK3", "type": 1 }, { "tag": "Gene Expression Regulation", "type": 1 }, { "tag": "Glycogen Synthase Kinase 3", "type": 1 }, { "tag": "Humans", "type": 1 }, { "tag": "Mice", "type": 1 }, { "tag": "Mice, Inbred C57BL", "type": 1 }, { "tag": "Mice, Nude", "type": 1 }, { "tag": "PYK2", "type": 1 }, { "tag": "Wnt Signaling Pathway", "type": 1 }, { "tag": "Wnt/b-catenin pathway", "type": 1 }, { "tag": "biochemistry", "type": 1 }, { "tag": "cell biology", "type": 1 }, { "tag": "human", "type": 1 }, { "tag": "intestinal tumorigenesis", "type": 1 }, { "tag": "mouse", "type": 1 }, { "tag": "phosphorylation", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2016-10-08T04:37:17Z", "dateModified": "2016-10-08T04:37:17Z" } }, { "key": "MJE5TMG4", "version": 98, "library": { "type": "group", "id": 689058, "name": "ALS432 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"https://www.accessdata.fda.gov/scripts/opdlisting/oopd/listResult.cfm", "accessDate": "2016-10-08T04:30:38Z", "shortTitle": "", "language": "", "rights": "", "extra": "", "tags": [], "collections": [], "relations": {}, "dateAdded": "2016-10-08T04:30:38Z", "dateModified": "2016-10-08T04:30:38Z" } }, { "key": "S2426GXH", "version": 97, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/S2426GXH", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/S2426GXH", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2639675, "username": "knguyen15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/knguyen15", "type": "text/html" } } }, "creatorSummary": "Li et al.", "parsedDate": "2014", "numChildren": 1 }, "data": { "key": "S2426GXH", "version": 97, "itemType": "journalArticle", "title": "Repurposing the FDA-approved pinworm drug pyrvinium as a novel chemotherapeutic agent for intestinal polyposis", "creators": [ { "creatorType": "author", "firstName": "Bin", "lastName": "Li" }, { "creatorType": "author", "firstName": "Colin A.", "lastName": "Flaveny" }, { "creatorType": "author", "firstName": "Camilla", "lastName": "Giambelli" }, { "creatorType": "author", "firstName": "Dennis Liang", "lastName": "Fei" }, { "creatorType": "author", "firstName": "Lu", "lastName": "Han" }, { "creatorType": "author", "firstName": "Brian I.", "lastName": "Hang" }, { "creatorType": "author", "firstName": "Feng", "lastName": "Bai" }, { "creatorType": "author", "firstName": "Xin-Hai", "lastName": "Pei" }, { "creatorType": "author", "firstName": "Vania", "lastName": "Nose" }, { "creatorType": "author", "firstName": "Oname", "lastName": "Burlingame" }, { "creatorType": "author", "firstName": "Anthony J.", "lastName": "Capobianco" }, { "creatorType": "author", "firstName": "Darren", "lastName": "Orton" }, { "creatorType": "author", "firstName": "Ethan", "lastName": "Lee" }, { "creatorType": "author", "firstName": "David J.", "lastName": "Robbins" } ], "abstractNote": "Mutations in the WNT-pathway regulator ADENOMATOUS POLYPOSIS COLI (APC) promote aberrant activation of the WNT pathway that is responsible for APC-associated diseases such as Familial Adenomatous Polyposis (FAP) and 85% of spontaneous colorectal cancers (CRC). FAP is characterized by multiple intestinal adenomas, which inexorably result in CRC. Surprisingly, given their common occurrence, there are few effective chemotherapeutic drugs for FAP. Here we show that the FDA-approved, anti-helminthic drug Pyrvinium attenuates the growth of WNT-dependent CRC cells and does so via activation of CK1α. Furthermore, we show that Pyrvinium can function as an in vivo inhibitor of WNT-signaling and polyposis in a mouse model of FAP: APCmin mice. Oral administration of Pyrvinium, a CK1α agonist, attenuated the levels of WNT-driven biomarkers and inhibited adenoma formation in APCmin mice. Considering its well-documented safe use for treating enterobiasis in humans, our findings suggest that Pyrvinium could be repurposed for the clinical treatment of APC-associated polyposes.", "publicationTitle": "PloS One", "publisher": "", "place": "", "date": "2014", "volume": "9", "issue": "7", "section": "", "partNumber": "", "partTitle": "", "pages": "e101969", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "PLoS ONE", "DOI": "10.1371/journal.pone.0101969", "citationKey": "", "url": "", "accessDate": "", "PMID": "", "PMCID": "", "ISSN": "1932-6203", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "eng", "libraryCatalog": "PubMed", "callNumber": "", "rights": "", "extra": "PMID: 25003333\nPMCID: PMC4086981", "tags": [ { "tag": "Adenomatous Polyposis Coli", "type": 1 }, { "tag": "Animals", "type": 1 }, { "tag": "Antineoplastic Agents", "type": 1 }, { "tag": "Cell Survival", "type": 1 }, { "tag": "Drug Approval", "type": 1 }, { "tag": "Drug Repositioning", "type": 1 }, { "tag": "Drug Screening Assays, Antitumor", "type": 1 }, { "tag": "HCT116 Cells", "type": 1 }, { "tag": "Humans", "type": 1 }, { "tag": "Mice, Inbred C57BL", "type": 1 }, { "tag": "Mice, Transgenic", "type": 1 }, { "tag": "Pyrvinium Compounds", "type": 1 }, { "tag": "Wnt Signaling Pathway", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2016-10-08T01:00:29Z", "dateModified": "2016-10-08T01:00:29Z" } }, { "key": "ITKSASAE", "version": 97, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/ITKSASAE", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/ITKSASAE", "type": "text/html" }, "up": { "href": "https://api.zotero.org/groups/689058/items/S2426GXH", "type": 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"charset": "", "tags": [], "relations": {}, "dateAdded": "2016-10-05T06:11:21Z", "dateModified": "2016-10-05T06:11:21Z" } }, { "key": "7GEF75RS", "version": 94, "library": { "type": "group", "id": 689058, "name": "ALS432 Orphan Drug", "links": { "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/689058/items/7GEF75RS", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/als432_orphan_drug/items/7GEF75RS", "type": "text/html" } }, "meta": { "createdByUser": { "id": 2607171, "username": "jlam15", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jlam15", "type": "text/html" } } }, "creatorSummary": "Fasano et al.", "parsedDate": "2012-11", "numChildren": 2 }, "data": { "key": "7GEF75RS", "version": 94, "itemType": "journalArticle", "title": "DHA induces apoptosis by altering the expression and cellular location of GRP78 in colon cancer cell lines", "creators": [ { "creatorType": "author", "firstName": "Elena", "lastName": "Fasano" }, { "creatorType": "author", "firstName": "Simona", "lastName": "Serini" }, { "creatorType": "author", "firstName": "Elisabetta", "lastName": "Piccioni" }, { "creatorType": "author", "firstName": "Amelia", "lastName": "Toesca" }, { "creatorType": "author", "firstName": "Giovanni", "lastName": "Monego" }, { "creatorType": "author", "firstName": "Achille R.", "lastName": "Cittadini" }, { "creatorType": "author", "firstName": "Franco O.", "lastName": "Ranelletti" }, { "creatorType": "author", "firstName": "Gabriella", "lastName": "Calviello" } ], "abstractNote": "n − 3 polyunsaturated fatty acids exert growth-inhibitory and pro-apoptotic effects in colon cancer cells. We hypothesized that the anti-apoptotic glucose related protein of 78 kDa (GRP78), originally described as a component of the unfolded protein response in endoplasmic reticulum (ER), could be a molecular target for docosahexaenoic acid (DHA) in these cells. GRP78 total and surface overexpression was previously associated with a poor prognosis in several cancers, whereas its down-regulation with decreased cancer growth in animal models. DHA treatment induced apoptosis in three colon cancer cell lines (HT-29, HCT116 and SW480), and inhibited their total and surface GRP78 expression. The cell ability to undergo DHA-induced apoptosis was inversely related to their level of GRP78 expression. The transfection of the low GRP78-expressing SW480 cells with GRP78-GFP cDNA significantly induced cell growth and inhibited the DHA-driven apoptosis, thus supporting the essential role of GRP78 in DHA pro-apoptotic effect. We suggest that pERK1/2 could be the first upstream target for DHA, and demonstrate that, downstream of GRP78, DHA may exert its proapoptotic role by augmenting the expression of the ER resident factors ERdj5 and inhibiting the phosphorylation of PKR-like ER kinase (PERK), known to be both physically associated with GRP78, and by activating caspase-4. Overall, the regulation of cellular GRP78 expression and location is suggested as a possible route through which DHA can exert pro-apoptotic and antitumoral effects in colon cancer cells.", "publicationTitle": "Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease", "publisher": "", "place": "", "date": "November 2012", "volume": "1822", "issue": "11", "section": "", "partNumber": "", "partTitle": "", "pages": "1762-1772", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease", "DOI": "10.1016/j.bbadis.2012.08.003", "citationKey": "", "url": "http://www.sciencedirect.com/science/article/pii/S0925443912001895", "accessDate": "2016-10-05T06:11:21Z", "PMID": "", "PMCID": "", "ISSN": "0925-4439", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "ScienceDirect", "callNumber": "", "rights": "", "extra": "", "tags": [ { "tag": "Apoptosis", "type": 1 }, { "tag": "Colon cancer cell", "type": 1 }, { "tag": "DHA", "type": 1 }, { "tag": "ERK1/2", "type": 1 }, { "tag": "GRP78", "type": 1 } ], "collections": [ "2SF4TMH6" ], "relations": {}, "dateAdded": "2016-10-05T06:11:21Z", "dateModified": "2016-10-05T06:11:21Z" } } ]