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dc.contributor.authorFeitelson, Mark A.-
dc.contributor.authorSánchez García, Isidro-
dc.date.accessioned2016-08-23T11:08:30Z-
dc.date.available2016-08-23T11:08:30Z-
dc.date.issued2015-
dc.identifierdoi: 10.1016/j.semcancer.2015.02.006-
dc.identifiere-issn: 1096-3650-
dc.identifierissn: 1044-579X-
dc.identifier.citationSeminars in Cancer Biology 35(Supl.): S25-S54 (2015)-
dc.identifier.urihttp://hdl.handle.net/10261/135784-
dc.descriptionUnder a Creative Commons license.-- et al.-
dc.description.abstractProliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression.-
dc.description.sponsorshipDrs. Feitelson and Arzumanyan were supported by NIH (AI076535) and by Temple University. Dr. Rob J. Kulathinal was supported by the National Science Foundation, and by the American Cancer Society. Dr. Marino was supported by grant from University Roma Tre (CLA 2013) and by the Italian Association for Cancer Research (no. IG15221). Dr. Georgakilas was supported by the EU Marie Curie Reintegration Grant (MC-CIG-303514), Greek National funds through the Operational Program ‘Educational and Lifelong Learning of the National Strategic Reference Framework (NSRF)- Research Funding Program: THALES (MIS 379346) and COST Action CM1201 ‘Biomimetic Radical Chemistry.’ Dr. Amedei was supported by the Italian Ministry of University and University of Italy. Dr. Amin was supported by the Terry Fox Foundation (TF-36), UAEU Program for Advanced Research (UPAR25183), Al-Jalila Foundation (AJF201454) and Zayed Center for Health Sciences (ZCHS2014). Dr. Sanchez-Garcia was supported by FEDER, by MICINN (SAF2012-32810), by NIH (R01 CA109335-04A1), by Junta de Castilla y León (BIO/SA06/13), by the ARIMMORA project (FP7-ENV-2011, EU 7th Framework Program) and by the EuroSyStem and the DECIDE Network (EU FP7). Dr. Sharma was funded by NIH grants (R01CA131294, CA155686), the Avon Foundation and a Breast Cancer Research Foundation grant (90047965). Dr. Saxena was supported by a grant from NIH (K01DK077137 and R03DK089130). Dr. Singh was supported by the Fast Track Scheme for Young Scientists, Department of Science and Technology, India (SR/FT/LS-063/2008). Dr. Honoki was supported by a grant from the Ministry of Education, Culture, Sports, Science and Technology, Japan (no. 24590493). Dr. Ciriolo was supported by the Italian Association for Cancer Research (AIRC – grant #IG10636). Dr. Aquilano was supported by MIUR-PRIN (20125S38FA 002) and Ministero della Salute (GR-2011-02348047). Dr. Chen was funded from the Ovarian and Prostate Cancer Research Trust, UK. Dr. Mohammed is supported by the Purdue University Center for Cancer Research. W. Nicol Keith & Alan Bilsland were supported by the University of Glasgow, Beatson Oncology Centre Fund, and Cancer Research UK (http://www.cancerresearchuk.org) grant C301/A14762.-
dc.publisherElsevier-
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/282891-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.subjectCancer stem cells-
dc.subjectProliferation-
dc.subjectNatural products-
dc.subjectTherapeutic targets-
dc.subjectCancer hallmarks-
dc.titleSustained proliferation in cancer: Mechanisms and novel therapeutic targets-
dc.typeartículo-
dc.identifier.doi10.1016/j.semcancer.2015.02.006-
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.semcancer.2015.02.006-
dc.date.updated2016-08-23T11:08:30Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.contributor.funderCancer Research UK-
dc.contributor.funderDepartment of Science and Technology (India)-
dc.contributor.funderBreast Cancer Research Foundation-
dc.contributor.funderAvon Foundation for Women-
dc.contributor.funderJunta de Castilla y León-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.contributor.funderMinistero dell'Istruzione, dell'Università e della Ricerca-
dc.contributor.funderEuropean Commission-
dc.contributor.funderAssociazione Italiana per la Ricerca sul Cancro-
dc.contributor.funderUniversità degli Studi Roma Tre-
dc.contributor.funderAmerican Cancer Society-
dc.contributor.funderTemple University-
dc.contributor.funderNational Science Foundation (US)-
dc.contributor.funderNational Institutes of Health (US)-
dc.contributor.funderUniversity of Glasgow-
dc.contributor.funderPurdue University-
dc.contributor.funderMinistry of Education, Culture, Sports, Science and Technology (Japan)-
dc.contributor.funderMinistero della Salute-
dc.contributor.funderProstate Cancer UK-
dc.relation.csic-
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dc.identifier.pmid25892662-
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item.openairetypeartículo-
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item.cerifentitytypePublications-
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