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dc.creatorFeitelson, Mark
dc.creatorArzumanyan, Alla
dc.creatorKulathinal, Rob
dc.creatorBlain, Stacy W.
dc.creatorHolcombe, Randall F.
dc.creatorMahajna, Jamal
dc.creatorMarino, Maria
dc.creatorMartinez-Chantar, Maria L.
dc.creatorNawroth, Roman
dc.creatorSanchez-Garcia, Isidro
dc.creatorSharma, Dipali
dc.creatorSaxena, Neeraj K.
dc.creatorSingh, Neetu
dc.creatorVlachostergios, Panagiotis J.
dc.creatorGuo, Shanchun
dc.creatorHonoki, Kanya
dc.creatorFujii, Hiromasa
dc.creatorGeorgakilas, Alexandros G.
dc.creatorBilsland, Alan
dc.creatorAmadei, Amadeo
dc.creatorNowsheen, Somaira
dc.date.accessioned2023-06-22T15:11:33Z
dc.date.available2023-06-22T15:11:33Z
dc.date.issued2015-11-18
dc.identifier.issn1096-3650
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/8731
dc.identifier.urihttp://hdl.handle.net/20.500.12613/8767
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.format.extent30 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartSeminars in Cancer Biology, Vol. 35, Supplement
dc.relation.isreferencedbyElsevier
dc.rightsAttribution-NonCommercial-NoDerivs CC BY-NC-ND
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectProliferation
dc.subjectNatural products
dc.subjectTherapeutic targets
dc.subjectCancer stem cells
dc.subjectCancer hallmarks
dc.titleSustained proliferation in cancer: Mechanisms and novel therapeutic targets
dc.typeText
dc.type.genreJournal article
dc.description.departmentBiology
dc.relation.doihttps://doi.org/10.1016/j.semcancer.2015.02.006
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeTemple University. College of Science and Technology
dc.creator.orcidFeitelson|0000-0002-4904-0498
dc.creator.orcidKulathinal|0000-0003-1907-2744
dc.temple.creatorFeitelson, Mark A.
dc.temple.creatorArzumanyan, Alla
dc.temple.creatorKulathinal, Rob J.
refterms.dateFOA2023-06-22T15:11:33Z


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