Signaling networks in TMPRSS2-ERG positive prostate cancers: Do we need a Pied Piper or sharpshooter to deal with at large fused oncoprotein

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dc.authoridMansoor, Qaisar/0000-0003-1341-7174
dc.authoridRomero, Mirna Azalea/0000-0001-9806-0789
dc.authoridFarooqi, Ammad/0000-0003-2899-5014
dc.contributor.authorLin, X.
dc.contributor.authorQureshi, M. Z.
dc.contributor.authorRomero, M. A.
dc.contributor.authorYaylim, I.
dc.contributor.authorArif, S.
dc.contributor.authorUcak, I.
dc.contributor.authorFayyaz, S.
dc.date.accessioned2024-11-07T13:35:17Z
dc.date.available2024-11-07T13:35:17Z
dc.date.issued2017
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractOverwhelmingly increasing scientific evidence has provided near complete resolution of prostate cancer landscape and it is now more understandable that wide ranging factors underlies its development and progression. Increasingly it is being realized that genetic/epigenetic factors, Intra-tumoral and inter-tumoral heterogeneity, loss of apoptosis, dysregulations of spatio-temporally controlled signaling cascades, Darwinian evolution in response to therapeutic pressures play instrumental role in prostate carcinogenesis. Moreover, multi-directional patterns of spread between primary tumors and metastatic sites have also been studied extensively in prostate cancer. Research over the years has gradually and systematically revealed closer association between tumor phenotype and type of gene fusion. Latest developments in deep sequencing technologies have shown that gene fusions originate in a non-random, cell type dependent manner and are much more frequent than previously surmised. These findings enabled sub-classification and categorization of seemingly identical diseases. Furthermore, research methodologies have shown that many gene fusions inform us about risk stratification and many chimeric proteins encoded by the fused genes are being studied as drug target/s. We partition this multi-component review into the molecular basis of formation of fusion transcripts, how protein network is regulated in fusion positive prostate cancer cells and therapeutic strategies which are currently being investigated to efficiently target fusion transcript and its protein product.
dc.identifier.doi10.14715/cmb/2017.63.2.1
dc.identifier.endpage8
dc.identifier.issn0145-5680
dc.identifier.issn1165-158X
dc.identifier.issue2
dc.identifier.pmid28364793
dc.identifier.scopus2-s2.0-85018215774
dc.identifier.scopusqualityQ4
dc.identifier.startpage1
dc.identifier.urihttps://doi.org/10.14715/cmb/2017.63.2.1
dc.identifier.urihttps://hdl.handle.net/11480/16434
dc.identifier.volume63
dc.identifier.wosWOS:000402148700001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherC M B Assoc
dc.relation.ispartofCellular and Molecular Biology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectTMPRSS2-ERG
dc.subjectProstate Cancer
dc.subjectApoptosis
dc.subjectSignaling
dc.titleSignaling networks in TMPRSS2-ERG positive prostate cancers: Do we need a Pied Piper or sharpshooter to deal with at large fused oncoprotein
dc.typeReview Article

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