06869nam 2201945z- 450 991055762350332120231214132838.0(CKB)5400000000045180(oapen)https://directory.doabooks.org/handle/20.500.12854/69075(EXLCZ)99540000000004518020202105d2020 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierTargeting STAT3 and STAT5 in CancerBasel, SwitzerlandMDPI - Multidisciplinary Digital Publishing Institute20201 electronic resource (578 p.)3-03943-036-X 3-03943-037-8 Every minute, 34 new patients are diagnosed with cancer globally. Although over the past 50 years treatments have improved and survival rates have increased dramatically for several types of cancers, many remain incurable. Several aggressive types of blood and solid cancers form when mutations occur in a critical cellular signaling pathway, the JAK-STAT pathway; (Janus Kinase-Signal Transducer and Activator of Transcription). Currently, there are no clinically available drugs that target the oncogenic STAT3/5 proteins in particular or their Gain of Function hyperactive mutant products. Here, we summarize targeting approaches on STAT3/5, as the field moves towards clinical applications as well as we illuminate on upstream or downstream JAK-STAT pathway interference with kinase inhibitors, heat shock protein blockers or changing nuclear import/export processes. We cover the design paradigms and medicinal chemistry approaches to illuminate progress and challenges in understanding the pleiotropic role of STAT3 and STAT5 in oncogenesis, the microenvironment, the immune system in particular, all culminating in a complex interplay towards cancer progression.Research & information: generalbicsscBiology, life sciencesbicsscmultiple myelomaSTAT3S3I-1757nanoparticleCD38siRNA/RNAipolyethyleniminePEIlipopolyplexsiRNA deliverygliomaglioblastomaSTAT5AKTERK1/2prolactinandrogensprostate cancerknockoutescape mechanismsstem/progenitor cellscell hierarchycancerCD4+ T cellsCD8+ T cellsmyeloid cellsimmune check pointhepatitis C virus (HCV)cirrhosishepatocellular carcinoma (HCC)endoplasmic reticulum (ER) stressoxidative stress (OS)unfolded protein response (UPR)microRNA-122 (miR-122)nuclear factor erythroid 2-related factor 2 (NRF2)signal transducer and activator of transcription 3 (STAT3)hepatocyte nuclear factor 4 alpha (HNF4A)solid cancerscell cycleapoptosisinflammationmitochondriastemnesstumor suppressionmelanomaautoimmune diseaseimmunotherapytumor-immune cell interactionsbreast cancerPD-L1M2 macrophagesNK cellsSTAT3 inhibitor XIIIhedgingtransaction costsdynamic programmingrisk managementpost-decision state variablecancer progressioncancer-stem cellcytokinetherapy resistancemetastasisimmunosuppressiontumor microenvironmentproliferationtyrosine kinase 2JAK family of protein tyrosine kinasessignal transducer and activator of transcriptioncytokine receptor signalinggain-of-function mutationtumorigenesisADAM17interleukin-6trans-signalingepidermal growth factor receptor (EGF-R)sheddingmetalloproteasetumor necrosis factor alpha (TNFα)inflammation associated cancercolon cancerlung cancerSH2 domainmutationsautosomal-dominant hyper IgE syndromeinflammatory hepatocellular adenomasT-cell large granular lymphocytic leukemiaT-cell prolymphocytic leukemiagrowth hormone insensitivity syndromenuclear pore complexnuclear transport receptorsnucleocytoplasmic shuttlingtargetingtumor-associated macrophagesadoptive T cell therapyimmune suppressionSTAT transcription factorsJAKSTATT-PLLT-cell leukemiameta-analysisSTAT5B signalingsmall-molecule inhibitorscancer modelscompanion animalscomparative oncologypharmacological inhibitorSTAT5 signalingchemotherapy resistancemyeloid leukemiaheat shock proteinschaperonesstabilizationtargeted therapyovarian cancerhematopoietic cancerstherapeutic targetingpharmacological inhibitorsmTORBone Marrow Failure SyndromeslymphocyteslymphomaT-cellsRHOANGSMPNJAK2 V617Fneoplastic stem cellsResearch & information: generalBiology, life sciencesMoriggl Richardedt1287874Gunning PatrickedtKeserü György MiklósedtMoriggl RichardothGunning PatrickothKeserü György MiklósothBOOK9910557623503321Targeting STAT3 and STAT5 in Cancer3020509UNINA