06756nam 2201933z- 450 991055762350332120210501(CKB)5400000000045180(oapen)https://directory.doabooks.org/handle/20.500.12854/69075(oapen)doab69075(EXLCZ)99540000000004518020202105d2020 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierTargeting STAT3 and STAT5 in CancerBasel, SwitzerlandMDPI - Multidisciplinary Digital Publishing Institute20201 online 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.Biology, life sciencesbicsscResearch & information: generalbicsscADAM17adoptive T cell therapyAKTandrogensapoptosisautoimmune diseaseautosomal-dominant hyper IgE syndromeBone Marrow Failure Syndromesbreast cancercancercancer modelscancer progressioncancer-stem cellCD38CD4+ T cellsCD8+ T cellscell cyclecell hierarchychaperoneschemotherapy resistancecirrhosiscolon cancercompanion animalscomparative oncologycytokinecytokine receptor signalingdynamic programmingendoplasmic reticulum (ER) stressepidermal growth factor receptor (EGF-R)ERK1/2escape mechanismsgain-of-function mutationglioblastomagliomagrowth hormone insensitivity syndromeheat shock proteinshedginghematopoietic cancershepatitis C virus (HCV)hepatocellular carcinoma (HCC)hepatocyte nuclear factor 4 alpha (HNF4A)immune check pointimmune suppressionimmunosuppressionimmunotherapyinflammationinflammation associated cancerinflammatory hepatocellular adenomasinterleukin-6JAKJAK family of protein tyrosine kinasesJAK2 V617Fknockoutlipopolyplexlung cancerlymphocyteslymphomaM2 macrophagesmelanomameta-analysismetalloproteasemetastasismicroRNA-122 (miR-122)mitochondriaMPNmTORmultiple myelomamutationsmyeloid cellsmyeloid leukemian/ananoparticleneoplastic stem cellsNGSNK cellsnuclear factor erythroid 2-related factor 2 (NRF2)nuclear pore complexnuclear transport receptorsnucleocytoplasmic shuttlingovarian canceroxidative stress (OS)PD-L1PEIpharmacological inhibitorpharmacological inhibitorspolyethyleniminepost-decision state variableprolactinproliferationprostate cancerRHOArisk managementS3I-1757SH2 domainsheddingsignal transducer and activator of transcriptionsignal transducer and activator of transcription 3 (STAT3)siRNA deliverysiRNA/RNAismall-molecule inhibitorssolid cancersstabilizationSTATSTAT transcription factorsSTAT3STAT3 inhibitor XIIISTAT5STAT5 signalingSTAT5B signalingstem/progenitor cellsstemnessT-cell large granular lymphocytic leukemiaT-cell leukemiaT-cell prolymphocytic leukemiaT-cellsT-PLLtargeted therapytargetingtherapeutic targetingtherapy resistancetrans-signalingtransaction coststumor microenvironmenttumor necrosis factor alpha (TNFα)tumor suppressiontumor-associated macrophagestumor-immune cell interactionstumorigenesistyrosine kinase 2unfolded protein response (UPR)Biology, life sciencesResearch & information: generalGunning PatrickedtKeserü G. MedtMoriggl RichardedtBOOK9910557623503321Targeting STAT3 and STAT5 in Cancer3020509UNINA