TY  - GEN
AU  - Moriggl,Richard
AU  - Gunning,Patrick
AU  - Keserü,György Miklós
AU  - Moriggl,Richard
AU  - Gunning,Patrick
AU  - Keserü,György Miklós
TI  - Targeting STAT3 and STAT5 in Cancer
SN  - books978-3-03943-037-6
PY  - 2020///
CY  - Basel, Switzerland
PB  - MDPI - Multidisciplinary Digital Publishing Institute
KW  - Research & information: general
KW  - bicssc
KW  - Biology, life sciences
KW  - multiple myeloma
KW  - STAT3
KW  - S3I-1757
KW  - nanoparticle
KW  - CD38
KW  - siRNA/RNAi
KW  - polyethylenimine
KW  - PEI
KW  - lipopolyplex
KW  - siRNA delivery
KW  - glioma
KW  - glioblastoma
KW  - STAT5
KW  - AKT
KW  - ERK1/2
KW  - prolactin
KW  - androgens
KW  - prostate cancer
KW  - knockout
KW  - escape mechanisms
KW  - stem/progenitor cells
KW  - cell hierarchy
KW  - cancer
KW  - CD4+ T cells
KW  - CD8+ T cells
KW  - myeloid cells
KW  - immune check point
KW  - hepatitis C virus (HCV)
KW  - cirrhosis
KW  - hepatocellular carcinoma (HCC)
KW  - endoplasmic reticulum (ER) stress
KW  - oxidative stress (OS)
KW  - unfolded protein response (UPR)
KW  - microRNA-122 (miR-122)
KW  - nuclear factor erythroid 2-related factor 2 (NRF2)
KW  - signal transducer and activator of transcription 3 (STAT3)
KW  - hepatocyte nuclear factor 4 alpha (HNF4A)
KW  - solid cancers
KW  - cell cycle
KW  - apoptosis
KW  - inflammation
KW  - mitochondria
KW  - stemness
KW  - tumor suppression
KW  - melanoma
KW  - autoimmune disease
KW  - immunotherapy
KW  - tumor–immune cell interactions
KW  - breast cancer
KW  - PD-L1
KW  - M2 macrophages
KW  - NK cells
KW  - STAT3 inhibitor XIII
KW  - hedging
KW  - transaction costs
KW  - dynamic programming
KW  - risk management
KW  - post-decision state variable
KW  - cancer progression
KW  - cancer-stem cell
KW  - cytokine
KW  - therapy resistance
KW  - metastasis
KW  - immunosuppression
KW  - tumor microenvironment
KW  - proliferation
KW  - tyrosine kinase 2
KW  - JAK family of protein tyrosine kinases
KW  - signal transducer and activator of transcription
KW  - cytokine receptor signaling
KW  - gain-of-function mutation
KW  - tumorigenesis
KW  - ADAM17
KW  - interleukin-6
KW  - trans-signaling
KW  - epidermal growth factor receptor (EGF-R)
KW  - shedding
KW  - metalloprotease
KW  - tumor necrosis factor alpha (TNFα)
KW  - inflammation associated cancer
KW  - colon cancer
KW  - lung cancer
KW  - SH2 domain
KW  - mutations
KW  - autosomal-dominant hyper IgE syndrome
KW  - inflammatory hepatocellular adenomas
KW  - T-cell large granular lymphocytic leukemia
KW  - T-cell prolymphocytic leukemia
KW  - growth hormone insensitivity syndrome
KW  - nuclear pore complex
KW  - nuclear transport receptors
KW  - nucleocytoplasmic shuttling
KW  - targeting
KW  - tumor-associated macrophages
KW  - adoptive T cell therapy
KW  - immune suppression
KW  - STAT transcription factors
KW  - JAK
KW  - STAT
KW  - T-PLL
KW  - T-cell leukemia
KW  - meta-analysis
KW  - STAT5B signaling
KW  - small-molecule inhibitors
KW  - cancer models
KW  - companion animals
KW  - comparative oncology
KW  - pharmacological inhibitor
KW  - STAT5 signaling
KW  - chemotherapy resistance
KW  - myeloid leukemia
KW  - heat shock proteins
KW  - chaperones
KW  - stabilization
KW  - targeted therapy
KW  - ovarian cancer
KW  - hematopoietic cancers
KW  - therapeutic targeting
KW  - pharmacological inhibitors
KW  - mTOR
KW  - Bone Marrow Failure Syndromes
KW  - lymphocytes
KW  - lymphoma
KW  - T-cells
KW  - RHOA
KW  - NGS
KW  - MPN
KW  - JAK2 V617F
KW  - neoplastic stem cells
KW  - n/a
N1  - Open Access
N2  - 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
UR  - https://mdpi.com/books/pdfview/book/2844
UR  - https://directory.doabooks.org/handle/20.500.12854/69075
ER  -