Relevant bibliographies by topics / STAT. Inhibitor

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Academic literature on the topic 'STAT. Inhibitor'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "STAT. Inhibitor"

1

Jones, Dan, Justin Windham, Brian Stewart, Luis Fayad, Alma Rodriguez, and Fredrick B. Hagemeister. "Differential JAK-STAT Pathway Activation in Primary Mediastinal Large B-Cell Lymphoma: Two Subgroups with Differential Cytokine Activation Patterns and Predicted Responses to Kinase Inhibitors." Blood 114, no. 22 (November 20, 2009): 968. http://dx.doi.org/10.1182/blood.v114.22.968.968.

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Abstract Abstract 968 Background: Primary mediastinal large B-cell lymphoma (PMBCL) is a specialized type of diffuse large B-cell lymphoma which shows diagnostic and pathogenetic overlap with mediastinal classical Hodgkin lymphoma. Approximately 60% of patients with PMBCL have good response to conventional chemoradiotherapy with the rest often showing distant relapses. Microarray studies of PMBCL have revealed overexpression of components and targets of the JAK-STAT signaling pathways including upregulation of IL13 receptor and STAT1; a subset of PMBCL have genome amplification of JAK2 or deletion of the JAK suppressor SOCS1. Given this complexity, we examined the most common mechanism and effects of JAK-STAT dysregulation in a series of newly diagnosed and recurrent PMBCL. Methods: Fifty-three biopsies from 23 patients with PMBCL were assessed and correlated with outcome. JAK2 and SOCS1 copy number status were determined by quantitative PCR on genomic DNA. JAK-STAT pathway activation was probed using reverse transcription quantitative (RQ)-PCR for JAK2, JAK3, and a panel of IL-4 and IL-13 transcriptional targets. JAK-STAT activation was assessed in tissue arrays using antisera against phospho-activation epitopes of STAT1, STAT3, STAT5, and STAT6 using immunohistochemistry (IHC). Activation patterns were modeled in the PMBCL cell line Karpas (K)1106P at baseline and following IL-4 and IL-13 stimulation with or without a range of small molecule inhibitors and blocking antibodies. Growth parameters were measured by MTT and protein levels by flow cytometry, Western blot, RQ-PCR and kinase profiling. Results: JAK2 genomic amplification was present in 40% of PMBCL and SOCS1 deletion in 10% as well as in the K1106P line. By phospho-activation IHC, tumors in 20/23 (87%) patients showed STAT activation, mostly due to STAT1 (60.8%) followed by STAT3 (26.1%), with 6 cases showing mixed patterns. In different tumors, localized and uniform STAT activation patterns were seen. Constitutive STAT activation was correlated with high expression of IL-4 transcription targets including CCL17 and IL13RA as well as JAK2 autophosphorylation and inferior outcome (p = .007). Tumors with more localized foci of activation were associated with alternate transcription patterns. In the K1106P cell line, IL-4 but not IL-13 treatment led to inducible STAT1 activation whereas baseline STAT3/6 activation was highly regulated by cytokine exposure. The JAK2 inhibitor JSI124 blocked IL-4 induced STAT1 activation whereas the JAK inhibitors AG-490, NSC7908 and WHI-P154 did not but did block IL-4/IL-13-induced STAT3 activation. The JAK3 inhibitor ZM39923 was most effective in blocking cell growth but did not block STAT1 activation. Conclusions: JAK2-STAT pathway activation characterizes nearly all cases of PMBCL but genetic mechanisms are distinct leading to distinct patterns of STAT1 activation (driven predominantly through the type I IL-4 receptor) and STAT3/6 activation (driven predominantly through the type II IL13RA/IL4RA) with differential effects on growth parameters and gene regulation. The patterns of STAT activation and target gene expression in primary tumors comprising these two groups mirrored the response to small molecule inhibitors following cytokine exposure in vitro in the K1106P line and highlights differences between IL-4 and IL-13 signaling in PMBCL. Profiling of PMBCL biopsies with phosphoactivation IHC for STAT isoforms may be useful to subcategorize cases and select the optimal JAK-STAT pathway inhibitors for adjuvant therapy. Disclosures: No relevant conflicts of interest to declare.
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Hu, Cheng-Ping, Jun-Tao Feng, Yu-Ling Tang, Jin-Qi Zhu, Min-Juan Lin, and Ming-En Yu. "LIF Upregulates Expression of NK-1R in NHBE Cells." Mediators of Inflammation 2006 (2006): 1–8. http://dx.doi.org/10.1155/mi/2006/84829.

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Leukemia inhibitory factor (LIF), a cytokine at the interface between neurobiology and immunology, is mainly mediated through JAK/STAT pathway and MAPK/ERK pathway. Evidence suggested LIF is related to the higher expression of neurokinin-1 receptor (NK-1R) in asthma. In this study, the immunohistochemistry stain showed the expressions of NK-1R, LIF, p-STAT3, and p-ERK1/2 in the lung tissues of allergic rats were increased compared with the controls, and the main positive cell type was airway epithelial cell. Normal human bronchial epithelial cells were treated with LIF in the presence or absence of AG490 (JAK2 inhibitor), PD98059 (MEK inhibitor), and the siRNA against STAT3. Western blot and RT-PCR indicated that LIF induced the expression of NK-1R, which was inhibited by the inhibitors mentioned above. No significant interaction was found between JAK/STAT pathway and MAPK/ERK pathway. In summary, bronchial epithelial cell changes in asthma are induced by LIF which promotes the expression of NK-1R, and JAK/STAT pathway and MAPK/ERK pathway may participate in this process.
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Zhang, Xuekang, Jun Zhou, Qian Hu, Zhengren Liu, Qiuhong Chen, Wenxiang Wang, Huaigen Zhang, Qin Zhang, and Yuanlu Huang. "The Role of Janus Kinase/Signal Transducer and Activator of Transcription Signalling on Preventing Intestinal Ischemia/Reperfusion Injury with Dexmedetomidine." Journal of Nanoscience and Nanotechnology 20, no. 5 (May 1, 2020): 3295–302. http://dx.doi.org/10.1166/jnn.2020.16416.

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Dexmedetomidine (Dex) works as a crucial agent for the treatment of intestinal ischemia/reperfusion (I/R), but its mechanism remains unclear. Recent articles demonstrated the pivotal role of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3) signalling in I/R. Therefore, it is reasonable to explore the associated mechanism of JAK2/STAT3 signalling in Dex treatment. The study purpose was to evaluate the JAK2/STAT3 signalling regulatory mechanisms of Dex in preventing I/R. Anaesthetized rats were subjected to superior mesenteric artery occlusion consisting of 1 h of ischemia and 2 h of reperfusion while served as controls. Animals received subcutaneous administration of 50 μg/kg Dex, JAK1 and JAK2 inhibitor, Ruxolitinib, selective JAK2 inhibitor, 10 mg/kg AG490 or STAT inhibitor and 0.4 mg/kg rapamycin; or Dex-treatment in the presence of α2-adrenoceptor antagonists Atip or Dex-treatment alone after I/R. Injury was scored histologically, apoptosis was detected via the apoptotic mediators caspase-3 and Bcl-2/Bax and the degree of activation of the JAK/STAT pathway was evaluated. Dex inhibited I/R injury by decreasing apoptosis significantly with rescue of cleaved caspase-3 and the Bcl-2/Bax ratio. Furthermore, phosphorylation of JAK2, STAT1 and STAT3 was affected, suggesting the involvement of activated JAK/STAT in response to Dex. Meanwhile, the JAK2 or STAT inhibitors AG490 and rapamycin, but not Ruxolitinib, exhibited a similar but even greater JAK2 and STAT3 regulatory effect, thus leading to a greater benefit. JAK2/STAT3 activation is crucial to the diminishing effect of Dex on mesenteric I/R injury; however, the efficacy and timing of Dex administration should be considered in clinical practice.
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Zhao, Lan-Juan, Sheng-Fei He, Yuan Liu, Ping Zhao, Zhong-Qi Bian, and Zhong-Tian Qi. "Inhibition of STAT Pathway Impairs Anti-Hepatitis C Virus Effect of Interferon Alpha." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 77–90. http://dx.doi.org/10.1159/000452526.

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Background/Aims: Signal transducer and activator of transcription (STAT) pathway plays an important role in antiviral efficacy of interferon alpha (IFN-α). IFN-α is the main therapeutic against hepatitis C virus (HCV) infection. We explored effects of IFN-α on HCV replication and antiviral gene expression by targeting STAT. Methods: In response to IFN-α, STAT status, HCV replication, and antiviral gene expression were analyzed in human hepatoma Huh7.5.1 cells before and after cell culture-derived HCV infection. Results: IFN-α treatment induced expression and phosphorylation of STAT1 and STAT2 in Huh7.5.1 cells. Pretreatment of Huh7.5.1 cells with a mAb to IFN alpha receptor (IFNAR) 2 decreased IFN-α-dependent phosphorylation of STAT1 and STAT2, whereas pretreatment with an IFNAR1 mAb increased such phosphorylation, suggesting that IFNAR mediates IFN-α-triggered STAT signaling. During HCV infection, STAT1 and STAT2 phosphorylation could be rescued by IFN-α and IFN-α-induced phosphorylation of STAT1 and STAT2 was impaired. Inhibition of STAT pathway by Jak inhibitor I significantly enhanced HCV RNA replication and viral protein expression. Antiviral genes coding for IFN regulatory factor 9 and IFN-stimulated gene 15 were up-regulated by IFN-α during HCV infection but such up-regulation was abrogated by Jak inhibitor I. Conclusion: These results establish that activation of STAT pathway is essential for anti-HCV efficacy of IFN-α. Impairment of IFN-α-triggered STAT signaling by HCV may account for evading IFN-α response.
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Kim, Byung-Su, Chansu Lee, Juwon Park, Kwang-Sung Ahn, Byoung Kook Kim, Seonyang Park, Young-Yiul Lee, and Sung-Soo Yoon. "Inactivation of JAK/STAT Cell Signaling by SK-7041, a Novel HDAC Inhibitor, Effectively Inhibits Growth of Acute Myeloid Leukemia Cells." Blood 112, no. 11 (November 16, 2008): 4005. http://dx.doi.org/10.1182/blood.v112.11.4005.4005.

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Abstract Activation of the JAK/STAT pathway appears common in AML, occurring in up to 70% of AML patients. Therefore, JAK/STAT signal inhibitors are promising as candidate anti-cancer agents in AML. Recently, we reported that SK-7041, an HDAC inhibitor, inhibited the growth of AML cells via activation of caspase-3 and down-regulation of cyclin D1. These findings lead us to further examine whether SK-7041 inhibits the growth of KG1 AML cells via inactivation of JAK/STAT signals. Multi-immunoblotting technique (Kinetworks™ analysis) showed that expression of p-STAT-3, p-STAT-5, and p-Erk was down-regulated in KG1 cells treated with SK-7041. These results were confirmed by individual western blot analysis. In addition, IL-6-induced activation of STAT-3 and Erk was inhibited by treatment of SK-7041. Combined treatment of SK-7041 and JAK inhibitor (AG490) showed additive anti-leukemic effect as evidenced by caspase-3 activation, down-regulation of cyclin D1 (cMYC), and inhibition of phosphorylation of STATs (−1, −3). These results suggest that HDAC inhibitor, SK-7041, inhibited AML cell growth via inactivation of JAK/STATs pathway.
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Barclay, J. L., T. Wonisch, S. T. Anderson, M. J. Waters, and J. D. Curlewis. "124. Regulation of SOCS3 expression by prostaglandin, prolactin and growth hormone: challenging the Jak/STAT signalling dogma." Reproduction, Fertility and Development 17, no. 9 (2005): 74. http://dx.doi.org/10.1071/srb05abs124.

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SOCS3 is an inhibitor of various cytokine-receptor signalling pathways and is therefore involved in suppression of cellular responsiveness to these critical regulators. SOCS3 expression is thought to be regulated by a STAT responsive element (SRE). However, our research suggests the involvement of other signalling pathways. In T-47D breast cancer cells, we found that PGE2 induces a 3–5 fold increase in SOCS3 mRNA, as determined by real-time PCR. This effect was not due to phosphorylation of STATs, or inhibited by the Jak2 inhibitor, AG490, but was inhibited by the PI3Kinase inhibitor, LY294002, Akt Inhibitor IV and partially inhibited by the PKA inhibitor, H89. It was not affected by inhibitors of MEK, PDK1, mTOR or p38-MAPK. We concurrently examined PRL-induced SOCS3 expression, and found that although STAT1 and 5 phosphorylation was increased, SOCS3 expression was again inhibited by Akt Inhibitor IV and H89 but unaffected by AG-490. To explore this further, we used a model of GH signalling, BaF3 cells stably expressing GH receptor. GH induced a 15–20 fold increase in SOCS3 mRNA, which was accompanied by increased STAT5 phosphorylation. However the SOCS3 response was not inhibited by AG-490 or H89, but was diminished by Akt Inhibitor IV. Analysis of the SOCS3 promoter revealed a FOXO binding site. When we mutated this site in a mouse SOCS3 promoter–luciferase construct, basal and GH-induced promoter activity was significantly increased. These results are consistent with FOXO acting as a repressor, which is inactivated by Akt. We propose that in T-47D cells, SOCS3 expression involves cross-talk between PI3K/Akt and cAMP/PKA, whereas in BaF3 cells, expression is enhanced by Akt phosphorylation and subsequent FOXO inactivation. These findings contrast with the accepted Jak/STAT regulation of SOCS3 expression. This work is supported by the Australian Research Council.
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Kitanaga, Yukihiro, Emiko Imamura, Yutaka Nakahara, Hidehiko Fukahori, Yasutomo Fujii, Satoshi Kubo, Shingo Nakayamada, and Yoshiya Tanaka. "In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors." Rheumatology 59, no. 8 (November 25, 2019): 1957–68. http://dx.doi.org/10.1093/rheumatology/kez526.

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Abstract Objectives Peficitinib, a novel Janus kinase (JAK) inhibitor, demonstrated promising results in treating RA in phase 3 clinical trials. This in vitro study was undertaken to characterize the pharmacological properties of peficitinib and investigate the involvement of JAK and signal transducer and activator of transcription (STAT) pathways in the pathological processes of SSc, which is also an autoimmune disease. Methods Phosphorylation levels of STAT molecules were assessed in peripheral blood mononuclear cells collected from patients with RA or SSc and healthy subjects, and in skin specimens obtained from 19 patients with SSc. In vitro inhibition of STAT phosphorylation and cytokine/chemokine production by peficitinib, tofacitinib and baricitinib were also characterized. Results Higher spontaneous STAT1 or STAT3 phosphorylation was observed in peripheral T-cells and monocytes from patients with RA and SSc compared with healthy subjects. In skin sections from patients with SSc, phosphorylated STAT3–positive cells were found in almost all cases, irrespective of disease subtype or patient characteristics. Conversely, phosphorylated STAT1-positive cells were observed only in samples from untreated patients with diffuse disease of short duration. Peficitinib inhibited STAT phosphorylation induced by various cytokines, with comparable efficacy to tofacitinib and baricitinib. Peficitinib also suppressed cytokine and chemokine production by peripheral blood mononuclear cells and skin fibroblasts. Conclusion Our results suggest that JAK/STAT pathways are constitutively activated in SSc and RA, and that the JAK inhibitor may represent a novel therapeutic option for SSc.
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Zhou, Jianbiao, Chonglei Bi, Lai Fong Poon, Viraj J. Janakakumara, Jiaying Khng, Hanry Yu, Keith B. Glaser, Daniel H. Albert, Davidsen K. Davidsen, and Chien-Shing Chen. "Overactivation of STAT Pathways and Overexpression of Survivin Confer Resistance to FLT3 Inhibitors and Could Be Therapeutic Targets in AML." Blood 110, no. 11 (November 16, 2007): 2367. http://dx.doi.org/10.1182/blood.v110.11.2367.2367.

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Abstract Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (FLT3) receptor plays an important role in the pathogenesis of acute myeloid leukemia (AML). A number of small molecule kinase inhibitors are currently proceeding in different phases of clinical trials. As with imatinib in CML, leukemic cells could develop resistance to these RTK inhibitors when used as monotherapy. Mutations in the ATP-binding pocket have been identified through PCR-based mutagenesis screening in Ba/F3-FLT3-ITD cells and selected for growth in the presence of PKC412, or in a resistant Ba/F3-FLT3-ITD cell line developed by cocultured with SU5416. Resistance to PKC412 resulting from the N676K point mutation in the FLT3 kinase domain has been described in a clinical trial patient. Selection of activating Ras mutations has been found in 2 out of 6 FLT3 inhibitor resistant cell lines, but no point mutation of FLT3 kinase domain was found in all 6 resistant cell lines. To further investigate other potential mechanisms of resistance to FLT3 inhibitors, we developed a resistant cell line by long-term culture of MV4-11 cells with ABT-869, designated as MV4-11-R (IC50: 52 vs 6 nM for the parental MV4-11 cell line), which is also cross resistant to other structurally unrelated inhibitors including SU5416, AG1296 and a FLT3 inhibitor III (MERCK). No point mutation in the kinase domain of FLT3 was found in MV4-11-R cells. Western blot and FACS analysis excluded overexpression of p-FLT3, FLT3 or 3 multidrug resistance related proteins (MDR, MRP1 and LRP) in this resistant line. Gene expression profiling revealed up-regulation of FLT3 ligand (FLT3LG) (2.4 fold) and Survivin (2 fold), while down-regulation of SOCS1, SOCS2, and SOCS3 was observed in MV4-11-R compared to MV4-11 parental cells. Overexpression of FLT3LG and Survivin was also demonstrated at the protein level. Survivin is a unique member of the inhibitor of apoptosis proteins (IAP) family and a known target of the STAT3 pathway. Down-regulation of suppressor of cytokine signaling (SOCS) proteins (negative regulators of STAT pathways) was observed even in the presence of overactivation of the STAT1, STAT3 and STAT5 pathways in the MV4-11-R line. We screened a panel of small molecule inhibitors including a STAT inhibitor (indirubin derivative IDR E804), 3 JAK inhbitors (Tyrene CR4, AG490, and JAK3 Inhibitor II), and a CDK/survivin inhibitor (NU6140). We found that MV4-11-R is most sensitive to IDR E804 (an inhibitor of CDKs and the SRC-STAT3 pathway). The IC50 value of ABT-869 in MV4-11-R was decreased from 52 to 6.2 nM in the presence of 2 nM of IDR E804. Further validation of the therapeutic effect of IDR E804 in combination with ABT-869 in the MV4-11-R mouse xenograft model is ongoing. Targeting Survivin by shRNA and a dominant-negative vector (survivin-T34A) induced MV4-11-R to undergo apoptosis. Taken together, these results demonstrate that overactivation of STAT pathways and overexpression of survivin are the main mechanism of resistance to ABT-869; suggesting that the STAT pathways and survivin could be potential targets for the treatment of patients who develop resistance to FLT3 inhibitors.
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Banes, Amy K., Séan Shaw, John Jenkins, Heather Redd, Farhad Amiri, David M. Pollock, and Mario B. Marrero. "Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli." American Journal of Physiology-Renal Physiology 286, no. 4 (April 2004): F653—F659. http://dx.doi.org/10.1152/ajprenal.00163.2003.

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Clinical and animal studies show that treatment with angiotensin-converting enzyme (ACE) inhibitors or ANG II-receptor antagonists slows progression of nephropathy in diabetes, indicating ANG II plays an important role in its development. We previously reported that hyperglycemia augments both ANG II-induced growth and activation of Janus kinase (JAK)2 and signal transducers and activators of transcription (STAT) proteins in cultured rat mesangial cells. Furthermore, we demonstrated that the tyrosine kinase enzyme JAK2 plays a key role in both ANG II- and hyperglycemia-induced growth in these cells. We hypothesized that the ACE inhibitor captopril and the ANG II-receptor antagonist candesartan would hinder hyperglycemic-induced activation of JAK and STAT proteins in rat glomeruli, demonstrating that ANG II plays an important role in the activation of these proteins in vivo. Adult male Sprague-Dawley rats were given either streptozotocin (STZ; 60 mg/kg iv) or vehicle, and glomeruli were isolated 2 wk later. Activation of JAK and STAT proteins was evaluated by Western blot analysis for specific tyrosine phosphorylation. Groups of rats were given captopril (75–85 mg·kg-1·day-1), candesartan (10 mg· kg-1·day-1), or the JAK2 inhibitor AG-490 (5 mg·kg-1·day-1) for the study's duration. STZ stimulated glomerular phosphorylation of JAK2, STAT1, STAT3, and STAT5. Phosphorylation was reduced in rats treated with captopril, candesartan, and AG-490. Furthermore, both candesartan and AG-490 inhibited STZ-induced increases in urinary protein excretion. In conclusion, our studies demonstrate that hyperglycemia induces activation of JAK2 and the STATs in vivo via an ANG II-dependent mechanism and that these proteins may be involved in the early kidney damage associated with diabetes.
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Alunno, Alessia, Ivan Padjen, Antonis Fanouriakis, and Dimitrios T. Boumpas. "Pathogenic and Therapeutic Relevance of JAK/STAT Signaling in Systemic Lupus Erythematosus: Integration of Distinct Inflammatory Pathways and the Prospect of Their Inhibition with an Oral Agent." Cells 8, no. 8 (August 15, 2019): 898. http://dx.doi.org/10.3390/cells8080898.

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Four Janus kinases (JAKs) (JAK1, JAK2, JAK3, TYK2) and seven signal transducers and activators of transcription (STATs) (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, STAT6) mediate the signal transduction of more than 50 cytokines and growth factors in many different cell types. Located intracellularly and downstream of cytokine receptors, JAKs integrate and balance the actions of various signaling pathways. With distinct panels of STAT-sensitive genes in different tissues, this highly heterogeneous system has broad in vivo functions playing a crucial role in the immune system. Thus, the JAK/STAT pathway is critical for resisting infection, maintaining immune tolerance, and enforcing barrier functions and immune surveillance against cancer. Breakdowns of this system and/or increased signal transduction may lead to autoimmunity and other diseases. Accordingly, the recent development and approval of the first small synthetic molecules targeting JAK molecules have opened new therapeutic avenues of potentially broad therapeutic relevance. Extensive data are now available regarding the JAK/STAT pathway in rheumatoid arthritis. Dysregulation of the cytokines is also a hallmark of systemic lupus erythematosus (SLE), and targeting the JAK/STAT proteins allows simultaneous suppression of multiple cytokines. Evidence from in vitro studies and animal models supports a pivotal role also in the pathogenesis of cutaneous lupus and SLE. This has important therapeutic implications, given the current paucity of targeted therapies especially in the latter. Herein, we summarize the currently available literature in experimental SLE, which has led to the recent promising Phase II clinical trial of a JAK inhibitor.
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Dissertations / Theses on the topic "STAT. Inhibitor"

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Younis, Usir, and Usir Younis. "Inhalational Delivery of a JAK3 Inhibitor for the Novel Treatment of Asthma and the Investigation of Pharmaceutical Salts in HFA Propellant Systems." Diss., The University of Arizona, 2018. http://hdl.handle.net/10150/626756.

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Asthma is a significant lung disease involving chronic inflammation and remodeling of the airways, resulting in reduced quality of life for those who suffer from the condition. Current therapeutic guidelines suggest the use of inhaled corticosteroids for long-term anti-inflammatory relief to manage moderate to severe chronic asthma; however, inhaled corticosteroids fail to provide prophylactic or reversal treatment of damaged airways incurred by chronic asthma as well as exhibiting adverse side effects (skeletal complications, diabetes, and weight gain).Therefore, there is a need for a new type of drug therapy to address these gaps in the treatment of chronic asthma. There is growing interest aimed towards the inhibition of the Janus Kinase and Signal Transducer and Activator of Transcription (JAK-STAT) pathway for the treatment of asthma. Despite the promising opportunity to investigate this new pathway towards this clinical application, no published work is available using an established and characterized JAK 1/3 inhibitor for the treatment of chronic asthma delivered via inhalation. This work investigated tofacitinib citrate, a selective JAK 3 inhibitor, and its potential to be delivered locally to the lungs for the treatment of chronic asthma. Several preformulation studies were conducted to determine the basic physical and chemical properties of the compound and its free base, tofacitinib, for proper inhalational formulation development. The drug was delivered to BALB/c mice challenged with house dust mite (HDM) allergen via nebulization utilizing a nose-only chamber. After a three week dosing schedule, mice treated with tofacitinib citrate exhibited an increase in monocyte cell numbers with a simultaneous decrease in eosinophil cell count, gathered from BAL fluid. Further, the experimental groups treated with tofacitinib citrate had a decrease in total protein concentrations in comparison to the experimental groups that were only challenged with HDM or were both exposed to HDM and vehicle. These findings demonstrated that the proper formulation was developed for nebulized delivery of tofacitinib citrate, and that the compound was capable of reducing total protein concentrations and eosinophil cell recruitment, both recognized as biomarkers for an asthmatic response. Although significant work is still needed to be done, these data hold promise for the potential of a locally delivered JAK 3 inhibitor as a treatment for chronic asthma. Further, the solubility of tofacitinib citrate and five other pharmaceutical salts were determined in HFA 134a, HFA 227, and DFP with varying cosolvent content (0-20% v/v ethanol). The experimental solubilities of the free acid and base compounds were larger than the solubilities of their respective salts in all three systems for tofacitinib, albuterol, and salicylic acid. Warfarin, phenytoin, and ciprofloxacin had similar solubilities with their respective salt forms. Solubilities also increased with increasing cosolvent concentration for all compounds investigated. The model propellant, DFP, provided a slightly stronger correlation of solubility values with HFA 134a in comparison to HFA 227. The observed solubility values were also compared to calculated values obtained from the ideal solubility model, where it was determined that the observed solubility was indeed also dependent on its surrounding solvent interactions and not solely on its ideal solubility (melting point). While some physical changes were observed for the pharmaceutical salts in HFA 134a and 227, more quantitative studies are needed for a larger database of compounds to better understand the factors that contribute to the solubility of pharmaceutical salts (and their correlation to DFP), in HFA-based systems. This information could potentially contribute to a predictive model, saving time and money during the process of pMDI formulation development.
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Torikoshi, Kazuo. "Protein inhibitor of activated STAT, PIASy regulates α-smooth muscle actin expression by interacting with E12 in mesangial cells." Kyoto University, 2013. http://hdl.handle.net/2433/174820.

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Martin, Nadine. "Rôle de la SUMO E3 ligase PIASy dans les mécanismes de contrôle de la prolifération cellulaire et de réponse aux dommages." Paris 6, 2007. http://www.theses.fr/2007PA066243.

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La modification des protéines par SUMO joue un rôle important dans de nombreuses fonctions cellulaires. Le travail présenté dans cette thèse vise à analyser l'action des protéines PIAS, régulateurs transcriptionnels et SUMO E3 ligases, et en particulier de PIASy dans le contexte de l'oncogenèse. Nous avons montré que PIASy induit la sénescence des fibroblastes primaires, en activant les voies Rb et p53, ou l'apoptose si la voie Rb est déficiente. Nous avons parallèlement identifié de nouveaux partenaires protéiques de PIASy. PIASy induit l'accumulation de FIP200 dans le noyau, ce qui inhibe l'action de FIP200 dans la voie mTOR. FIP200 coopère avec PIASy pour activer l'expression du gène p21. Par ailleurs, la modification de PARP-1 par SUMO stimulée par PIASy régule la réponse au choc thermique. Ainsi, ce travail a mis en évidence un rôle important de PIASy dans le contrôle de la prolifération cellulaire et la réponse aux dommages, et a précisé son action au niveau moléculaire
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Aubert-Jürgens, Ana. "STAT3 inhibitors for cancer treatment." [S.l.] : [s.n.], 2005. http://elib.tu-darmstadt.de/diss/000563.

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Ricard, Laure. "Les lymphocytes T folliculaires auxiliaires dans la sclérodermie systémique." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS340.

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La sclérodermie systémique (SSc) est une maladie auto-immune, caractérisée par une atteinte microvasculaire oblitérante, de la fibrose et des anomalies de l'immunité humorale. Les lymphocytes T folliculaires auxiliaires (Tfh) CD4+CXCR5+PD1+ coopèrent avec les lymphocytes B pour induire leur différenciation en plasmocytes sécréteurs d’immunoglobulines (Ig). Les Tfh circulants (cTfh) sont augmentés dans plusieurs maladies auto-immunes et les Tfh infiltrent la peau des patients SSc. Nous avons observé que les cTfh des patients SSc étaient augmentés en comparaison avec les témoins et notamment dans des formes sévères de SSc. Les cTfh des patients SSc ont un phénotype activé avec une forte expression de BCL-6 et des capacités augmentées à produire de l’IL-21. In vitro, les cTfh de patients SSc sont aussi plus efficaces pour stimuler la différenciation des plasmablastes (PB) ainsi que leur production d’Ig. Le blocage de l’IL-21 ainsi que le ruxolitinib, un inhibiteur de la voie JAK1/2 diminuaient la capacité des cTfh à stimuler la différenciation des PB et leur sécrétion d’Ig. Les mécanismes à l’origine de cette expansion aberrante des cTfh dans la SSc demeurent à définir. Les cellules dendritiques, les monocytes ainsi que des anomalies épigénétiques pourraient être à l’origine de cette expansion des cTfh. L’hématopoïèse clonale (HC) est définie par l’acquisition de mutations somatiques dans les cellules souches hématopoïétiques menant à des clones détectables. Nous avons observé une forte prévalence d’HC dans la SSc. Le gène le plus fréquemment muté était DNMT3A impliqué dans la régulation épigénétique. Le rôle de ces mutations dans la physiopathologie de la SSc reste à démontrer
Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis, vascular microangiopathy and deregulated immune system with the presence of autoantibodies. Follicular helper T (Tfh) cells, defined as CD4+CXCR5+PD-1+ cooperate with B lymphocytes to induce the differentiation of plasmocytes secreting immunoglobulins (Ig). Circulating Tfh (cTfh) cells are increased in several autoimmune diseases, and Tfh cells can infiltrate the skin of SSc patients. We demonstrate that cTfh cell are increased in SSc patients compared with healthy controls (HC), which was more potent in severe forms of SSc. cTfh cells from SSc patients present an activated Tfh phenotype, with high expression of BCL-6 and increased capacity to produce IL-21 in comparison to HC. In vitro, cTfh cells from SSc patients had higher capacity to stimulate the differentiation of plasmablasts and their secretion of Ig through the IL-21 pathway. Blocking IL-21 or using the JAK1/2 inhibitor (ruxolitinib) reduced the Tfh cells’ capacity to stimulate the plasmablasts and decreased the Ig production. Mechanisms leading to this aberrant cTfh expansion remain to be established. Monocytes and dendritic cells could participate to this cTfh expansion. Epigenetics abnormalities could also contribute to cTfh activation in SSc. Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the acquisition of somatic mutations in hematopoietic stem cells leading to detectable clones. We observed a high prevalence of CHIP in SSc patients. The most common mutation occurred in DNMT3A gene involved in epigenetic regulation. The implication of these mutations in SSc pathophysiology remains to be demonstrated
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Ball, Sarah Lynnette. "Small molecule inhibitors, LLL12 and celecoxib, effectively inhibit STAT3 phosphorylation, decrease cellular viability and induce apoptosis in medulloblastoma and glioblastoma cell lines." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1298906960.

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Hill, Jacqueline M. "Transition state analogues as inhibitors of metallo-proteases." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260112.

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Fisher, Michael I. "Transition state analogue inhibitors of the aspartyl proteases." Thesis, University of Huddersfield, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363233.

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Ekegren, Jenny. "Design and Synthesis of Novel HIV-1 Protease Inhibitors Comprising a Tertiary Alcohol in the Transition-State Mimic." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6737.

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Ghafoory, Shima. "Development of a screening assay for inhibitors of inflammation useful against pancreatic cancer." Thesis, Mälardalen University, Mälardalen University, School of Sustainable Development of Society and Technology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-7797.

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Pancreatic cancer is the fourth most lethal cancer and ranks as the eighth most commonly diagnosed cancer worldwide. This is due to its rapid proliferation, strong metastatic potential and its delayed detection. One major risk factor for developing pancreatic cancer is the aggressive inflammatory disease chronic pancreatitis. Chronic inflammation frequently precedes the development of certain pancreatic cancers.

Inflammation is a protective and necessary process by which the body can alert the immune system of the existence of a wound or infection and mount an immune response to remove the harmful stimuli and start wound healing. The cross-talking of cells of the immune system and infected cells happens through cytokines, soluble proteins that activate and recruit other immune cells to increase the system’s response to the pathogen. Failure to resolve the injury can result in persistent cytokine production that in turn allows a cell that is damaged or altered to survive when in normal conditions it would be killed. Inflammation is thought to create a microenvironment that facilitates the initiation and/or growth of pancreatic cancer cells.

Cytokines use two important kinases for their signaling: Janus Kinases (JAKs) and Signal Transducers and Activators of Transcription (STATs). The JAKs are activated upon the binding of cytokines to their corresponding receptors. When activated, the JAKs activate STATs through tyrosine phosphorylation. The STATs transduce signals to the nucleus of the cells to induce expression of critical genes essential in normal physiological cellular events such as differentiation, proliferation, cell survival, apoptosis and angiogenesis. STAT3 (a member of the STAT family) is constitutively activated in some pancreatic cancers, promoting cell cycle progression, cellular transformations and preventing apoptosis. Therefore, STAT3 is a promising target for cancer treatment. Novel therapies that inhibit STAT3 activity in cancers are urgently needed. Natural products are a very good resource for the discovery of new drugs against pancreatic cancer.

Covering more than 70% of the Earths surface, The Ocean is an excellent source of bioactive natural products. Harbor Branch Oceanographic Institute’s Center for Marine Biomedical and Biotechnology Research (HBOI-CMBBR) situated in Florida, aims to find new marine natural products useful in disease prevention and drug therapy. Their current focus is to look for novel treatments for preventing both the formation of new pancreatic tumors and the metastasis of existing tumors.

The hypothesis of this degree project was that novel inhibitors of STAT3 useful in the treatment of pancreatitis and/or pancreatic cancer could be found from marine-natural products. The first specific aim of this degree project was to set up an assay to identify bioactive marine natural products as inhibitors of inflammation. Furthermore the assay was validated using a commercially available inhibitor of inflammation (Cucurbitacin I). The last aim was to further validate the assay by screening pure compounds and peak library material from the HBOI marine specimen collection.

At the end of the experimentation time, the assay still was not set-up as there were difficulties in proper cell culture techniques and the cell line did not respond as advertised. While the results were not as expected, the work performed resulted in familiarization with research laboratory practices and increased laboratory skills. Moreover, the results from the assays point to future directions to accomplish this project.


Development of a screening assay for inhibitors of inflammation useful against pancreatic cancer
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Books on the topic "STAT. Inhibitor"

1

Ward, Alister C., ed. STAT Inhibitors in Cancer. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42949-6.

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Ward, Alister C. STAT Inhibitors in Cancer. Humana, 2016.

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Ward, Alister C. STAT Inhibitors in Cancer. Humana, 2018.

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Brunner, Hans R. Ace-Inhibition: State of the Art. S Karger Pub, 1989.

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(Editor), A. Raman, and Paul Labine (Editor), eds. Reviews on Corrosion Inhibitors Science and Technology: Papers Presented at the Corrosion/89 Symposium "Review of Corrosion Inhibition Science." Sponsored ... Group T-3A-15 N Inhibitors, State-Of-The a. Nace, 1993.

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Bernhard, Elsener, European Federation of Corrosion, and Institute of Materials (Great Britain), eds. Corrosion inhibitors for steel in concrete: State of the art report. London: published for the European Federation of Corrosion by Maney on behalf of the Institute of Materials, 2001.

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Martin, Richard. Inhibition of the RTEM-1 [beta]-lactamase by transition-state analogs. 1996.

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Young, Benjamin. Classes of Antiretrovirals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0019.

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Results of the randomized, international INSIGHT START clinical trial provide definitive proof of the benefit of antiretroviral therapy initiation in asymptomatic individuals with CD4+ counts greater than 500 cells/mm3. There are six different classes of antiretroviral agents: two types of reverse transcriptase inhibitors, two types of entry inhibitors, one class of inhibitors of HIV protease, and one class of inhibitors of HIV integrase. Combination antiretroviral therapy is recommended for all people living with HIV. The primary goal of combination antiretroviral therapy is to achieve viral suppression. Each antiretroviral class targets a unique step in the replication cycle of HIV-1.
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Alikhan, Raza. Normal haemostatic function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0283.

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Humans have evolved an intricate system that maintains blood in a fluid state. This relies on an intact vascular endothelium modulating vascular tone and forming a barrier between blood components and reactive subendothelial components. It also involves the production of inhibitors of both blood coagulation and platelet aggregation. In addition, haemostatic systems are primed to convert blood from its fluid state to a solid state, to allow the formation of a haemostatic plug, following vessel injury, to stem the flow of blood from or within a blood vessel. This chapter reviews the physiology of haemostasis.
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Book chapters on the topic "STAT. Inhibitor"

1

Dempsey, Brian R., Anne C. Rintala-Dempsey, Gary S. Shaw, Yuan Xiao Zhu, A. Keith Stewart, Jaime O. Claudio, Constance E. Runyan, et al. "SSI (STAT-Induced STAT Inhibitor)." In Encyclopedia of Signaling Molecules, 1787. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101283.

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Borgés, Sahra, Elara Moudilou, Cécile Vouyovitch, Jean Chiesa, Peter Lobie, Hichem Mertani, and Mireille Raccurt. "Involvement of a JAK/STAT Pathway Inhibitor: Cytokine Inducible SH2 Containing Protein in Breast Cancer." In Hormonal Carcinogenesis V, 321–29. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_30.

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Argyropoulos, Vasilike, Stamatis C. Boyatzis, Maria Giannoulaki, Elodie Guilminot, and Aggeliki Zacharopoulou. "Organic Green Corrosion Inhibitors Derived from Natural and/or Biological Sources for Conservation of Metals Cultural Heritage." In Microorganisms in the Deterioration and Preservation of Cultural Heritage, 341–67. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69411-1_15.

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AbstractIn the last decade, there has been an increase in research related to green corrosion inhibitors for conservation of metals cultural heritage to help promote sustainable practices in the field that are safe, environmentally friendly, and ecologically acceptable. The most common are organic substances derived either from natural and/or biological sources: plant extracts and oils, amino acids, microorganisms, and biopolymers. The chapter will provide a review of these substances as corrosion inhibitors for metals conservation, by discussing the state-of-the-art research to date, with a special focus on cysteine. Most of the research has focused on the examination of such inhibitors on metal coupons with or without corrosion products using electrochemical techniques or weight-loss measurements to determine their effectiveness. Some of these studies have also considered the conservation principles for practice, i.e., reversibility of the treatment and the visual aspect of the modification of the treated metal surface. However, before such green inhibitors can be routinely applied by conservators, more research is required on their application to real artefacts/monuments using in situ corrosion measurements. Furthermore, given that the composition of a green inhibitor is highly dependent on its extraction process, research must also involve identifying the specific adsorption models and involved mechanisms to ensure reproducibility of results.
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Kumar, Janani. "Inhibitors of Upstream Inducers of STAT Activation." In Cancer Drug Discovery and Development, 177–90. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42949-6_7.

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Muller, William A. "PECAM: Regulating the start of diapedesis." In Adhesion Molecules: Function and Inhibition, 201–20. Basel: Birkhäuser Basel, 2007. http://dx.doi.org/10.1007/978-3-7643-7975-9_8.

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Revhaug, A. "Use of Cyclooxygenase Inhibitors in the Acute Catabolic State." In Acute Catabolic State, 217–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-48801-6_19.

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Shouksmith, Andrew E., and Patrick T. Gunning. "Chapter 6. Targeting Signal Transducer and Activator of Transcripion (STAT) 3 with Small Molecules." In Small-molecule Transcription Factor Inhibitors in Oncology, 147–68. Cambridge: Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/9781782624011-00147.

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Bharadwaj, Uddalak, Moses M. Kasembeli, and David J. Tweardy. "STAT3 Inhibitors in Cancer: A Comprehensive Update." In Cancer Drug Discovery and Development, 95–161. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42949-6_5.

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Luly, Jay R., Anthony K. L. Fung, Jacob J. Plattner, Patrick A. Marcotte, Nwe BaMaung, Jeffrey L. Soderquist, and Herman H. Stein. "Transition-state analog inhibitors of human renin." In Peptides, 487–89. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-010-9595-2_145.

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Liu, Suhu, and David Frank. "Translating STAT Inhibitors from the Lab to the Clinic." In Cancer Drug Discovery and Development, 49–68. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42949-6_3.

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Conference papers on the topic "STAT. Inhibitor"

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De Velasco, Marco A., Yurie Kura, Naomi Ando, Emiko Fukushima, Yuji Hatanaka, Yutaka Yamamoto, Nobutaka Shimizu, et al. "Abstract 906: Therapeutic potential of JAK/STAT signal inhibition in prostate cancer by the JAK inhibitor AZD1480." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-906.

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Pesch, Andrea M., Thomas L. Gonzalez, Benjamin C. Chandler, Siqi Sun, Christina L. Gersch, José M. Larios, Wadie S. David, Corey W. Speers, and James M. Rae. "Abstract 4766: Transcriptomic profiling reveals a potential role for JAK/STAT inhibition in CDK4/6 inhibitor-resistant, ER+ breast cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4766.

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Pesch, Andrea M., Thomas L. Gonzalez, Benjamin C. Chandler, Siqi Sun, Christina L. Gersch, José M. Larios, Wadie S. David, Corey W. Speers, and James M. Rae. "Abstract 4766: Transcriptomic profiling reveals a potential role for JAK/STAT inhibition in CDK4/6 inhibitor-resistant, ER+ breast cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4766.

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Bose, Mukulika, Aabha Vora, Taylor Colleton, and Pinku Mukherjee. "Abstract 1837: MUC1 confers sensitivity to STAT-3 inhibitor napabucasin in pancreatic ductal adenocarcinoma cells." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1837.

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Madden, Timothy, Mary Johansen, Kirk S. Culotta, Amy Heimberger, Izabela Fokt, Charles Conrad, and Waldemar Priebe. "Abstract 3783: Pharmacokinetics and CNS biodistribution of WP1066, a novel small molecule inhibitor of STAT-3 phosphorylation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3783.

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Brewer, Charlene, Rifat Jan, Analese Smith, Tabitha King, Peter J. Sims, and Joan S. Lewis-Wambi. "Abstract 265: STAT-1 activation enhances phospholipid scramblase 1-mediated apoptosis in aromatase inhibitor resistant breast cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-265.

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Chen, Huawei (Ray), Geraldine Bebernitz, Kirsten Bell, Erica Anderson, Nanhua Deng, Jason Kettle, Paul Lyne, and Richard Woessner. "Abstract 4046: Targeting jak/stat adaptive mechanism with jak1 inhibitor azd4205 reduces residual disease and prolongs benefit of osimertinib." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4046.

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Proia, David A., Kevin P. Foley, Alexander F. Rosenberg, Tim Korbut, Jim Sang, Donald Smith, Chaohua Zhang, Keizo Koya, and Ronald K. Blackman. "Abstract 2640: Multimodal action of the Hsp90 inhibitor STA-9090 in treating cancer cells with activated JAK/STAT signaling." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2640.

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Wachikwu-Elechi, Virtue Urunwo, Sunday Sunday Ikiensikimama, Joseph Atubokiki Ajienka, Onyewuchi Emmanuel Akaranta, and Okon Efiong Okon. "Suppression Performance of an Unmodified Bio-Extract for Simulated Offshore Gas Hydrate Mitigation." In SPE Annual Technical Conference and Exhibition. SPE, 2021. http://dx.doi.org/10.2118/206304-ms.

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Abstract Gas hydrate inhibition through the use of chemicals has been ongoing over the years and these chemicals are toxic, synthetic and expensive, adding to the cost of doing oil and gas business, and also leads to environmental degradation. The call for greener environment has necessitated the search for more eco-friendly gas hydrate inhibitors. This paper takes a look at the use of a bio-extract in its unmodified state to inhibit gas hydrate using a locally made mini flow loop for gas hydrate studies. The bio extract was compared to a conventional gas hydrate inhibitor 2-Di(methylaminoethyl)methacrylate (2-DMAEM). For all the weight percentages considered (0.01-0.05wt%), the bio-extract had better pressure profiles. At the end of the experiment which lasted for 120 minutes, this is attributed to the fact that the pressures in the system were more regulated which prevented rapid gas dissolution in water. The Bio-extract is plant based, locally available in the commercial quantity and is eco-friendly so it should be harnessed as gas hydrate inhibitors in lieu of the expensive and imported conventional hydrate inhibitor 2-DMAEM which non-eco-friendly.
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Ranjan, Alok, Sanjay K. Srivastava, Parul Gupta, Ashlee Birkenfeld, Duy Hua, and Jianyu Lu. "Abstract C58: GS-19, a novel GSK inhibitor suppresses the growth of pancreatic cancer cells by inhibiting EGFR/AKT/STAT-3 signaling." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c58.

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Reports on the topic "STAT. Inhibitor"

1

Schneider, Brandt. Role of the Cdk Inhibitor Sic 1 in Start. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359281.

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Schneider, Brandt. Role of the Cdk Inhibitor Sic 1 in Start. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392485.

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Schneider, Brandt. Role of the Cdk Inhibitor Sic 1 in Start. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada378108.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613987.

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Brooks-Kayal, Amy, Lauren Frey, and Bret N. Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada614126.

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Brooks-Kayal, Amy, and Bret Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada612534.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568150.

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Brooks-Kayal, Amy. Jak/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568663.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada586062.

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Seto, Christopher. Anticancer Agents Based on a New Class of Transition-State Analog Inhibitors for Serine and Cysteine Proteases. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada383963.

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