Auswahl der wissenschaftlichen Literatur zum Thema „STAT inhibitors“
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Zeitschriftenartikel zum Thema "STAT inhibitors"
Ebersbach, Celina, Alicia-Marie K. Beier, Christian Thomas und Holger H. H. Erb. „Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer“. Cancers 13, Nr. 19 (28.09.2021): 4854. http://dx.doi.org/10.3390/cancers13194854.
Der volle Inhalt der QuelleLee, Hyun-Ku, Gita Singh und Sujay Singh. „STAT reporter cell line systems as a tool for cancer therapeutic target screening.“ Journal of Immunology 200, Nr. 1_Supplement (01.05.2018): 169.8. http://dx.doi.org/10.4049/jimmunol.200.supp.169.8.
Der volle Inhalt der QuelleJones, Dan, Justin Windham, Brian Stewart, Luis Fayad, Alma Rodriguez und 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, Nr. 22 (20.11.2009): 968. http://dx.doi.org/10.1182/blood.v114.22.968.968.
Der volle Inhalt der QuelleStanding, David, Emma Feess, Satvik Kodiyalam, Michael Kuehn, Zachary Hamel, Jaimie Johnson, Sufi Mary Thomas und Shrikant Anant. „The Role of STATs in Ovarian Cancer: Exploring Their Potential for Therapy“. Cancers 15, Nr. 9 (26.04.2023): 2485. http://dx.doi.org/10.3390/cancers15092485.
Der volle Inhalt der QuelleRodman, Esther, Michael Emch, Elizabeth Bruinsma, Xiaonan Hou, John Weroha und John Hawse. „Abstract 1129: Interrogating JAK/STAT signaling in ovarian cancer as a potential oncogenic driver and therapeutic target“. Cancer Research 82, Nr. 12_Supplement (15.06.2022): 1129. http://dx.doi.org/10.1158/1538-7445.am2022-1129.
Der volle Inhalt der QuelleZhou, Jianbiao, Chonglei Bi, Lai Fong Poon, Viraj J. Janakakumara, Jiaying Khng, Hanry Yu, Keith B. Glaser, Daniel H. Albert, Davidsen K. Davidsen und 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, Nr. 11 (16.11.2007): 2367. http://dx.doi.org/10.1182/blood.v110.11.2367.2367.
Der volle Inhalt der QuelleSuzuki, Asuka, Toshikatsu Hanada, Keiichi Mitsuyama, Takafumi Yoshida, Shintaro Kamizono, Tomoaki Hoshino, Masato Kubo et al. „Cis3/Socs3/Ssi3 Plays a Negative Regulatory Role in Stat3 Activation and Intestinal Inflammation“. Journal of Experimental Medicine 193, Nr. 4 (12.02.2001): 471–82. http://dx.doi.org/10.1084/jem.193.4.471.
Der volle Inhalt der QuelleGalli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes und Gustavo Martelli Palomino. „The JAK-STAT Pathway and the JAK Inhibitors“. Journal of Clinical Research in Dermatology 7, Nr. 5 (30.11.2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.
Der volle Inhalt der QuelleWang, Weiyuan, Melanie Cristina Lopez McDonald, Rajashree Hariprasad, Tiara Hamilton und David A. Frank. „Oncogenic STAT Transcription Factors as Targets for Cancer Therapy: Innovative Strategies and Clinical Translation“. Cancers 16, Nr. 7 (31.03.2024): 1387. http://dx.doi.org/10.3390/cancers16071387.
Der volle Inhalt der QuelleHu, Cheng-Ping, Jun-Tao Feng, Yu-Ling Tang, Jin-Qi Zhu, Min-Juan Lin und 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.
Der volle Inhalt der QuelleDissertationen zum Thema "STAT inhibitors"
Etter, Jonathan Parker. „Development of Inhibitors in the IL-6/GP130/JAK/STAT Pathway as Therapeutic Agents“. The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376525461.
Der volle Inhalt der QuelleGhafoory, 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.
Der volle Inhalt der QuellePancreatic 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
Berrabah, Sofia. „Etude de nouvelles cibles thérapeutiques dans les lymphomes compliquant la maladie cœliaque“. Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5201.
Der volle Inhalt der QuelleRefractory coeliac disease type II (RCDII), also called intraepithelial lymphoma, is a rare but severe complication of coeliac disease characterized by the clonal expansion of a small subset of innate intraepithelial lymphocytes (IEL), present in the normal human and murine intestine. Our lab has shown that this population displays shared features between T and natural killer (NK) cells. These so-called iCD3+ innate IEL are mainly characterized by intracellular expression of CD3, which is not detected at the cell surface, expression of NK receptors as well as DNA rearrangement of T cell receptor genes. Our lab has also shown that iCD3+ innate IEL originate from bone marrow precursors through coordinated NOTCH1 and interleukin (IL)-15 signals. During lymphomagenesis, iCD3+ innate IEL of most RCDII patients were shown to have acquired somatic gain-of-function mutations in JAK1 and/or STAT3 that confer increased sensitivity to interleukin-15, a cytokine overexpressed in the intestine of coeliac patients, thereby promoting their clonal expansion. Thus, our hypothesis is that JAK1/STAT3 mutations play a key role in initiating lymphomagenesis associated to coeliac disease in an IL-15-rich environment and that they could represent an attractive therapeutic target.The first objective of my thesis was to study the interest of JAK/STAT inhibitors for RCDII treatment. First, we have tested in vitro different JAK/STAT inhibitors on IL-15-dependent RCDII or normal IEL-T cell lines. We have shown that these inhibitors decrease the proliferation and phosphorylation of STAT3 and increase cellular apoptosis in both RCDII and normal T cell lines. Secondly, we have established a xenograft model based on the injection of cells derived from biopsy or blood from one RCDII patient into immunodeficient mice overexpressing the human IL-15 transgene in their gut epithelium (Rag-/-Gc-/- IL-15TgE; IRGC) to test the efficacy of JAK/STAT inhibitors in vivo. Treatment of xenografted mice with ruxolitinib, a potent inhibitor of JAK1/JAK2 decreased the frequency, number and cytotoxic potential of human tumoral cells and allowed clinical restoration. These preliminary results are encouraging but need to be confirmed. The second objective of my thesis was to test whether the Stat3 pD661V mutation is sufficient to induce the intraepithelial lymphoma in an IL-15-rich context in IRGC mice. We have successfully generated murine iCD3+ innate IEL in vitro, resembling their human counterparts from common lymphoid precursors by combining NOTCH and IL-15 signals. We then transduced CLP with a retroviral vector containing wild-type or mutated Stat3 pD661V. The transduced cells were injected into IRGC mice that subsequently were followed-up during a period of 8 weeks. In vitro generated iCD3+ innate IEL preferentially homed to the intestine. However, no development of intraepithelial lymphoma was observed suggesting that the Stat3 pD661V variant alone is not sufficient to induce the intraepithelial lymphoma. These preliminary results need to be reproduced and confirmed. The murine model used to test the role of STAT3 will now be used to evaluate the respective contribution of canonical mutations in JAK1 and STAT3 and of other recurrent mutations identified in RCDII
Gomes, Guilherme Wataru. „Expressão gênica dos transportadores de membrana ABCB1,ABCG2, SLC22A1 e SLCO1A2 em linhagens celulares tratadas com inibidor comercial da via JAK-STAT“. Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-16032016-095918/.
Der volle Inhalt der QuelleBACKGROUND: JAK-STAT pathway signaling disregulation is a hallmark of myeloproliferative neoplasms (MPN), hematopoietic stem cell clonal diseases, among which is myelofibrosis (MF). Several JAK inhibitors have been developed for MF treatment and are found in different stages of clinical development. Because the recent development of these compounds, the role of drug transporters in their pharmacokinetics is poorly understood. These proteins perform celular influx and effux of endogenous substrates and xenobiotics, and changes in the expression of these drugs transporters may affect the response to these drugs. AIM: To evaluate the effect of a JAK-STAT pathway commercial inhibitor in gene expression of drug transporters ABCB1, ABCG2, SLC22A1 and SLCO1A2 in HepG2, Caco-2 and HEL92.1.7 cells. METHODS: Hepatocellular carcinoma cell line HepG2, colorectal adenocarcinoma cell line Caco-2 and human erythroleukemia homozygous JAK2V617F cell line HEL92.1.7 were grown and treated with the JAK-STAT pathway inhibitor JAK Inhibitor I. In order to determine the optimal concentration for treatment with the inhibitor, cells were treated with several concentrations of JAK inhibitor by 24 hours, and cell viability and DNA fragmentation tests were performed. Once the treatment conditions were standardized, total RNA were obtained from the cells, and cDNA was synthesized in order to evaluate the mRNA expression of ABCB1, ABCG2, SLC22A1 and SLCO1A2 genes, performed by real time PCR. We also evaluate the expression of drug efflux transporters ABCB1 and ABCG2 by flow cytometry, using primary antibodies directed to these proteins. RESULTS: In HepG2 cells, it was observed an increase in ABCB1 mRNA expression in cells treated with 4,00 µM of JAK inhibitor, when compared with controls (cells exposed only to the vehicle) (P=0.041). There was no change in ABCB2 and SLC22A1 mRNA expression with the treatment with JAK inhibitor in this cell line (P>0.05); SLCO1A2 mRNA was not detected in this cell line. In Caco-2 cells, ABCB1, ABCG2, SLC22A1 and SLCO1A2 mRNA expression did not change with treatment with the JAK inhibitor at the concentrations used (0.25 µM to 1.00 µM) by 24 hours (P>0.05). In HEL92.1.7 cells, it was not observed differences in ABCB1, ABCG2 and SLC22A1 mRNA expression with the treatment with 1 µM of JAK inhibitor by 24 hours when compared with controls (P>0.05); in this cell line, SLCO1A2 mRNA was not detected. Protein expression of ABCB1 and ABCG2 drug transporters has not changed with treatment with the JAK inhibitor under the conditions used in the three cell lines studied. CONCLUSIONS: Only HepG2 cells presented an increase in mRNA expression of drug efflux transporter ABCB1 in presence of high levels of JAK inhibitor, suggesting that JAK inhibitors could modulate this transporter gene expression in liver. Treatment with JAK-STAT pathway inhibitor was not associated with changes in ABCB1 and ABCG2 protein expression in all cell lines studied.
Khatchaturyan, Levon [Verfasser], Udo [Akademischer Betreuer] Markert, Uta-Christina [Akademischer Betreuer] Hipler und Ulrike [Akademischer Betreuer] Kämmerer. „Die Rolle von PIAS (Protein Inhibitors of Activated STATs) in der Regulation von STAT (Signal Transducer and Activator of Transcription) : vermittelten Funktionen trophoblastärer Zellen / Levon Khachaturyan. Gutachter: Udo Markert ; Uta-Christina Hipler ; Ulrike Kämmerer“. Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2012. http://d-nb.info/1020402113/34.
Der volle Inhalt der QuelleAubert-Jürgens, Ana. „STAT3 inhibitors for cancer treatment“. [S.l.] : [s.n.], 2005. http://elib.tu-darmstadt.de/diss/000563.
Der volle Inhalt der QuelleHill, 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.
Der volle Inhalt der QuelleFisher, 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.
Der volle Inhalt der QuelleBhasin, Deepak. „Small Molecule Inhibitors asAnticancer Agents“. The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1305826098.
Der volle Inhalt der QuelleHaque, Mohammad Rashedul. „Novel STAT3 small-molecule inhibitors as potential anticancer agents“. Thesis, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535504.
Der volle Inhalt der QuelleBücher zum Thema "STAT inhibitors"
Ward, Alister C., Hrsg. STAT Inhibitors in Cancer. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42949-6.
Der volle Inhalt der QuelleBernhard, Elsener, European Federation of Corrosion und Institute of Materials (Great Britain), Hrsg. 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.
Den vollen Inhalt der Quelle findenWard, Alister C. STAT Inhibitors in Cancer. Humana, 2018.
Den vollen Inhalt der Quelle findenWard, Alister C. STAT Inhibitors in Cancer. Humana, 2016.
Den vollen Inhalt der Quelle findenWard, Alister C. STAT Inhibitors in Cancer. Springer London, Limited, 2016.
Den vollen Inhalt der Quelle findenFleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.
Der volle Inhalt der QuelleWu, Joseph M., und Tze-Chen Hsieh. Resveratrol : State-Of-The-Art Science and Health Applications: Actionable Targets and Mechanisms of Resveratrol. World Scientific Publishing Co Pte Ltd, 2019.
Den vollen Inhalt der Quelle findenYoung, Benjamin. Classes of Antiretrovirals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0019.
Der volle Inhalt der Quelle(Editor), A. Raman, und Paul Labine (Editor), Hrsg. 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.
Den vollen Inhalt der Quelle findenElsener, B. Matsci : Corrosion Inhibitors for Steel In Concrete : State of the Art Report: Proceedings of an Efc Workshop. Taylor & Francis Group, 2001.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "STAT inhibitors"
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.
Der volle Inhalt der QuelleLiu, Suhu, und 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.
Der volle Inhalt der QuelleShouksmith, Andrew E., und 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.
Der volle Inhalt der QuelleYang, Jennifer, und Gregory B. Lesinski. „Curcumin Analogs as Inhibitors of the Jak-STAT Signal Transduction Pathway“. In Novel Apoptotic Regulators in Carcinogenesis, 247–66. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4917-7_10.
Der volle Inhalt der QuelleScott, Linda M. „Inhibitors of the JAK/STAT Pathway, with a Focus on Ruxolitinib and Similar Agents“. In Resistance to Targeted Anti-Cancer Therapeutics, 107–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75184-9_6.
Der volle Inhalt der QuelleDempsey, 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.
Der volle Inhalt der QuelleArgyropoulos, Vasilike, Stamatis C. Boyatzis, Maria Giannoulaki, Elodie Guilminot und 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.
Der volle Inhalt der QuelleRevhaug, 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.
Der volle Inhalt der QuelleLuly, Jay R., Anthony K. L. Fung, Jacob J. Plattner, Patrick A. Marcotte, Nwe BaMaung, Jeffrey L. Soderquist und 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.
Der volle Inhalt der QuelleBharadwaj, Uddalak, Moses M. Kasembeli und 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.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "STAT inhibitors"
Fanouriakis, Antonis. „28 JAK-STAT inhibitors in systemic lupus erythematosus“. In 12th Annual Meeting of the Lupus Academy; Virtual Pre-meeting: September 1, 2023; Hybrid Annual Meeting (Barcelona): September 8–10, 2023. Lupus Foundation of America, 2023. http://dx.doi.org/10.1136/lupus-2023-la.28.
Der volle Inhalt der QuelleHu, Wanting. „Progress of JAK/STAT 3 and its inhibitors in the treatment of cancer“. In 2ND INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FSBE 2019). AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0000440.
Der volle Inhalt der QuelleMorena, Isabel de la, Juan Alberto Paz Solarte, Diego Bedoya und Pilar Trenor Larraz. „AB0435 REAL WORLD DATA OF A PATIENT COHORT WITH RHEUMATOID ARTRITIS TREATED WITH JAK/STAT INHIBITORS“. In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8254.
Der volle Inhalt der QuelleBreedy, Sloan, Wishrawana S. Ratnayake, Christopher Apostolatos, Avijit Dey und Mildred Acevedo-Duncan. „Abstract 5216: Atypical PKC inhibitors ICA-1S and ζ-Stat show inhibition of neuroblastoma cell proliferation“. 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.am2020-5216.
Der volle Inhalt der QuelleAbdelhamid, Dalia, Mike Corcoran, Jonathan P. Etter, Sheng Hu, Bulbul Pandit, Chenglong Li, Pui-Kai Li und James R. Fuchs. „Abstract 4502: Synthesis and evaluation of curcumin-like compounds as inhibitors of the JAK/STAT pathway in cancer“. 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.am10-4502.
Der volle Inhalt der QuelleCairo, Stefano, Olivier Déas, Truong-an Tran und Jean-Gabriel Judde. „Abstract 2811: High IFN/STAT-related gene expression is associated with sensitivity to PARP inhibitors of triple negative breast cancer“. In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2811.
Der volle Inhalt der QuelleCortez, Maria A., Lauren Averett Byers, You Hong Fan, Lixia Diao, Philip Groth, Julianne Paul, Jing Wang et al. „Abstract 2498: Proteomic analysis reveals Src/Stat and EGFR/MAPK pathways as potential mechanism of resistance to PI3K inhibitors in lung cancer.“ 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.am2013-2498.
Der volle Inhalt der QuelleMao, Yumeng, Isabel Poschke, Yago Pico de Coaña, Erik Wennerberg, Andreas Lundqvist und Rolf Kiessling. „Abstract A63: Melanoma-educated CD14+ monocytes become myeloid-derived suppressor cell-like and are potent inhibitors of autologous T cells through Cox-2 production and STAT-3 signaling.“ In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a63.
Der volle Inhalt der QuelleTan, Bee Chea, Ismail Mohd Saaid, Siti Qurratu'Aini Mahat, Suzalina Zainal, Petrus Tri Bhaskoro und Astriyana Anuar. „Evaluation of Polyamidoamine-Assisted Scale Inhibitors to Mitigate Silicate Scale Formation in Near Wellbore Region“. In SPE/IATMI Asia Pacific Oil & Gas Conference and Exhibition. SPE, 2023. http://dx.doi.org/10.2118/215266-ms.
Der volle Inhalt der QuelleCovey, Todd M., Santosh Putta, Michael Gulrajani, Aileen C. Cohen und Alessandra Cesano. „Abstract B182: Single cell network profiling (SCNP) by flow cytometry as a tool to measure potency and selectivity of JAK/STAT inhibitors in PBMC and whole blood discrete cell subsets“. In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b182.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "STAT inhibitors"
Tian, Cong, Jianlong Shu, Wenhui Shao, Zhengxin Zhou, Huayang Guo und Jingang Wang. The efficacy and safety of IL Inhibitors, TNF-α Inhibitors, and JAK Inhibitor on ankylosing spondylitis: A Bayesian network meta-analysis of a “randomized, double-blind, placebo-controlled” trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0117.
Der volle Inhalt der QuelleSchneider, 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.
Der volle Inhalt der QuelleSchneider, 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.
Der volle Inhalt der QuelleSchneider, 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.
Der volle Inhalt der QuelleSeto, Christopher T. 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 1999. http://dx.doi.org/10.21236/ada377205.
Der volle Inhalt der QuelleSeto, 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.
Der volle Inhalt der QuelleCoiwell, J., S. Pednekar und M. Han. L51540 Corrosion Criteria for J-Tube Risers. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), November 1987. http://dx.doi.org/10.55274/r0011426.
Der volle Inhalt der QuelleBhagawati, Rishiraj, Dolf J. H. te Lintelo, John Msuya und Tumaini Mikindo. Nutrition Accountability through Sub-National Scorecards in Tanzania – Policy Innovations and Field Realities. Institute of Development Studies (IDS), Dezember 2021. http://dx.doi.org/10.19088/ids.2021.067.
Der volle Inhalt der QuelleBarash, Itamar, J. Mina Bissell, Alexander Faerman und Moshe Shani. Modification of Milk Composition via Transgenesis: The Role of the Extracellular Matrix in Regulating Transgene Expression. United States Department of Agriculture, Juli 1995. http://dx.doi.org/10.32747/1995.7570558.bard.
Der volle Inhalt der QuelleAltstein, Miriam, und Ronald J. Nachman. Rational Design of Insect Control Agent Prototypes Based on Pyrokinin/PBAN Neuropeptide Antagonists. United States Department of Agriculture, August 2013. http://dx.doi.org/10.32747/2013.7593398.bard.
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