Добірка наукової літератури з теми "Somatic gain of mutation STAT3"
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Статті в журналах з теми "Somatic gain of mutation STAT3":
Koskela, Hanna, Samuli Eldfors, Henrikki Almusa, Emma Andersson, Pekka Ellonen, Henrik Edgren, Pirjo Koistinen, et al. "Recurrent Missense Mutations in the STAT3 Gene in LGL Leukemia Provide Insights to Pathogenetic Mechanisms and Suggest Potential Diagnostic and Therapeutic Applications." Blood 118, no. 21 (November 18, 2011): 936. http://dx.doi.org/10.1182/blood.v118.21.936.936.
Chomczynski, Peter W., Michael J. Clemente, Srinivasa Reddy Sanikommu, Alek d. Nielsen, Cassandra M. Hirsch, Hanna Rajala, Mikkael A. Sekeres, et al. "Next-Generation Sequencing Analysis of Clonal Hierarchy and Dynamics in T-Large Granular Lymphocyte Leukemia Suggests Emergence of STAT3 Clones within Pre-Existing Dominant T-Cell Repertoire Responses Otherwise Silenced in Normal Individuals." Blood 128, no. 22 (December 2, 2016): 2731. http://dx.doi.org/10.1182/blood.v128.22.2731.2731.
Lesmana, Harry, Marcela Popescu, Sara Lewis, Sushree Sangita Sahoo, Charnise Goodings-Harris, Mihaela Onciu, John Kim Choi, Clifford Takemoto, Kim E. Nichols, and Marcin Wlodarski. "Germline Gain-of-Function JAK3 Mutation in Familial Chronic Lymphoproliferative Disorder of NK Cells." Blood 136, Supplement 1 (November 5, 2020): 9–10. http://dx.doi.org/10.1182/blood-2020-142078.
Rajala, Hanna L. M., Thomas Olson, Sonja Lagström, Pekka Ellonen, Syed Arshi Uz Zaman, Emma I. Andersson, Michael J. Clemente, et al. "Multiple STAT3 Mutations In Different Lymphocyte Clones Of Large Granular Lymphocytic Leukemia Patients." Blood 122, no. 21 (November 15, 2013): 2559. http://dx.doi.org/10.1182/blood.v122.21.2559.2559.
Nabhani, Schafiq, Hagit Miskin, Cyrill Schipp, Dan Harlev, Shoshana Revel-Vilk, Michael Gombert, Sebastian Ginzel, Arndt Borkhardt, Polina Stepensky, and Ute Fischer. "Activating Mutation of STAT3 Protects Lymphocytes from Apoptosis and Leads to a Clinical Phenotype Resembling the Autoimmune Lymphoproliferative Syndrome." Blood 126, no. 23 (December 3, 2015): 2218. http://dx.doi.org/10.1182/blood.v126.23.2218.2218.
Wang, T. Tiffany, Jun Yang, Shubha Dighe, Matthew W. Schmachtenberg, Nathan T. Leigh, Emily Farber, Suna Onengut-Gumuscu, et al. "Whole Genome Sequencing of Spontaneously Occurring Rat Natural Killer Large Granular Lymphocyte Leukemia Identifies JAK1 Somatic Activating Mutation." Cancers 12, no. 1 (January 3, 2020): 126. http://dx.doi.org/10.3390/cancers12010126.
Kim, Daehong, Mikko Myllymäki, Matti Kankainen, Timo Jarvinen, Giljun Park, Roberta Bruhn, Edward L. Murphy, and Satu Mustjoki. "Somatic STAT3 Mutations in CD8+ T Cells of HTLV-2 Positive Blood Donors." Blood 138, Supplement 1 (November 5, 2021): 3133. http://dx.doi.org/10.1182/blood-2021-146326.
Kunter, Ghada M., Fulu Liu, Maxwell Krem, and Daniel Link. "G-CSF Receptor Mutations Found in Patients with Severe Congenital Neutropenia Confer a Strong Competitive Growth Advantage at the Hematopoietic Stem Cell Level That Is Mediated by STAT5 Activation." Blood 108, no. 11 (November 16, 2006): 632. http://dx.doi.org/10.1182/blood.v108.11.632.632.
Mailloux, Adam W., Jeff Painter, Eric Padron, Thomas P. Loughran та Pearlie K. Epling-Burnette. "Common γ Chain (γc) Cytokine Hypersensitivity Leads To T-Cell Homeostatic Deregulation Independent Of STAT3 Mutation In Large Granular Lymphocyte Leukemia". Blood 122, № 21 (15 листопада 2013): 1628. http://dx.doi.org/10.1182/blood.v122.21.1628.1628.
Pastore, Friederike, Aishwarya Krishnan, Henrik M. Hammarén, Olli Silvennoinen, Benedict Yan, and Ross L. Levine. "JAK2S523L, a novel gain-of-function mutation in a critical autoregulatory residue in JAK2V617F− MPNs." Blood Advances 4, no. 18 (September 21, 2020): 4554–59. http://dx.doi.org/10.1182/bloodadvances.2019001283.
Дисертації з теми "Somatic gain of mutation STAT3":
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.
Refractory 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
Menon, Priyanka Rajeev. "The importance of homotypic interactions of unphosphorylated STAT proteins in cytokine-induced signal transduction." Doctoral thesis, 2021. http://hdl.handle.net/21.11130/00-1735-0000-0005-15A2-C.
Частини книг з теми "Somatic gain of mutation STAT3":
Thomas, Duncan C. "Basic Concepts of Molecular Genetics." In Statistical Methods in Genetic Epidemiology, 25–44. Oxford University PressNew York, NY, 2004. http://dx.doi.org/10.1093/oso/9780195159394.003.0002.
Keppler-Noreuil, Kim M. "PIK3CA-Related Overgrowth Spectrum." In Overgrowth Syndromes, 217–40. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190944896.003.0012.
Тези доповідей конференцій з теми "Somatic gain of mutation STAT3":
Eldfors, Samuli, Hanna LM Rajala, Pekka Ellonen, Emma I. Andersson, Sonja Lagström, Henrikki Almusa, Henrik Edgren, et al. "Abstract 3164: Somatic mutation analysis pipeline for exome-sequencing data identifies oncogenic STAT3 mutations in T-LGL leukemia." 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.am2013-3164.
Gonzalez-Mancera, M. S., B. Johnson, M. Murthi, G. E. Holt, M. A. Campos, and M. Mirsaeidi. "STAT3 Gain-of-Function Mutation in a Patient with Recurrent Bronchopulmonary Infections and Multi-Organ Involvement." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1362.
Crescenzo, Ramona, Valentina Fragliasso, Marcello Gaudiano, Marco Pizzi, and Giorgio Inghirami. "Abstract 2885: Somatic mutation of STAT3 leads to the preferential Th17 differentiation in human naïve CD4-positive cells and favor TCR-mediated proliferation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2885.
Звіти організацій з теми "Somatic gain of mutation STAT3":
Weller, Joel I., Derek M. Bickhart, Micha Ron, Eyal Seroussi, George Liu, and George R. Wiggans. Determination of actual polymorphisms responsible for economic trait variation in dairy cattle. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600017.bard.