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Relevant bibliographies by topics / JAK/STAT Signaling Pathway

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Academic literature on the topic 'JAK/STAT Signaling Pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "JAK/STAT Signaling Pathway"

1

Tian, SS, P. Tapley, C. Sincich, RB Stein, J. Rosen, and P. Lamb. "Multiple signaling pathways induced by granulocyte colony-stimulating factor involving activation of JAKs, STAT5, and/or STAT3 are required for regulation of three distinct classes of immediate early genes." Blood 88, no. 12 (1996): 4435–44. http://dx.doi.org/10.1182/blood.v88.12.4435.bloodjournal88124435.

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Granulocyte colony-stimulating factor (G-CSF) is the major regulator of proliferation and differentiation of neutrophilic granulocyte precursor cells. G-CSF activates multiple signaling molecules, including the JAK1 and JAK2 kinases and the STAT transcription factors. To investigate G-CSF signaling events regulated by the JAK-STAT pathway, we have generated UT7-epo cells stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutants. Gel mobility shift and immunoprecipitation/Western analysis showed that STAT5 is rapidly activated by G-CSF in cells expressing

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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 (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/ST

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Raivola, Juuli, Teemu Haikarainen, and Olli Silvennoinen. "Characterization of JAK1 Pseudokinase Domain in Cytokine Signaling." Cancers 12, no. 1 (2019): 78. http://dx.doi.org/10.3390/cancers12010078.

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The Janus kinase-signal transducer and activator of transcription protein (JAK-STAT) pathway mediates essential biological functions from immune responses to haematopoiesis. Deregulated JAK-STAT signaling causes myeloproliferative neoplasms, leukaemia, and lymphomas, as well as autoimmune diseases. Thereby JAKs have gained significant relevance as therapeutic targets. However, there is still a clinical need for better JAK inhibitors and novel strategies targeting regions outside the conserved kinase domain have gained interest. In-depth knowledge about the molecular details of JAK activation i

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Malemud, Charles J. "The role of the JAK/STAT signal pathway in rheumatoid arthritis." Therapeutic Advances in Musculoskeletal Disease 10, no. 5-6 (2018): 117–27. http://dx.doi.org/10.1177/1759720x18776224.

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Proinflammatory cytokine activation of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signal transduction pathway is a critical event in the pathogenesis and progression of rheumatoid arthritis. Under normal conditions, JAK/STAT signaling reflects the influence of negative regulators of JAK/STAT, exemplified by the suppressor of cytokine signaling and protein inhibitor of activated STAT. However, in rheumatoid arthritis (RA) both of these regulators are dysfunctional. Thus, continuous activation of JAK/STAT signaling in RA synovial joints results in the elevated

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Sonkin, Dmitriy, Catherine Regnier, Xianhui Rong, et al. "Identification of pSTAT5 gene signature in hematologic malignancy." Journal of Clinical Oncology 31, no. 15_suppl (2013): 7111. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.7111.

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7111 Background: The JAK/STAT pathway is an important signaling pathway downstream of multiple cytokine and growth factor receptors. Receptor-associated JAKs are activated following receptor-ligand binding. Activated JAKs phosphorylate STAT proteins, which then dimerize and translocate to the nucleus where they modulate the expression of target genes. Dysregulated JAK/STAT signaling has been implicated in the pathogenesis of multiple human malignancies. Activating mutations in JAK2 and the associated activation of STAT5 in myeloproliferative neoplasia is one example of the involvement of this

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Andl, Claudia D., Takaaki Mizushima, Kenji Oyama, Mark Bowser, Hiroshi Nakagawa, and Anil K. Rustgi. "EGFR-induced cell migration is mediated predominantly by the JAK-STAT pathway in primary esophageal keratinocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 6 (2004): G1227—G1237. http://dx.doi.org/10.1152/ajpgi.00253.2004.

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The epidermal growth factor receptor (EGFR) activates several signaling cascades in response to epidermal growth factor stimulation. One of these signaling events involves tyrosine phosphorylation of signal transducer and activator of transcription (STAT), whereas another involves activation of the phosphatidylinositol 3-OH kinase pathway. Two possibilities for STAT activation exist: a janus kinase (JAK)-dependent and a JAK-independent mechanism. Herein, we demonstrate that EGFR overexpression in primary esophageal keratinocytes activates STAT in a JAK-dependent fashion with the functional con

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Palmroth, M., K. Kuuliala, R. Peltomaa, et al. "AB0250 TOFACITINIB SUPPRESSES SEVERAL JAK-STAT PATHWAYS IN RHEUMATOID ARTHRITIS AND BASELINE SIGNALING PROFILE ASSOCIATES WITH TREATMENT RESPONSE." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1150.2–1151. http://dx.doi.org/10.1136/annrheumdis-2021-eular.448.

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Background:Cytokines are important mediators of inflammation and tissue destruction in rheumatoid arthritis (RA) 1. Several cytokines involved in RA pathogenesis act through Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway 2. The effects of JAK-inhibitor tofacitinib on cytokine signaling in vitro are well established, while in vivo evidence in patients remains scarce.Objectives:To investigate in vivo in rheumatoid arthritis patients i) which JAK-STAT pathways are inhibited by tofacitinib and ii) if baseline signaling profile is associated with the treatment re

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Takeda, Takashi, Hirohisa Kurachi, Toshiya Yamamoto, et al. "Participation of JAK, STAT and unknown proteins in human placental lactogen-induced signaling: a unique signaling pathway different from prolactin and growth hormone." Journal of Endocrinology 153, no. 1 (1997): R1—R3. http://dx.doi.org/10.1677/joe.0.153r001.

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Abstract The signal transduction mechanism involved in human placental lactogen (hPL) was studied. We have identified that hPL rapidly stimulated the tyrosine phosphorylation of at least 7 proteins including Janus Kinases (JAK1 and JAK2) and a signal transducer and activator of transcription protein (Stat3). This is the first evidence that the JAK-STAT pathway is involved in the hPL signaling. Moreover, two unknown proteins which were different from STAT proteins (Stat1, 3 and 5) in sizes were predominantly tyrosine-phosphorylated. Because human growth hormone (hGH) activates Stat1, 3, 5 and h

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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 (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 dele

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Zheng, Ying, Hongwei Qin, Stuart J. Frank, et al. "A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway." Blood 118, no. 1 (2011): 156–66. http://dx.doi.org/10.1182/blood-2010-01-266320.

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Abstract JAK-STAT signaling is involved in the regulation of cell survival, proliferation, and differentiation. JAK tyrosine kinases can be transiently activated by cytokines or growth factors in normal cells, whereas they become constitutively activated as a result of mutations that affect their function in tumors. Specifically, the JAK2V617F mutation is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these diseases. In the present study, we report that the kinase CK2 is a novel interaction partner of JAKs and is essential

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Dissertations / Theses on the topic "JAK/STAT Signaling Pathway"

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Saharinen, Pipsa. "Signaling through the Jak-Stat pathway : regulation of tyrosine kinase activity." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/saharinen/.

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Lukashova, Viktoria. "Involvement of the Jak/STAT pathway in platelet-activating factor receptor signaling." Thèse, Sherbrooke : Université de Sherbrooke, 2003. http://savoirs.usherbrooke.ca/handle/11143/4173.

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Giedt, Michelle Suzanne. "JAK/STAT SIGNALING REGULATES GAMETOGENESIS AND AGE-RELATED REPRODUCTIVE MAINTENANCE." UKnowledge, 2018. https://uknowledge.uky.edu/biology_etds/52.

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Cell signaling is central to integration of internal and external cues that regulate development and homeostasis. Most development is thought of as pre-adult, but limited developmental processes occur in adults. Gametogenesis incorporates elements of both these facets, with a distinct developmental plan for gamete synthesis which is regulated by integration of homeostatic inputs such as nutrient status, and environmental cues. Signaling pathways integrate and transduce information from these cues to evoke a response. A decline in homeostasis and subsequent cues occurs over time, in the case of

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Leal, Cervantes Ana Irene. "Transcriptional consequences of Jak-Stat signalling in haematopoiesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709253.

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Kalymbetov, Anuar [Verfasser]. "Role of JAK/STAT signalling pathway in PAH / Anuar Kalymbetov." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1120270227/34.

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Park-Min, Kyung-Hyun. "The crosstalk between ITAM-associated receptors and Jak-STAT signaling pathways /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1296119161&sid=8&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Guo, Qian. "THE FUNCTION OF Socs GENES IN DROSOPHILA DEVELOPMENT AND SIGNALING PATHWAYS." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_theses/466.

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The duration and intensity of the JAK/stat signaling must be tightly regulated to prevent excessive transcriptional response and to reset the pathway to receive additional signals. Socs are the largest class of these regulators in mammals. Eight Socs genes have been found in mammals. CIS, and SOCS1-3, the canonical Socs, are transcriptionally activated by and down-regulate the JAK signaling. Socs4-7, the non-canonical Socs, are less studied and their relationship with the JAK/STAT pathway has not been well established. The Drosophila genome encodes three non-canonical Socs homologues, Socs16D,

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DiNapoli, Vincent A. "Alterations in JAK/STAT signaling pathway and blood-brain barrier function mechanisms underlying worsened outcome following stroke in the aged rat /." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5142.

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Thesis (Ph. D.)--West Virginia University, 2007.<br>Title from document title page. Document formatted into pages; contains x, 154 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 135-149).

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Hamedi, Mojgan. "The expression of Suppressor of Cytokine Signalling (SOCS), JAK-STAT signalling pathway and cytokine profile in Behçet's disease." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8557.

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Behçet’s disease (BD) is a chronic, multi systemic, recurrent vasculitis disease of unknown aetiology. The clinical manifestations are composed of relapsing episodes of recurrent oral ulcers, uveitis, skin lesions and genital ulcers along with musculoskeletal and neurological involvement. Pro-inflammatory cytokines are a key feature of the disease but the triggers for their induction are not well understood and/or controversial. Many cytokines (including IFNγ, IL-12, IL-23, IL-10 and IL-6) activate the JAK-STAT signalling pathway which is negatively regulated by Suppressor of Cytokine Signalli

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Collura, Kaitlin Marie. "Palmitoylation-Dependent Regulation of the DLK/JNK/cJun and the GP130/JAK/STAT Retrograde Signaling Pathways." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/426710.

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Biomedical Sciences<br>Ph.D.<br>Palmitoylation is the post-translational addition of the 16-carbon fatty acid palmitate to protein cysteine residues. This process is best known for its roles in targeting proteins to lipid membranes, including both the plasma membrane and vesicles. Palmitoylation occurs in all eukaryotic cells, but appears to be particularly important in neurons, because genetic mutation or loss of several palmitoyl acyltransferases (PATs, the enzymes that catalyze palmitoylation), leads to predominantly neuropathological defects. In addition, a growing number of recent studies

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Books on the topic "JAK/STAT Signaling Pathway"

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Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. Springer, 1996.

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Decker, Thomas, and Mathias Müller, eds. Jak-Stat Signaling : From Basics to Disease. Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.

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Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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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

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Wilks, Andrew F. Intracellular Signal Transduction: The Jak-Stat Pathway. Springer, 2013.

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Harpur, Ailsa G., and Andrew F. Wilks. The Jak-Stat Pathway (Molecular Biology Intelligence Unit). Springer, 1996.

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Jakstat Signalling Methods And Protocols. Humana Press, 2012.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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Book chapters on the topic "JAK/STAT Signaling Pathway"

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Leonard, Warren J. "The JAK-STAT Pathway." In Hormone Signaling. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_6.

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Croker, Ben A., and Nicos A. Nicola. "The Jak-Stat Pathway of Cytokine Signaling." In Hematopoietic Growth Factors in Oncology. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_3.

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Ivashkiv, Lionel B. "Crosstalk with the Jak-STAT Pathway in Inflammation." In Jak-Stat Signaling : From Basics to Disease. Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8_19.

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Luo, Na, and Justin M. Balko. "Role of JAK-STAT Pathway in Cancer Signaling." In Predictive Biomarkers in Oncology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95228-4_26.

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Mehta, Poonam, and Rajender Singh. "JAK-STAT pathway: Testicular development, spermatogenesis and fertility." In Molecular Signaling in Spermatogenesis and Male Infertility. CRC Press, 2019. http://dx.doi.org/10.1201/9780429244216-15.

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Durbin, Joan E. "Jak-Stat Pathway in Response to Virus Infection." In Cellular Signaling and Innate Immune Responses to RNA Virus Infections. ASM Press, 2014. http://dx.doi.org/10.1128/9781555815561.ch6.

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Vaddi, Kris. "The Role of the JAK/STAT Signalling Pathway in Immunoregulation of Gastrointestinal Cancers." In Immunotherapy for Gastrointestinal Cancer. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43063-8_7.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_157-1.

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Caldow, Marissa K., and David Cameron-Smith. "JAK/STAT Pathway." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_242.

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Zhang, Wei, and Xiufen Zou. "The Data-Based Mathematical Modeling and Parameter Identification in JAK-STAT Signaling Pathway by Using a Hybrid Evolutionary Algorithm." In Advances in Computation and Intelligence. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-16493-4_52.

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Conference papers on the topic "JAK/STAT Signaling Pathway"

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Mohbeddin, Abeer, Nawar Haj Ahmed, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Innate Immunity on Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0224.

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Apart from its traditional role in disease control, recent body of evidence has implicated a role of the immune system in regulating metabolic homeostasis. Owing to the importance of this “immune-metabolic alignment” in dictating a state of health or disease, a proper mechanistic understanding of this alignment is crucial in opening up for promising therapeutic approaches against a broad range of chronic, metabolic, and inflammatory disorders like obesity, diabetes, and inflammatory bowel syndrome. In this project, we addressed the role of the Janus kinase/signal transducer and activator of tr

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Gago-Dominguez, Manuela, Maria E. Martinez, Roger Milne, et al. "Abstract 4621: Polymorphisms in JAK/STAT signaling pathway genes and risk of breast cancer." 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.am2020-4621.

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Hui-Fen, Liao, Hsuan-Yu Peng, and Yu-Jen Chen. "Abstract 3552: JAK/Stat3 signaling pathway modulates human megakaryocytic differentiation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3552.

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Maude, Shannon L., Sibasish Dolai, Cristina Delagdo-Martin, et al. "Abstract 997: Targeting the Jak/Stat signaling pathway is highly effective in xenograft models of early T cell precursor (ETP) acute lymphoblastic leukemia (ALL)." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-997.

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Olejniczak, Scott H., Gaspare La Rocca, Megan Radler, and Craig B. Thompson. "Abstract 973: Coordinated regulation of cap-dependent translation and microRNA function by convergent signaling through the PI3K/Akt/mTOR and Jak/Stat/Pim signaling pathways." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-973.

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Tagami, Naoko, Satoshi Serada, Minoru Fujimoto, Atsushi Tanemura, Ichiro Katayama, and Tetsuji Naka. "Abstract 1348: Suppressor of cytokine signaling (SOCS)-1 suppresses a proliferation of malignant melanoma cellsviathe suppression of JAK/STAT and the activation of p53 signaling pathways." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1348.

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Li, H., and H. Zeng. "AB0188 Effect of MIR-19A and MIR-21 on the JAK/STAT signaling pathway in the peripheral blood mononuclear cells of patients with systemic juvenile idiopathic arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2060.

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Su, Liping, Xiongyan Wu, Quan Zhou, Chenchen Wang, and Bingya Liu. "Abstract 4803: Cancer-associated fibroblast promotes gastric cancer invasion and epithelial-mesenchymal transition via the IL-6/JAK/STAT3 signaling pathway." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4803.

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Yue, Wen, Yong Lin, Chunxia Chen, Darren R. Carpizo, Robert S. DiPaola, and Xiang-Lin Tan. "Abstract 2153: Metformin and aspirin synergistically inhibit mTOR and JAK/STAT3 signaling pathway and induce cell death in pancreatic cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2153.

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Yadav, Arti, Bhavna Kumar, Jharna Datta, Theodoros N. Teknos, and Pawan Kumar. "Abstract 3362: IL-6 promotes head and neck tumor metastasis by inducing epithelial-mesenchymal transition via the JAK-STAT3-SNAIL signaling pathway." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3362.

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Reports on the topic "JAK/STAT Signaling Pathway"

1

Clevenger, Charles V., and Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada543162.

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Clevenger, Charles. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada551381.

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Clevenger, Charles, and Anthony Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada551383.

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Kossiakoff, Anthony A. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada552192.

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Clevenger, Charles V., and Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada560592.

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Kossiakoff, Anthony A., and Charles V. Clevenger. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada560996.

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