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Relevant bibliographies by topics / JAK/STAT

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Academic literature on the topic 'JAK/STAT'

Author: Grafiati

Published: 4 June 2021

Last updated: 24 August 2024

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Journal articles on the topic "JAK/STAT"

1

Barry, Sean P. "JAK-STAT." JAK-STAT 1, no. 2 (April 2012): 90–91. http://dx.doi.org/10.4161/jkst.20939.

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Minaudo, Carla. "Vía JAK-STAT e inhibidores JAK." Dermatología Argentina 28, no. 2 (June 1, 2022): 55–62. http://dx.doi.org/10.47196/da.v28i2.2324.

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La vía JAK-STAT (Janus Kinasas) es una cadena de traducción de señales intracelulares, que se activa a través de receptores de citoquinas I y II. Mediante esta vía, varias moléculas de importancia en dermatología ejercen sus efectos: IL2, IL4, IL7, IL5, IL6, IL9, IL12, IL13, IL15, IL21, IL23, INFa e INFb, entre otras. También es la señal intracelular de hormonas como la prolactina y la hormona de crecimiento. La inhibición de distintos componentes de esta vía es utilizada como terapéutica en enfermedades reumatológicas y un número cada vez mayor de patologías cutáneas. Los inhibidores JAK surgieron en la práctica médica hace aproximadamente 11 años, con el ruxolitinib y poco tiempo después el tofacitinib. En la actualidad, se dispone de varias moléculas aprobadas y muchas otras en etapa experimental. En este artículo se desarrollarán la organización intracelular y las funciones de la vía JAK-STAT con sus variantes principales relacionadas a enfermedades inmunomediadas, así como las características más relevantes de los inhibidores JAK.

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Galli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes, and Gustavo Martelli Palomino. "The JAK-STAT Pathway and the JAK Inhibitors." Journal of Clinical Research in Dermatology 7, no. 5 (November 30, 2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.

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Dozens of cytokines that bind Type I and Type II receptors use the Janus Kinases (JAK) and the Signal Transducer and Activator of Transcription (STAT) proteins pathway for intracellular signaling, orchestrating hematopoiesis, inducing inflammation, and controlling the immune response. Currently, oral JAK inhibitors are being used to treat many inflammatory and myeloproliferative diseases and are also under investigation in several clinical trials for skin diseases. Thus, dermatologists should understand how the JAK-STAT pathway works as well as the mechanism of action of the JAK inhibitors which will certainly become an important part of the dermatologist’s treatment armamentarium in the next few years. Keywords: JAK inhibitors; Janus Kinases; JAK-STAT Pathway List of Abbreviations: AD: Atopic Dermatitis ADP: Adenosine diphosphate Dmards: Disease-Modifying Antirheumatic Drugs JAK: Janus kinase(s) Jaki: Janus kinase Inhibitor(s) PIAS: Protein Inhibitor of Activated STAT P-STAT: Phosphorylated STAT STAT: Signal Transducer and Activator of Transcription TYK2: Tyrosine Kinase 2 Wsxws: Tryptophan-Serine-X-Tryptophan-Serine

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Harrison, D. A. "The JAK/STAT Pathway." Cold Spring Harbor Perspectives in Biology 4, no. 3 (March 1, 2012): a011205. http://dx.doi.org/10.1101/cshperspect.a011205.

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Wells, William A. "A JAK/STAT invasion." Journal of Cell Biology 156, no. 3 (January 28, 2002): 413. http://dx.doi.org/10.1083/jcb1563rr2.

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Aaronson, D. S., and C. M. Horvath. "The JAK-STAT Pathway." Science Signaling 2003, no. 197 (August 26, 2003): cm11. http://dx.doi.org/10.1126/stke.2003.197.cm11.

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Myllymäki, H., and M. Rämet. "JAK/STAT Pathway inDrosophilaImmunity." Scandinavian Journal of Immunology 79, no. 6 (May 21, 2014): 377–85. http://dx.doi.org/10.1111/sji.12170.

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Imada, Kazuroni, and Warren J. Leonard. "The Jak-STAT pathway." Molecular Immunology 37, no. 1-2 (January 2000): 1–11. http://dx.doi.org/10.1016/s0161-5890(00)00018-3.

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Ladyman, Sharon R., and David R. Grattan. "JAK-STAT and feeding." JAK-STAT 2, no. 2 (April 2013): e23675. http://dx.doi.org/10.4161/jkst.23675.

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Hombría, James Castelli-Gair, and Sol Sotillos. "JAK-STAT pathway inDrosophilamorphogenesis." JAK-STAT 2, no. 3 (July 15, 2013): e26089. http://dx.doi.org/10.4161/jkst.26089.

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Dissertations / Theses on the topic "JAK/STAT"

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Is'Harc, Hayaatun. "JAK/STAT signalling." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272414.

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Dawson, M. A. F. "JAK-STAT signalling at chromatin." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.

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The aim of my work was to explore the possibility that the mammalian JAK2 signalling pathway influences the structure and function of chromatin. I have demonstrated that JAK2 is present in the nucleus of both human haematopoietic cell lines and primary cells. My results suggest that JAK2 functions as a histone tyrosine kinase and phosphorylates histone H3 at tyrosine-41 (H3Y41). This novel histone modification, the first described tyrosine phosphorylation on any of the non-variant histones, regulates the binding of heterochromatin protein 1-alpha (HP1α) at a new binding site on chromatin. HP1α uses its chromo-shadow domain to bind the H3Y41 region. Phosphorylation of H3Y41 by JAK2 reduces its affinity for chromatin. This reciprocal relationship was given a functional context by demonstrating its relationship to the expression of a key haematopoietic oncogene Imo2. Genome-wide studies demonstrate that H3Y41ph is present at the 5’ end of genes and is highly correlated with active transcription. This is the first comprehensive genome wide mapping of a histone phosphorylation mark and potentially highlights a role for this novel modification in the regulation of transcription. H3Y41ph was also present at specific cis-regulatory elements on JAK2-STAT5 target genes and genome-wide mapping of STAT5 binding confirmed that STAT5 binding and H3Y41ph was coincident at a significant number of sites within the human genome. This interesting observation suggests that canonical JAK2-STAT5 signalling is not confined to the cytoplasma but also occurs at chromatin. These findings extend the existing paradigm of JAK-STAT signalling and provide a platform for a better understanding of this critical signalling pathway, which is important in both normal development and oncogenesis.

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Broughton, Nicola Ann. "Specificity in JAK/STAT signal transduction." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300540.

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Zhu, Wei. "Negative regulation of JAK/STAT pathway /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3112843.

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Vogt, Katja L. "Endocytic regulation of JAK/STAT signalling." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6655/.

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Moore, Rachel. "Regulation of JAK/STAT signalling by endocytosis." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22459/.

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The JAK/STAT pathway is a highly evolutionarily conserved signal transduction pathway, whose activation can lead to a broad range of cellular outcomes. The pathway is used repeatedly during multiple developmental stages and in adult tissue, and therefore tight regulation is required to enable accurate responses in a context specific manner. Internalisation and endocytic trafficking of signalling components provides a mechanism whereby spatial compartmentalisation can enable distinct signalling outputs. Within this study I have investigated the role of endocytosis in the regulation of the Drosophila melanogaster JAK/STAT pathway, and demonstrated that internalisation and endocytic trafficking differentially regulates target genes. Although the JAK/STAT pathway is transcriptionally competent and can regulate the expression of particular targets when the activated receptor is at the cell surface, receptor endocytosis and localisation to distinct endosomes is required for the expression of other targets. This appears to be context-dependent, as high levels of ligand stimulation overcomes endocytic regulation. STAT92E, the Drosophila JAK/STAT transcription factor, is a target of endocytic regulation. Although it is efficiently activated and undergoes nuclear translocation when endocytosis is perturbed, it is not capable of regulating a subset of target genes and therefore further STAT92E interacting partners and/or post translational modification must be required to fine-tune its transcriptional competency during endocytic trafficking. Utilising mass spectrometry I identified a novel STAT92E phosphorylation site, at threonine 702. Mutation of this threonine to prevent its phosphorylation, resulted in inhibition of STAT92E signalling and nuclear translocation, and also prevented phosphorylation of a highly conserved tyrosine residue at position 704, which is crucial for ligand activated JAK/STAT signalling outputs. Therefore, this study has enhanced our understanding of mechanisms that can modulate JAK/STAT activity. I have revealed an important role for endocytosis in fine- tuning Drosophila JAK/STAT signalling outputs and also identified a novel phosphorylation site which is crucial in the activity of STAT92E.

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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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Röder, Sabine. "Signaltransduktion durch JAK-STAT-Moleküle bei der Polyzythämia vera." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972175741.

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Moubarak, Patricia. "Expression und Regulation von JAK/STAT-Proteinen im Pankreas." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-53862.

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Pean, Claire. "JAK-STAT pathway in the control of mycobacterial infections." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/jakstat-pathway-in-the-control-of-mycobacterial-infections(cb788a0d-1c53-4f5c-8513-64c8cb50e08e).html.

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Though mammalian JAKs and STATs have been extensively studied over the past 20 years, many aspects of their in vivo function remain unclear. In particular, their roles in control of infection with pathogens remain murky and confusing. One difficulty in understanding how these pathways regulate inflammation is the presence of complex compensatory mechanisms between the different JAK and STAT proteins. In the Dionne lab, we use the fruit-fly Drosophila melanogaster as a model to study the in vivo functions of the JAK/STAT pathway in mycobacterial infection. Flies contain only one JAK (hop), one STAT (STAT92E), and three identified interleukin-like signals to activate signalling (upd, upd2, upd3). I show that, in Drosophila, the STAT-activating cytokine Upd3 is harmful to the host upon mycobacterial infection. Flies lacking upd3, or in which the JAk/STAT pathway is inhibited in phagocytes, show improved survival, decreased mycobacterial numbers, and delayed immune cell death. Strikingly, I find that JAK/STAT signalling acts in concert with other inflammatory signals to regulate expression of Atg2 in Drosophila phagocytes. In isolation or upon infection, STAT activation inhibits Atg2 expression and the ability of other, unknown signals to promote Atg2 expression. Increased Atg2 expression, as is seen in infected animals lacking either the cytokine Upd3 or STAT92E, promotes killing of intracellular bacteria and accumulation of large lipid droplets of unusual shape. I suggest an autophagy-independent mechanism by which Atg2 could reduce bacterial growth, involving the control of lipid body morphology. In this thesis, I show a mechanism by which JAK/STAT controls bacterial growth through inhibition of autophagy gene expression and demonstrate that this inhibition is detrimental to the survival of the host. In addition, I demonstrate that upd3 signalling is also required for glucose homeostasis suggesting a role for Upd3 in regulating gluconeogenesis and glycolysis.

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Books on the topic "JAK/STAT"

1

Nicholson, Sandra E., and Nicos A. Nicola, eds. JAK-STAT Signalling. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.

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Anastasis, Stephanou, ed. JAK-STAT pathway in disease. Austin, Tex: Landes Bioscience, 2009.

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Decker, Thomas, and Mathias Müller, eds. Jak-Stat Signaling : From Basics to Disease. Vienna: 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. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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

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6

Köberlein, Bernd. Interaktion von Hepatitis-B- und -C-Viren mit der inflammatorischen JAK-STAT-Signaltransduktion. Tübingen, Kastanienweg 5: B. Köberlein, 2008.

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7

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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Stephanou, Anastasis, and Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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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"

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Caldow, Marissa K., and David Cameron-Smith. "JAK/STAT Pathway." In Encyclopedia of Exercise Medicine in Health and Disease, 495–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_242.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_157-1.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology, 889–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_157.

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Leonard, Warren J. "The JAK-STAT Pathway." In Hormone Signaling, 103–20. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_6.

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Vangara, Bhavana S., and Jennifer R. Grandis. "Jak/STAT Signaling in HNC." In Molecular Determinants of Head and Neck Cancer, 163–77. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8815-6_8.

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Stine, Rachel R., and Erika L. Matunis. "JAK-STAT Signaling in Stem Cells." In Transcriptional and Translational Regulation of Stem Cells, 247–67. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6621-1_14.

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Siddiqui, M. A. Q., and Eduardo Mascareno. "JAK/Stat Signaling in Cardiac Diseases." In Signal Transduction and Cardiac Hypertrophy, 349–56. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_25.

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Vogl, Claus, Priyank Shukla, and Ingo Ebersberger. "Evolution of Jak and Stat Proteins." In Jak-Stat Signaling : From Basics to Disease, 99–114. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8_7.

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Wilks, Andrew F., and Ailsa G. Harpur. "STFs: STAT-Containing Transcription Factors." In Intracellular Signal Transduction: The JAK-STAT Pathway, 79–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4_5.

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Croker, Ben A., and Nicos A. Nicola. "The Jak-Stat Pathway of Cytokine Signaling." In Hematopoietic Growth Factors in Oncology, 45–64. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_3.

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Conference papers on the topic "JAK/STAT"

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Beeckmans, H., J. E. Mcdonough, L. De Sadeleer, A. Sacreas, A. Vanstapel, J. Kaes, A. Van Herck, et al. "JAK-STAT pathway is upregulated in CLAD." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1390.

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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 transcription (JAK/STAT) innate immune pathway in regulating different metabolic parameters using the Drosophila melanogaster (DM) fruit fly model organism. Mutant JAK/STAT pathway flies with a systemic knockdown of either Domeless (Dome) [domeG0282], the receptor that activates JAK/STAT signaling, or the signal-transducer and activator of transcription protein at 92E (Stat92E) [stat92EEY10528], were used. The results of the study revealed that blocking JAK/STAT signaling alters the metabolic profile of mutant flies. Both domeG0282 and stat92EEY10528 mutants had an increase in body weight, lipid deprivation from their fat body (lipid storage organ in flies), irregular accumulation of lipid droplets in the gut, systemic elevation of glucose and triglyceride levels, and differential down-regulation in the relative gene expression of different peptide hormones (Tachykinin, Allatostatin C, and Diuretic hormone 31) known to regulate metabolic homeostasis in flies. Because the JAK/STAT pathway is evolutionary conserved between invertebrates and vertebrates, our potential findings in the fruit fly serves as a platform for further immune-metabolic translational studies in more complex mammalian systems including humans.

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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.

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Elahi, Abul, Jonathan M. Hernandez, and David Shibata. "Abstract 3064: HPP1 tumor suppression and 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.am10-3064.

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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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Montazeri Aliabadi, Hamidreza, Emira Bousoik, and Parvin Mahdipoor. "Abstract B087: A systematic approach to JAK/STAT pathway shut-down." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b087.

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Alapatt, Catherine F., Amanda Greenspan, and Mohammad Fardos. "Janus Kinase (JAK) Inhibitors: A New Frontier in the Treatment of Vitiligo." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. http://dx.doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.180_2024.

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Up to 70 million people worldwide suffer from vitiligo, an autoimmune disease characterized by the destruction of melanin. Current treatment options vary in efficacy. The disease manifests clinically as white circular macules of depigmentation seen primarily on the face and appendages.1 The pathophysiology of vitiligo is multifactorial and still being studied. One proposed mechanism behind the pathophysiology of vitiligo involves the upregulation of interferon gamma (IFN-γ) with downstream effects on JAK/STAT pathways resulting in CXCL10 transcription.1,2 Here we discuss Ruxolitinib, a topical JAK inhibitor, that recently passed its clinical trial phase, and Ritlecitinib, an oral JAK inhibitor which is currently undergoing clinical trials.3,4 These drugs are a reflection of the recent increase in targeted therapies for dermatologic diseases. The promising results of these drugs are widening the possible treatment options for patients that suffer from vitiligo.

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Clarke, DL, EL Hardaker, MC Catley, MA Birrell, and MG Belvisi. "Inhibition of JAK/STAT Signalling: A Novel Therapy for Steroid Resistant Asthma?." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5599.

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Denk, Dagmar, Klaus Fortschegger, and Sabine Strehl. "Abstract 2171: The fusion protein PAX5-JAK2 constitutively activates JAK-STAT signaling." 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.am2011-2171.

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Jingjing, Gong, Izhar S. Batth, and Addanki P. Kumar. "Abstract 3544: Jak/Stat signaling: A potential target for pancreatic cancer management." 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.am2011-3544.

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Reports on the topic "JAK/STAT"

1

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, 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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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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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485255.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada472476.

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Clevenger, Charles V., and Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 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. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada551381.

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