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Bibliographies thématiques / Inhibiteur de la tyrosine kinase / Livres

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Livres sur le sujet « Inhibiteur de la tyrosine kinase »

Auteur : Grafiati

Publié le 17 mai 2025

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1

Focosi, Daniele, dir. Resistance to Tyrosine Kinase Inhibitors. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46091-8.

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2

Mustelin, Tomas. Src family tyrosine kinases in leukocytes. Austin : R.G. Landes, 1994.

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3

Heilmeyer, L. M. G. 1937- et NATO Advanced Study Institute on Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling (1992 : Acquafredda di Maratea, Italy), dir. Tyrosine phosphorylation/dephosphorylation and downstream signalling. Berlin : Springer-Verlag, 1993.

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4

D, Fabbro, et McCormick Frank 1950-, dir. Protein tyrosine kinases : From inhibitors to useful drugs. Totowa, N.J : Humana Press, 2006.

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5

Germano, Serena. Receptor tyrosine kinases : Methods and protocols. New York : Humana Press, 2015.

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6

Shulman, Johanna. Biochemical analysis of activating mutations of the Kit receptor tyrosine kinase. Ottawa : National Library of Canada, 1998.

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7

Gibson, Spencer Bruce. Role of the TEC family tyrosine kinase EMT in T cell activation. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1997.

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8

Easterfield, Howard James. Analogues of phosphotyrosine : New components of ligands for protein tyrosine kinase enzymes. Birmingham : University of Birmingham, 1999.

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9

Cudmore, Stephen Bruce. The effect of postnatal development on synaptic tyrosine kinase of rat forebrain. Ottawa : National Library of Canada, 1991.

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10

Ho, Jacqueline. A requirement for the receptor tyrosine kinase, Flk1, in hematopoiesis and vasculogenesis. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1999.

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11

Danielian, Sylvia. Protéines tyrosine kinases et signalisation cellulaire : Le modèle des lymphocytes T. Paris : Editions INSERM, 1993.

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12

Schmidt, Holger. NMR-Lösungsstruktur der humanen Hck SH3-Domäne im Komplex mit einem artifiziellen, hochoffinen Peptid-Liganden. Jülich : Forschungszentrum Jülich, Zentralbibliothek, 2006.

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13

Kellie, Stuart. Tyrosine kinases and neoplastic transformation. Austin : R.G. Landes, 1994.

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14

Tran, Thi Tuyen. Analyse der Bindungsspezifität der humanen Lck-SH3-Domäne anhand artifizieller und physiologischer Peptid-Liganden und strukturelle Charakterisierung dieser Peptide im Komplex mit SH3-Domänen. Jülich : Forschungszentrum Jülich, Zentralbibliothek, 2005.

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15

Technologie, Karlsruher Institut für, dir. Phosphorylation and Regulation of the Wnt co-Receptor LRP6 by Cyclin Dependent Kinase 14/Cyclin Y and Tyrosine Kinase Fer. [S.l : s.n.], 2014.

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16

Keane, Noeleen Emily. Nuclear magnetic resonance studies of the human insulin receptor tyrosine kinase autophosphorylation and activity. Birmingham : University of Birmingham, 1994.

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17

Lam, Lily Po Yee. A transforming mutation induces dimerization and enhances activity of the c-kit soluble tyrosine kinase domain. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1999.

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18

Viegas, Muriel. The intrinsic tyrosine kinase activity of the epidermal growth factor receptor is necessary for phospholipase A2 activation. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1993.

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19

Karlsson, Torbjörn. Possible role of the receptor tyrosine kinase- and Src homology 3 domain-interacting protein Shb for apoptosis and differentiation. Uppsala : Uppsala Universitet, 1997.

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20

Rommel, Christian. Phosphoinositide 3-kinase in Health and Disease : Volume 2. Berlin, Heidelberg : Springer-Verlag Berlin Heidelberg, 2011.

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21

Alaimo, Darrick James. Hepatic insulin receptor tyrosine kinase activity in diabetes : Modulation by assorted adenosine triphosphatases/phosphatases which copurify in partially purified preparations of the insulin receptor. [s.l : s.n.], 1992.

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22

Ivashchenko, I͡U. D.(I͡Uriĭ Dmitrievich). Polipeptidnye faktory rosta i kant͡serogenez. Kiev : Nauk. dumka, 1990.

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23

1952-, Drescher U., dir. Molecular bases of axonal growth and pathfinding. Berlin : Springer, 1997.

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24

1949-, Lichtner R. B., et Harkins R. N. 1947-, dir. EGF receptor in tumor growth and progression. Berlin : Springer, 1997.

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25

Matthews, David J. Targeting protein kinases for cancer therapy. Hoboken, N.J : John Wiley & Sons, 2009.

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26

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

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

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27

Eisen, Tim. The patient with renal cell cancer. Sous la direction de Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.

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28

Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer International Publishing AG, 2018.

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29

Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer, 2016.

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30

Focosi, Daniele. Resistance to Tyrosine Kinase Inhibitors. Springer, 2016.

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31

McCann, Shaun R. Leukaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0007.

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The word leukaemia still is associated with foreboding and a fear of premature death. Steady advances have been made in the treatment of childhood leukaemia but, with notable exceptions, the same is not true in adults. The so-called genetic/molecular revolution has extended the understanding of the pathogenesis of many forms of leukaemia but, as yet, has rarely facilitated cure. With the introduction of tyrosine kinase inhibitor therapy, chronic myeloid leukaemia is the obvious exception but it still needs to be seen as to whether the cytogenetic/molecular revolution can provide cures for many elderly patients with leukaemia, as such patients respond poorly to chemotherapy. Haematopoietic stem cell transplantation, although toxic, expensive, and difficult, still provides a cure for many patients. In spite of all these advances, however, most adults with acute leukaemia or myelodysplastic syndrome are destined to die from their disease, and the causes of these fatal illnesses continue to elude researchers.

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32

Beyer, Elsa Margaret. System-level studies of cell fate decisions mediated by receptor tyrosine kinases. 2010.

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33

Wybenga-Groot, Leanne Elizabeth. Regulation of Eph receptor tyrosine kinase catalytic function. 2005.

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34

The Protein Kinase Factsbook : Protein-Tyrosine Kinases (Factsbook). Academic Press, 1995.

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35

(Editor), Grahame Hardie, et Steven Hanks (Editor), dir. The Protein Kinase Factsbook : Protein-Tyrosine Kinases (Factsbook). Academic Press, 1995.

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36

Dikic, Inga. Signal Transduction by Proline-Rich Tyrosine Kinase Pyk2. Uppsala Universitet, 2002.

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37

Krall, Jordan Asher. System-level studies of receptor Tyrosine Kinase signaling networks. 2009.

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38

Hanks, Steven, et Grahame Hardie. Protein Kinase Factsbook, Two-Volume Set : Protein-Tyrosine Kinases. Elsevier Science & Technology Books, 1995.

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39

Friedman, Adam Amiel. Genomic dissection of receptor tyrosine kinase activation of extracellular signal-regulated kinase in Drosophila. 2007.

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40

Ellis, Paul D. *. Synaptic tyrosine kinase : partial characterization and identification of endogenous substrates. 1988.

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41

Puil, Lorri Jane. Protein-tyrosine kinase signalling pathways in normal hematopoiesis and leukemogenesis. 1998.

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42

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Family and Subfamilies. Springer, 2016.

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43

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Family and Subfamilies. Springer International Publishing AG, 2015.

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44

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Family and Subfamilies. Springer, 2015.

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45

Germano, Serena. Receptor Tyrosine Kinases : Methods and Protocols. Springer New York, 2016.

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46

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Structure, Functions and Role in Human Disease. Springer New York, 2016.

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47

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Structure, Functions and Role in Human Disease. Springer, 2014.

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48

Yarden, Yosef, et Deric L. Wheeler. Receptor Tyrosine Kinases : Structure, Functions and Role in Human Disease. Springer, 2014.

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49

Makowiecki, Mark Paul. Characterizing the role of EphB4 receptor tyrosine kinase during Xenopus gastrulation. 2005.

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50

3BP-2 : A novel substrate of the FLT3 receptor tyrosine kinase. Ottawa : National Library of Canada, 1996.

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