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Bibliographies thématiques / Tyrosine Kinase Inhibitors (TKIs) / Livres

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Livres sur le sujet « Tyrosine Kinase Inhibitors (TKIs) »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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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

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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3

Phosphoinositide 3-kinase in health and disease. Heidelberg : Springer Verlag, 2010.

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4

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

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5

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

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6

E, Gerritsen Mary, dir. Targeting protein kinases for cancer therapy. Hoboken, N.J : John Wiley & Sons, 2010.

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7

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

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8

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

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9

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

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10

McCormick, Frank, et Doriano Fabbro. Protein Tyrosine Kinases : From Inhibitors to Useful Drugs. Humana Press, 2010.

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11

McCormick, Frank. Protein Tyrosine Kinases : From Inhibitors to Useful Drugs. Humana Press, 2005.

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12

(Editor), Doriano Fabbro, et Frank McCormick (Editor), dir. Protein Tyrosine Kinases : From Inhibitors to Useful Drugs (Cancer Drug Discovery and Development). Humana Press, 2005.

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13

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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14

Rommel, Christian, Peter K. Vogt et Bart Vanhaesebroeck. Phosphoinositide 3-kinase in Health and Disease : Volume 1. Springer, 2012.

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15

Rommel, Christian, Peter K. Vogt et Bart Vanhaesebroeck. Phosphoinositide 3-kinase in Health and Disease : Volume 1. Springer, 2010.

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16

Rommel, Christian, Peter K. Vogt et Bart Vanhaesebroeck. Phosphoinositide 3-kinase in Health and Disease : Volume 2. Springer, 2010.

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17

Rommel, Christian, Peter K. Vogt et Bart Vanhaesebroeck. Phosphoinositide 3-Kinase in Health and Disease : Volume 2. Springer Berlin / Heidelberg, 2012.

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18

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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19

Kuwabara, Satoshi. Neuromuscular junction disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0014.

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Ten seminal papers on disorders of the neuromuscular junction are described, covering historical aspects, recent advances in immunological, biological, and genetic researches, and future perspectives. Early descriptions of myasthenia gravis (MG) date back to the seventeenth century, and MG acquired its name in the nineteenth century. The first symptomatic treatment with cholinesterase inhibitors was reported in 1934, leading to the development of modern immunological therapies. Following the discovery of anti-MuSK (muscle-specific tyrosine kinase) antibody in 2001, MG is currently classified into three categories: AChR-positive, MuSK-positive, and dual-seronegative. Lambert-Eaton myasthenic syndrome was recognized in 1956, followed by the discovery of antibodies to voltage-gated calcium channels in the pre-synaptic membrane, facilitating diagnosis and improving the understanding of the pathophysiological mechanisms. Since the late twentieth century, many types of congenital myasthenic syndromes with pre-synaptic, synaptic, and post-synaptic defects have been identified, and a classification based on molecular genetics is in evolution.

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20

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne et Gareth Morris-Stiff. Bone and soft tissue malignancies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199689842.003.0025.

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Haematological malignancies examines the epidemiology, genetics, clinical presentation and classification of these diseases, and presents current treatment approaches for each. First are the acute leukaemias, and the management of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML). Chronic myeloid leukaemia, its genetics and sensitivity to tyrosine kinase inhibitors, is described. Myelodysplastic syndromes and their management, are followed by chronic lymphoid leukaemias, a large heterogeneous group of diseases, and their treatment. Hodgkin lymphoma, its pathology and presentation, staging and role of PET scanning, is described along with current treatment with chemotherapy and limited radiotherapy. Non-Hodgkin lymphoma is another heterogeneous group of diseases, divided into low-grade and high-grade pathology, and varying in their genetics, presentation, and management. Rituximab is a key component of chemotherapy regimens against B-cell lymphoma. Myeloma and other plasma cell dyscrasias are described, and treatment options reviewed. Myeloma remains incurable, but with appropriate management consistent with prolonged good quality life. Treatment includes chemotherapy, bisphosphonate therapy, analgesics and radiotherapy, Throughout this chapter is emphasised the importance of clinical trials in driving the rapid improvements in treatment of these diseases.

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