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050 4 _aRC643
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066 _c(S
245 0 0 _aChemotherapy for Leukemia :
_bNovel Drugs and Treatment
_cTakanori Ueda editor.
264 1 _aSingapore
_bSpringer International Publishing
_c2017
264 4 _c2017
300 _a1 recurso en línea
_bilustraciones (algunas a color)
336 _astill image
_bsti
_2rdacontent
336 _aTexto
_btxt
_2rdacontent
337 _aelectrónico
_bc
_2rdamedia
338 _arecurso electrónico
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
504 _aIncluye referencias bibliográficas
505 0 _6880-01
_aPreface; Contents; 1: An Overview; 1.1 Category 1 Drugs; 1.2 Category 2 Drugs; 1.3 Category 3 Drugs; 1.4 Leukemic Stem Cells; References; Part I: Bcr-Abl Tyrosine Kinase Inhibitors (TKIs); 2: Imatinib: Basic Results; 2.1 Development of Imatinib; 2.2 Molecular Biology of CML; 2.2.1 Ph Chromosome; 2.2.2 Structure and Intramolecular Interaction of BCR-ABL; 2.2.3 Signaling Pathways Downstream of BCR-ABL; 2.3 Mechanism of BCR-ABL Inhibition by Imatinib; 2.3.1 Imatinib: Chemical Structure; 2.3.2 Imatinib and ABL Kinase Domain Interactions; 2.3.3 Imatinib: Pharmacodynamic Properties.
505 8 _a2.3.4 Effects of Imatinib on CML Mouse2.3.5 Mechanism of Imatinib-Induced Apoptosis; 2.4 Imatinib Resistance and Targeting Strategies to Overcome the Resistance; 2.4.1 BCR-ABL-Dependent Imatinib Resistance; 2.4.1.1 BCR-ABL Kinase Domain Mutations; 2.4.1.2 Gene Amplification and Upregulation of BCR-ABL Protein; 2.4.2 BCR-ABL-Independent Imatinib Resistance; 2.4.2.1 Alternative Signaling Pathways; 2.4.2.2 Genetic Instability; 2.4.2.3 Stem Cells and Bone Marrow Niche; 2.4.2.4 Imatinib Influx or Efflux; 2.5 Effects of Imatinib on Other Tyrosine Kinases; References.
505 8 _a3.12 Treatment-Free Remission3.13 Mathematical Models of Dynamics of CML; 3.14 Guidelines for CML; 3.15 Conclusion; References; 4: Dasatinib, Nilotinib, Bosutinib, Ponatinib, and Other TKIs; 4.1 Introduction; 4.2 Second-Generation ABL TKIs; 4.2.1 Dasatinib (Sprycel®); 4.2.1.1 Structure and Preclinical Studies; 4.2.1.2 Pharmacokinetics; 4.2.1.3 Clinical Effects; 4.2.1.4 Adverse Effects; 4.2.1.5 Indications and Usage; 4.2.1.6 Immunoeffects; 4.2.1.7 Stop Studies; 4.2.2 Nilotinib (Tasigna®); 4.2.2.1 Structure and Preclinical Studies; 4.2.2.2 Pharmacokinetics.
505 8 _a4.2.2.3 Clinical Effects4.2.2.4 Adverse Effects; 4.2.2.5 Indication and Usage; 4.2.2.6 Immunoeffects; 4.2.2.7 Stop Studies; 4.2.3 Bosutinib (Bosulif®); 4.2.3.1 Structure and Preclinical Studies; 4.2.3.2 Pharmacokinetics; 4.2.3.3 Clinical Effects; 4.2.3.4 Adverse Effects; 4.2.3.5 Indication and Usage; 4.2.3.6 Immunoeffects; 4.2.3.7 Stop Studies; 4.2.4 Bafetinib (Formerly INNO-406); 4.3 Third-Generation ABL TKIs; 4.3.1 Ponatinib (Iclusig®); 4.3.1.1 Structure and Preclinical Studies; 4.3.1.2 Pharmacokinetics; 4.3.1.3 Clinical Effects; 4.3.1.4 Adverse Effects.
520 3 _aThis book focuses on the latest progress in chemotherapy for leukemia and related diseases, including still-ongoing but promising studies. The effectiveness of treatment for chronic myeloid leukemia and acute promyelocytic leukemia has been dramatically improved in recent years. This improvement has been made possible with the development of molecular targeted agents such as bcr-abl tyrosine kinase inhibitors and all-trans retinoic acid. The antibody for the unique target of chemokine receptor 4 for adult T-cell leukemia/lymphoma, or FLT3 inhibitors (signaling inhibitors) has been applied to other leukemias. Also, chemotherapeutic agents including antimetabolite analogues such as clofarabine, and azacitidine (an epigenetic regulator) have undergone progressive development. Meanwhile, the novel concept of therapy targeting leukemic stem cells has been developed. The contributors discuss prospective results of basic and preclinical studies and clinical possibilities based on the effects for leukemic stem cells. This work facilitates a comprehensive understanding of modern treatment methodology for leukemia. The volume therefore will greatly benefit not only hematologists but also oncologists, all physicians who specialize in blood cancer, and pharmacologists who are involved in the development of therapeutic agents for leukemia.
650 7 _aLeucemia
_xChemotherapy.
_2embne
_0(OCoLC)fst00996896
_0
_9140673
700 1 _aUeda, Takanori,
_eeditor literario
856 4 0 _uhttps://go.openathens.net/redirector/universidadeuropea.es?url=http://link.springer.com/10.1007/978-981-10-3332-2
_zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
880 8 _6505-01/(S
_a3: Imatinib: Clinical Pharmacology and Therapeutic Results3.1 Introduction; 3.2 Definition of Responses to TKIs; 3.3 Clinical Trials of Imatinib for CML; 3.3.1 Phase 1 Study for CML in CP; 3.3.2 Phase 2 Studies for CML in CP, CML in AP, and CML in BP; 3.3.3 Outcomes of Imatinib Treatment in Newly Diagnosed CML-CP; 3.4 Adverse Events; 3.5 Dosing Issue; 3.6 Imatinib and Interferon α Combination; 3.7 Pharmacokinetics of Imatinib Therapy; 3.8 Prognostic Factors; 3.9 Monitoring the Response to Treatment of TKIs; 3.10 Prognosis Based on Response; 3.11 Resistance to Imatinib.
988 _aSpringer_Medicine_2017
998 _b02/2018
_dz
_e-
_zSI
999 _c95836
_d95836
_x1