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  • 1
    UID:
    (DE-605)HT000612031
    Format: 50 S.
    Note: MUENCHEN, MED. FAK., DISS. V. 22.7.1969
    Language: Undetermined
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  • 2
    Online Resource
    Online Resource
    Cham : Springer
    UID:
    (DE-605)HT019454875
    Format: 1 Online-Ressource (x, 255 Seiten) , Illustrationen , 26 cm
    ISBN: 9783319331980
    Series Statement: Hematologic malignancies
    Note: Includes bibliographical references
    Additional Edition: Erscheint auch als Druck-Ausgabe 9783319331973
    Language: English
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  • 3
    UID:
    (DE-627)1571808302
    Format: 4
    ISSN: 1592-8721
    Content: One of the great success stories of modern hematology is reaching its next and possibly final phase: the achievement of treatment-free remissions in stable deep molecular responders with chronic myeloid leukemia (CML) which may well be equivalent to cure. Although only the minority of patients
    Note: Gesehen am 09.04.2018
    In: Haematologica, Pavia : Ferrata Storti Foundation, 2014, 102(2017), 3, Seite 418-421, 1592-8721
    In: volume:102
    In: year:2017
    In: number:3
    In: pages:418-421
    In: extent:4
    Language: English
    URL: Volltext  (kostenfrei registrierungspflichtig)
    URL: Volltext  (kostenfrei registrierungspflichtig)
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  • 4
    Online Resource
    Online Resource
    Cham : Springer International Publishing | Cham : Springer
    UID:
    (DE-604)BV047389754
    Format: 1 Online-Ressource (IX, 273 p. 42 illus., 35 illus. in color)
    Edition: 2nd ed. 2021
    ISBN: 9783030719135
    Series Statement: Hematologic Malignancies
    Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-030-71912-8
    Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-030-71914-2
    Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-3-030-71915-9
    Language: English
    URL: Volltext  (URL des Erstveröffentlichers)
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  • 5
    UID:
    (DE-627)1669010996
    Format: 9
    ISSN: 1096-8652
    Content: SIMPLICITY (NCT01244750) is an observational study exploring tyrosine kinase inhibitor (TKI) use and management patterns in patients with chronic phase-chronic myeloid leukemia in the US and Europe in routine clinical practice. Herein we describe interruptions, discontinuations and switching of TKI therapy during the initial 2 years of treatment among 1121 patients prospectively enrolled between October 1, 2010 and March 7, 2017. Patient characteristics were broadly similar between the imatinib (n = 370), dasatinib (n = 376), and nilotinib (n = 375) cohorts. Treatment interruptions occurred in 16.4% (year 1) and 4.0% (year 2) of patients, mainly attributed to hematologic intolerances. Treatment discontinuations occurred in 21.8% (year 1) and 10.2% (year 2) of patients, with the highest rate within the first 3 months for intolerance. Switching of TKI was seen in 17.8% (year 1) and 9.5% (year 2) of patients. Significant associations were found between TKI switching and female gender (year 1), age ≥65 years at diagnosis (year 2) and treatment with imatinib (year 2). Intolerance was the most common reason given for patients discontinuing and for switching TKI therapy; however resistance was also cited. Lack of response monitoring in routine clinical practice may have resulted in lower identification of resistance in this dataset. Data from SIMPLICITY suggest that, in routine clinical practice, intolerance and resistance to TKIs influence decisions to change treatment. Changes in TKI therapy are frequent, with nearly a third of patients discontinuing their first-line TKI.
    Note: First published: 05 October 2018 , Gesehen am 11.07.2019
    In: American journal of hematology, New York, NY : Wiley-Liss, 1976, 94(2019), 1, Seite 46-54, 1096-8652
    In: volume:94
    In: year:2019
    In: number:1
    In: pages:46-54
    In: extent:9
    Language: English
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  • 6
    UID:
    (DE-101)482571314
    Format: 50 S. mit Abb. , 8
    Note: München, Med. F., Diss. v. 22. Juli 1969
    Language: German
    Keywords: Hochschulschrift
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  • 7
    Online Resource
    Online Resource
    Cham : Springer International Publishing
    UID:
    (DE-605)HT020976916
    Format: 1 Online-Ressource (IX, 273 p. 42 illus., 35 illus. in color)
    Edition: 2nd ed. 2021
    ISBN: 9783030719135
    Series Statement: Hematologic Malignancies
    Additional Edition: Printed edition 9783030719128
    Additional Edition: Printed edition 9783030719142
    Additional Edition: Printed edition 9783030719159
    Language: English
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  • 8
    UID:
    (DE-101)1153937190
    Format: Online-Ressource
    ISSN: 2296-5262
    In: volume:24
    In: number:4
    In: year:2001
    In: pages:380-384
    In: Oncology research and treatment, Basel : Karger, 2014-, 24, Heft 4 (2001), 380-384, 2296-5262
    Language: German
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  • 9
    UID:
    (DE-627)1571784993
    Format: 11
    ISSN: 1528-0020
    Content: Blast crisis (BC) remains the major challenge in the management of chronic myeloid leukemia (CML). It is now generally accepted that BC is the consequence of continued BCR-ABL activity leading to genetic instability, DNA damage, and impaired DNA repair. Most patients with BC carry multiple mutations, and up to 80% show additional chromosomal aberrations in a nonrandom pattern. Treatment with tyrosine kinase inhibitors has improved survival in BC modestly, but most long-term survivors are those who have been transplanted. Patients in BC should be treated with a tyrosine kinase inhibitor according to mutation profile, with or without chemotherapy, with the goal of achieving a second chronic phase and proceeding to allogeneic stem cell transplantation as quickly as possible. Although long-term remissions are rare, allogeneic stem cell transplantation provides the best chance of a cure in BC. Investigational agents are not likely to provide an alternative in the near future. In view of these limited options, prevention of BC by a rigorous and early elimination of BCR-ABL is recommended. Early response indicators should be used to select patients for alternative therapies and early transplantation. Every attempt should be made to reduce or eliminate BCR-ABL consistent with good patient care as far as possible.
    Note: Gesehen am 06.04.2018
    In: Blood, Washington, DC : American Society of Hematology, 1946, 120(2012), 4, Seite 737-747, 1528-0020
    In: volume:120
    In: year:2012
    In: number:4
    In: pages:737-747
    In: extent:11
    Language: English
    URL: Volltext  (kostenfrei)
    URL: Volltext  (kostenfrei)
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  • 10
    Online Resource
    Online Resource
    Cham : Springer International Publishing
    UID:
    (DE-627)866582576
    Format: 1 Online-Ressource (261 p)
    ISBN: 9783319331973
    Series Statement: Hematologic Malignancies
    Content: Contents -- Introduction: Chronic Myeloid Leukemia (CML) in the Era of Tyrosine Kinase Inhibition -- 1: Cytogenetics of Chronic Myeloid Leukemia (CML) -- 1.1 The Discovery of the Philadelphia Chromosome (Ph) -- 1.2 The Translocation t(9 -- 22) -- 1.3 Relevance of Additional Cytogenetic Aberrations in a Ph-Positive Clone -- 1.4 Ph-Negative Clones -- 1.5 Significance of Cytogenetics for Current and Future Diagnosis and Monitoring of CML -- References -- 2: The Biology and Pathogenesis of Chronic Myeloid Leukemia -- 2.1 Clinical Overview -- 2.1.1 Diagnosis
    Content: 2.1.2 CML Evolution and Prognosis -- 2.1.3 Treatment -- 2.2 The Molecular Biology of CML -- 2.2.1 The t(9 -- 22) Translocation and the BCR-ABL1 Gene -- 2.2.2 Protein Structure -- 2.2.3 The Consequence of BCR-ABL1 -- 2.3 Important Pathways Affected by BCR-ABL1 Activity -- 2.3.1 JAK/STAT -- 2.3.2 PI3K/AKT and Autophagy -- 2.3.3 Ras/MEK Pathway -- 2.3.4 Src Kinases -- 2.3.5 Crkl -- 2.3.6 Long Noncoding (lnc) RNA-BGL3 -- 2.3.7 Apoptosis Deregulation -- 2.4 CML Stem Cells -- 2.4.1 LSCs Are Refractory to TKIs -- 2.4.2 β-Catenin -- 2.4.3 Smo -- 2.4.4 PP2A-JAK2-SET -- 2.4.5 FoxO
    Content: 2.4.6 Alox5 and Alox15 -- 2.4.7 Bone Marrow Microenvironment -- 2.5 Biology of Blast Crisis -- 2.5.1 BCR-ABL1 and BC-CML -- 2.5.1.1 DNA Damage/Repair -- 2.5.1.2 C/EBPα and hnRNP-E2 -- 2.5.1.3 IRF-8 -- 2.5.2 Examples of Important Pathways Involved in BC-CML -- 2.5.2.1 MYC -- 2.5.2.2 p53 -- 2.5.2.3 Musashi-2 (Msi2) -- 2.5.2.4 XPO1 -- 2.5.2.5 SIRT1 -- 2.5.2.6 ADAR1 -- 2.5.2.7 Screening for Novel BC Driver Genes -- 2.6 Concluding Remarks -- References -- 3: The Choice of First-Line Chronic Myelogenous Leukemia Treatment -- 3.1 Introduction
    Content: 3.2 Second-Generation TKIs in First-Line Treatment -- 3.3 High-Dose Imatinib for First-­Line Treatment -- 3.4 Combination Therapy: Imatinib Plus Interferon Alpha -- Conclusions -- References -- 4: A Review and an Update of European LeukemiaNet Recommendations for the Management of Chronic Myeloid Leukemia -- 4.1 Chronic Phase (CP), Accelerated Phase (AP), and Blastic Phase -- 4.2 Risk, Baseline -- 4.3 Response to Treatment -- 4.4 First-Line Treatment -- 4.5 Second-Line Treatment -- 4.6 Treatment Continuation or Discontinuation, Treatment- Free Remission (TFR), Cure
    Content: 4.7 Treatment of Accelerated and Blastic Phase -- Conclusions -- References -- 5: Management of Adverse Events Associated with ATP-Competitive BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia -- 5.1 Introduction -- 5.2 Myelosuppression -- 5.3 Dermatologic Adverse Events -- 5.4 Gastrointestinal Adverse Events -- 5.5 Hepatic and Pancreatic Disorders -- 5.6 Musculoskeletal Symptoms -- 5.7 Fluid Retention -- 5.8 Pulmonary Toxicity -- 5.9 Cardiovascular Toxicity -- 5.9.1 QT Interval Prolongation -- 5.9.2 Systemic Arterial Hypertension -- 5.9.3 Congestive Heart Failure
    Content: 5.9.4 Arterial Occlusion
    Note: Description based upon print version of record
    Additional Edition: 9783319331980
    Additional Edition: 9783319331973
    Additional Edition: Print version Hehlmann, Rüdiger Chronic Myeloid Leukemia Cham : Springer International Publishing,c2016 9783319331973
    Language: English
    Keywords: Electronic books
    URL: Volltext  (lizenzpflichtig)
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