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  1. Book: Venetoclax - ein neuer Therapiestandard in der AML

    Döhner, Hartmut

    (Tumor-Diagnostik & Therapie : Drug Report ; [42,6, Beilage])

    2021  

    Author's details Auor Prof. Dr. Hartmut Döhner
    Series title Tumor-Diagnostik & Therapie : Drug Report ; [42,6, Beilage]
    Tumordiagnostik & Therapie
    Tumor-Diagnostik & Therapie
    Collection Tumordiagnostik & Therapie
    Tumor-Diagnostik & Therapie
    Language German
    Size 11 Seiten, Illustrationen, Diagramme
    Publisher Thieme
    Publishing place Stuttgart
    Publishing country Germany
    Document type Book
    HBZ-ID HT021303060
    Database Catalogue ZB MED Medicine, Health

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    Zs A 1590 -[42,6,Beil.]- not available for loan Zeitschriften-Lesesaal

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  2. Book: Midostaurin

    Döhner, Hartmut / Reiter, Andreas

    Multi-Target-Kinase-Hemmer

    (Drug report ; 12. Jahrgang, Heft 1 (Februar 2018))

    2018  

    Author's details Autoren Prof. Dr. Hartmut Döhner, Prof. Dr. med. Andreas Reiter
    Series title Drug report ; 12. Jahrgang, Heft 1 (Februar 2018)
    Collection
    Language German
    Size 15 Seiten, Illustrationen, Diagramme
    Publisher Thieme
    Publishing place Stuttgart
    Publishing country Germany
    Document type Book
    HBZ-ID HT019710267
    Database Catalogue ZB MED Medicine, Health

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    Zs A 6601 -12,1- verfügbar in Königswinter Königswinter

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  3. Article ; Online: All systems are not GO: ongoing challenges in interpreting gemtuzumab ozogamicin clinical trial results - Authors' reply.

    Döhner, Hartmut / Benner, Axel / Ganser, Arnold

    The Lancet. Haematology

    2023  Volume 10, Issue 9, Page(s) e707

    MeSH term(s) Humans ; Gemtuzumab/therapeutic use ; Longitudinal Studies ; Clinical Trials as Topic
    Chemical Substances Gemtuzumab (93NS566KF7)
    Language English
    Publishing date 2023-08-29
    Publishing country England
    Document type Letter ; Comment
    ISSN 2352-3026
    ISSN (online) 2352-3026
    DOI 10.1016/S2352-3026(23)00242-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: How I treat refractory and relapsed acute myeloid leukemia.

    Thol, Felicitas / Döhner, Hartmut / Ganser, Arnold

    Blood

    2023  Volume 143, Issue 1, Page(s) 11–20

    Abstract: Abstract: Most patients with acute myeloid leukemia (AML) develop refractory/relapsed (R/R) disease even in the presence of novel and targeted therapies. Given the biological complexity of the disease and differences in frontline treatments, there are ... ...

    Abstract Abstract: Most patients with acute myeloid leukemia (AML) develop refractory/relapsed (R/R) disease even in the presence of novel and targeted therapies. Given the biological complexity of the disease and differences in frontline treatments, there are therapies approved for only subgroups of R/R AML, and enrollment in clinical trials should be first priority. Allogeneic hematopoietic cell transplantation (HCT) is the only potentially curative strategy for most patients. Therapeutic approaches, including allogeneic HCT, triggered by the presence of measurable residual disease (MRD), have recently evolved to prevent overt hematologic relapse. Salvage therapy with chemotherapy or targeted therapy is frequently administered before HCT to reduce the leukemic burden. Gilteritinib is approved by the Food and Drug Administration and European Medicines Agency for patients with relapsed FLT3 mutated AML, whereas targeted therapy for relapsed IDH1/2 mutated AML has only FDA approval. Patients who are R/R after azacitidine and venetoclax (AZA/VEN) have a dismal outcome. In this setting, even available targeted therapies show unsatisfactory results. Examples of ongoing developments include menin inhibitors, a targeted therapy for patients with mutated NPM1 or KMT2A rearrangements, antibodies targeting the macrophage immune checkpoint CD47, and triple combinations involving AZA/VEN. The latter cause significant myelosuppressive effects, which make it challenging to find the right schedule and dose.
    MeSH term(s) Humans ; Hematopoietic Stem Cell Transplantation ; Azacitidine/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Leukemia, Myeloid, Acute/therapy ; Leukemia, Myeloid, Acute/drug therapy ; Salvage Therapy
    Chemical Substances Azacitidine (M801H13NRU)
    Language English
    Publishing date 2023-11-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2023022481
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Ivosidenib and Azacitidine in IDH1-Mutated AML. Reply.

    Montesinos, Pau / de Botton, Stephane / Döhner, Hartmut

    The New England journal of medicine

    2022  Volume 386, Issue 26, Page(s) 2536–2537

    MeSH term(s) Azacitidine/therapeutic use ; Glycine/analogs & derivatives ; Humans ; Isocitrate Dehydrogenase/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Pyridines/therapeutic use
    Chemical Substances Pyridines ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.) ; Azacitidine (M801H13NRU) ; ivosidenib (Q2PCN8MAM6) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2022-06-29
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2206489
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Oral Azacitidine Maintenance for Acute Myeloid Leukemia. Reply.

    Wei, Andrew H / Döhner, Hartmut / Roboz, Gail J

    The New England journal of medicine

    2021  Volume 384, Issue 13, Page(s) e51

    MeSH term(s) Azacitidine ; Humans ; Leukemia, Myeloid, Acute/drug therapy
    Chemical Substances Azacitidine (M801H13NRU)
    Language English
    Publishing date 2021-03-31
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2101283
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  7. Article ; Online: Neurologic Complications of the Central Nervous System after Allogeneic Stem Cell Transplantation: The Role of Transplantation-Associated Thrombotic Microangiopathy as a Potential Underreported Cause.

    Sala, Elisa / Neagoie, Adela M / Lewerenz, Jan / Saadati, Maral / Benner, Axel / Gantner, Andrea / Wais, Verena / Döhner, Hartmut / Bunjes, Donald

    Transplantation and cellular therapy

    2024  

    Abstract: Neurologic complications (NCs), especially those of the central nervous system (CNS), represent a severe complication after allogeneic stem cell transplantation (allo-HSCT) and are associated with relevant morbidity and mortality. We aimed to ... ...

    Abstract Neurologic complications (NCs), especially those of the central nervous system (CNS), represent a severe complication after allogeneic stem cell transplantation (allo-HSCT) and are associated with relevant morbidity and mortality. We aimed to characterize the potential risk factors for the development of CNS-NC, with a special focus on the role of calcineurin inhibitors (CNIs) as a predisposing factor. For this purpose, we compared cyclosporin A (CsA) versus tacrolimus (TAC) with respect to their influence on the incidence and type of CNS-NC after allo-HSCT. We retrospectively analyzed the incidence, risk factors, and impact on outcomes of CNS-NC diagnosed during the post-transplantation follow-up in patients with different high-risk hematologic malignancies who underwent allo-HSCT at our institution over a 20-year period. All patients included in the analysis received CNI (CsA or TAC) as graft-versus-host disease (GVHD) prophylaxis. We evaluated a total of 739 consecutive patients who underwent transplantation between December 1999 and April 2019. During a median follow-up of 6.8 years, we observed a CNS-NC incidence of 17%. The development of CNS-NC was associated with decreased overall survival (OS) and increased transplantation-related mortality (TRM). The most frequent CNS-NCs were infections (30%) and neurologic adverse events related to the administration of CNI, TAC, or CsA as GVHD prophylaxis (42%). In the multivariable analysis, age, total body irradiation (TBI), and severe acute GVHD and chronic GVHD were significant risk factors in the development of CNS-NCs. TAC compared with CsA emerged as an independent predisposing factor for CNS-NCs. The TAC-associated risk of CNS-NCs was related mostly to the occurrence of transplantation-associated thrombotic microangiopathy (TA-TMA) with neurologic manifestations (neuro-TA-TMA), although the general TA-TMA incidence was comparable in the 2 CNI subgroups. CNS-NCs are associated with poor prognosis after allo-HSCT, with TAC emerging as a potential yet insufficiently characterized predisposing factor.
    Language English
    Publishing date 2024-03-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3062231-1
    ISSN 2666-6367
    ISSN (online) 2666-6367
    DOI 10.1016/j.jtct.2024.03.017
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    Zs.A 5082: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  8. Article ; Online: Towards precision medicine for AML.

    Döhner, Hartmut / Wei, Andrew H / Löwenberg, Bob

    Nature reviews. Clinical oncology

    2021  Volume 18, Issue 9, Page(s) 577–590

    Abstract: With rapid advances in sequencing technologies, tremendous progress has been made in understanding the molecular pathogenesis of acute myeloid leukaemia (AML), thus revealing enormous genetic and clonal heterogeneity, and paving the way for precision ... ...

    Abstract With rapid advances in sequencing technologies, tremendous progress has been made in understanding the molecular pathogenesis of acute myeloid leukaemia (AML), thus revealing enormous genetic and clonal heterogeneity, and paving the way for precision medicine approaches. The successful development of precision medicine for patients with AML has been exemplified by the introduction of targeted FLT3, IDH1/IDH2 and BCL-2 inhibitors. When used as single agents, these inhibitors display moderate antileukaemic activity. However, augmented clinical activity has been demonstrated when they are administered in combination with drugs with broader mechanisms of action targeting epigenetic and/or other oncogenic signalling pathways or with conventional cytotoxic agents. The development of immunotherapies has been hampered by the expression of antigens that are expressed by both leukaemic and non-malignant haematopoietic progenitor cells; nonetheless, a diverse range of immunotherapies are now entering clinical development. This myriad of emerging agents also creates challenges, such as how to safely combine agents with different mechanisms of action, the need to circumvent primary and secondary resistance, and new challenges in future clinical trial design. In this Review, we discuss the current state of precision medicine for AML, including both the potential to improve patient outcomes and the related challenges.
    MeSH term(s) Antineoplastic Agents/therapeutic use ; Epigenesis, Genetic/physiology ; Humans ; Leukemia, Myeloid, Acute/epidemiology ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Leukemia, Myeloid, Acute/therapy ; Molecular Targeted Therapy/methods ; Mutation ; Precision Medicine/methods ; Precision Medicine/trends
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2021-05-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2491410-1
    ISSN 1759-4782 ; 1759-4774
    ISSN (online) 1759-4782
    ISSN 1759-4774
    DOI 10.1038/s41571-021-00509-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6029: Show issues Location:
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  9. Article ; Online: Distinguishing AML from MDS: a fixed blast percentage may no longer be optimal.

    Estey, Elihu / Hasserjian, Robert P / Döhner, Hartmut

    Blood

    2021  Volume 139, Issue 3, Page(s) 323–332

    Abstract: Patients with acute myeloid leukemia (AML) have conventionally received more intense therapy than patients with myelodysplastic syndrome (MDS). Although less intense therapies are being used more often in AML, the dichotomy between AML and MDS remains, ... ...

    Abstract Patients with acute myeloid leukemia (AML) have conventionally received more intense therapy than patients with myelodysplastic syndrome (MDS). Although less intense therapies are being used more often in AML, the dichotomy between AML and MDS remains, with the presence of ≥20% myeloblasts in marrow or peripheral blood generally regarded as defining AML. Consequently, patients with 19% blasts are typically ineligible for AML studies, and patients with 21% blasts are ineligible for MDS studies. Here we cite biologic and clinical data to question this practice. Biologically, abnormalities in chromosome 3q26 and mutations in NPM1 and FLT3, regarded as AML associated, also occur in MDS. The genetic signatures of MDS, particularly cases with 10% to 19% blasts (MDS-EB2), resemble those of AML following a preceding MDS (secondary AML). Mutationally, secondary AML appears at least as similar to MDS-EB2 as to de novo AML. Patients presenting with de novo AML but with secondary-type AML mutations seem to have the same poor prognosis associated with clinically defined secondary AML. Seattle data indicate that after accounting for European LeukemiaNet 2017 risk, age, performance status, clinically secondary AML, and treatment including allogeneic transplantation, patients with World Health Organization-defined AML (n = 769) have similar rates of overall survival, event-free survival, and complete remission (CR)/CR with incomplete hematologic recovery as patients with MDS-EB2 (n = 202). We suggest defining patients with 10% to 30% blasts (AML/MDS) as eligible for both AML and MDS studies. This would permit empiric testing of the independent effect of blast percentage on outcome, allow patients access to more therapies, and potentially simplify the regulatory approval process.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Chromosome Aberrations ; Diagnosis, Differential ; Female ; Gene Rearrangement ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Male ; Middle Aged ; Mutation ; Myelodysplastic Syndromes/diagnosis ; Myelodysplastic Syndromes/genetics ; Nucleophosmin/genetics ; Young Adult
    Chemical Substances NPM1 protein, human ; Nucleophosmin (117896-08-9)
    Language English
    Publishing date 2021-06-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021011304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The International Consensus Classification of acute leukemias of ambiguous lineage.

    Weinberg, Olga K / Arber, Daniel A / Döhner, Hartmut / Mullighan, Charles G / Orgel, Etan / Porwit, Anna / Stone, Richard M / Borowitz, Michael J

    Blood

    2023  Volume 141, Issue 18, Page(s) 2275–2277

    MeSH term(s) Humans ; Consensus ; Leukemia ; Acute Disease ; Immunophenotyping
    Language English
    Publishing date 2023-03-06
    Publishing country United States
    Document type Letter
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022019493
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