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  1. Book ; Thesis: Validation eines Proxy-basierten SARC-F-Fragebogens zum gegenwärtigen und retrospektiven Screening von Sarkopenie-assoziierten funktionellen Einschränkungen

    Maurus, Johannes / Müller-Tidow, Carsten

    2023  

    Institution Universität Heidelberg
    Author's details vorgelegt von Johannes Maurus ; Doktorvater: Herr Prof. Dr. med. Carsten Müller-Tidow
    Language German
    Size 89 Blätter, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2023
    HBZ-ID HT030727522
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Thesis: A novel mass spectrometry-based approach reveals constitutive A>>XL receptor turnover by ectodomain shedding as a possible mechanism to prevent cell transformation

    Tix, Tobias / Müller-Tidow, Carsten

    2021  

    Institution Universität Heidelberg
    Author's details vorgelegt von Tobias Tix ; Doktorvater: Herr Prof. Dr. med. Carsten Müller-Tidow
    Language English
    Size 75 Blätter, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2023
    Note Text Englisch, Zusammenfassung in englischer und deutscher Sprache ; Literaturverzeichnis Blatt 57-73
    HBZ-ID HT030722421
    Database Catalogue ZB MED Medicine, Health

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  3. Article: Genome editing in clinical practice: A model study for next-gen hematopoietic cell transplants in hematologic malignancies.

    Derigs, Patrick / Müller-Tidow, Carsten

    Molecular therapy. Methods & clinical development

    2024  Volume 32, Issue 1, Page(s) 101210

    Language English
    Publishing date 2024-02-26
    Publishing country United States
    Document type News
    ZDB-ID 2872938-9
    ISSN 2329-0501 ; 2329-0501
    ISSN (online) 2329-0501
    ISSN 2329-0501
    DOI 10.1016/j.omtm.2024.101210
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: Myeloische Neoplasien

    Hofmann, Wolf-Karsten / Müller-Tidow, Carsten

    2020  

    Keywords myelodysplastisches Syndrom ; myeloische Leukämie ; Neoplasien ; AML ; MDS ; Stammzelltransplantation ; Knochenmarkkrankheit ; Diagnostik ; Therapie
    Subject Medizinische Behandlung ; Behandlung ; Krankenbehandlung ; Knochenmark ; Medizinische Diagnostik ; Medizin ; Klinische Diagnostik ; Diagnostisches Verfahren
    Subject code 610
    Language German
    Size XII, 256 Seiten, Illustrationen, 24 cm x 17 cm
    Publisher de Gruyter
    Publishing place Berlin
    Publishing country Germany
    Document type Book
    HBZ-ID HT020347754
    ISBN 978-3-11-059750-9 ; 3-11-059750-0 ; 9783110599794 ; 9783110598551 ; 3110599791 ; 3110598558
    Database Catalogue ZB MED Medicine, Health

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  5. Article ; Online: AKTing on XPO1 inhibition in AML.

    Göllner, Stefanie / Müller-Tidow, Carsten

    Nature cancer

    2022  Volume 3, Issue 7, Page(s) 787–789

    MeSH term(s) Humans ; Karyopherins ; Leukemia, Myeloid, Acute/drug therapy ; Receptors, Cytoplasmic and Nuclear
    Chemical Substances Karyopherins ; Receptors, Cytoplasmic and Nuclear
    Language English
    Publishing date 2022-07-26
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-022-00395-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The relevance of the hematopoietic niche for therapy resistance in acute myeloid leukemia.

    Allert, Catana / Müller-Tidow, Carsten / Blank, Maximilian Felix

    International journal of cancer

    2023  Volume 154, Issue 2, Page(s) 197–209

    Abstract: The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling ... ...

    Abstract The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling pathways which lead to resistance and impede effective therapy. Therefore, the underlying processes and mechanisms represent attractive therapeutic leverage points for overcoming therapy resistance in AML. Here, we briefly discuss resistance mechanisms based on cell interactions and secreted soluble factors in the hematopoietic niche and provide an overview of niche-related therapeutic targets currently undergoing preclinical and clinical investigation which may help improve the outcome in AML therapy.
    MeSH term(s) Humans ; Hematopoietic Stem Cells/metabolism ; Bone Marrow/metabolism ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/metabolism ; Signal Transduction ; Cell Communication ; Tumor Microenvironment
    Language English
    Publishing date 2023-08-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.34684
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Therapy resistance mechanisms in hematological malignancies.

    Hofmann, Wolf-Karsten / Trumpp, Andreas / Müller-Tidow, Carsten

    International journal of cancer

    2022  Volume 152, Issue 3, Page(s) 340–347

    Abstract: Hematologic malignancies are model diseases for understanding neoplastic transformation and serve as prototypes for developing effective therapies. Indeed, the concept of systemic cancer therapy originated in hematologic malignancies and has guided the ... ...

    Abstract Hematologic malignancies are model diseases for understanding neoplastic transformation and serve as prototypes for developing effective therapies. Indeed, the concept of systemic cancer therapy originated in hematologic malignancies and has guided the development of chemotherapy, cellular therapies, immunotherapy and modern precision oncology. Despite significant advances in the treatment of leukemias, lymphomas and multiple myelomas, treatment resistance associated with molecular and clinical relapse remains very common. Therapy of relapsed and refractory disease remains extremely difficult, and failure of disease control at this stage remains the leading cause of mortality in patients with hematologic malignancies. In recent years, many efforts have been made to identify the genetic and epigenetic mechanisms that drive the development of hematologic malignancies to the stage of full-blown disease requiring clinical intervention. In contrast, the mechanisms responsible for treatment resistance in hematologic malignancies remain poorly understood. For example, the molecular characteristics of therapy-resistant persisting cells in minimal residual disease (MRD) remain rather elusive. In this mini-review we want to discuss that cellular heterogeneity and plasticity, together with adaptive genetic and epigenetic processes, lead to reduced sensitivity to various treatment regimens such as chemotherapy and pathway inhibitors such as tyrosine kinase inhibitors. However, resistance mechanisms may be conserved across biologically distinct cancer entities. Recent technological advances have made it possible to explore the underlying mechanisms of therapy resistance with unprecedented resolution and depth. These include novel multi-omics technologies with single cell resolution combined with advanced biocomputational approaches, along with artificial intelligence (AI) and sophisticated disease models for functional validation.
    MeSH term(s) Humans ; Artificial Intelligence ; Precision Medicine ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/genetics ; Immunotherapy ; Neoplasm, Residual
    Language English
    Publishing date 2022-08-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.34243
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Symptomatic Patients with Hyperleukocytic FLT3-ITD Mutated Acute Myeloid Leukemia Might Benefit from Leukapheresis.

    Farid, Kiavasch Mohammad Nejad / Sauer, Tim / Schmitt, Michael / Müller-Tidow, Carsten / Schmitt, Anita

    Cancers

    2023  Volume 16, Issue 1

    Abstract: Purpose: We aimed to identify subsets of patients who benefit from emergency LA and to establish a therapeutic algorithm for AML patients with hyperleukocytosis.: Methods: In this single-center retrospective cohort study, a total of 20 consecutive ... ...

    Abstract Purpose: We aimed to identify subsets of patients who benefit from emergency LA and to establish a therapeutic algorithm for AML patients with hyperleukocytosis.
    Methods: In this single-center retrospective cohort study, a total of 20 consecutive patients underwent LA because of their clinical symptoms. Overall survival (OS) analysis was conducted using the Kaplan-Meier plot method. Univariate and multivariate analyses (using multiple logistic regression) were performed. At the time of diagnosis, all patients received a standard diagnostic workup for AML including FLT3-ITD mutational analysis.
    Results: FLT3-ITD mut AML patients receiving LA had a median OS of 437 days (range 5-2379 days) with a corresponding 14-day survival of 92.3%, while FLT3 wt AML patients displayed a significantly lower median OS of only 5 days (range 1-203 days) with a corresponding 14-day survival of 14.3% (
    Conclusions: Among patients with clinical symptoms of leukostasis, the subset of FLT3-ITD mut AML patients showed a better outcome with lower early mortality after emergency LA. Based on these observations, we established a therapeutic algorithm for AML patients with hyperleukocytosis.
    Language English
    Publishing date 2023-12-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16010058
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: NPM1 functions in epitranscriptomics.

    Zhou, Fengbiao / Müller-Tidow, Carsten

    Nature genetics

    2019  Volume 51, Issue 10, Page(s) 1436–1437

    MeSH term(s) Dyskeratosis Congenita/genetics ; Dyskeratosis Congenita/pathology ; Epigenomics/methods ; Gene Expression Profiling ; Humans ; Nuclear Proteins/chemistry ; Nuclear Proteins/genetics ; RNA Processing, Post-Transcriptional ; RNA, Messenger/genetics ; RNA, Ribosomal/genetics ; Transcriptome
    Chemical Substances Nuclear Proteins ; RNA, Messenger ; RNA, Ribosomal ; nucleophosmin (117896-08-9)
    Language English
    Publishing date 2019-09-30
    Publishing country United States
    Document type News
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-019-0510-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book ; Online: Decitabin

    Wörmann, Bernhard / Braess, Jan / Lübbert, Michael / Müller-Tidow, Carsten / Platzbecker, Uwe / Strupp, Corinna

    Stellungnahme zur Nutzenbewertung des G-BA von Arzneimitteln für seltene Leiden gemäß § 35a SGB V und der Dossierbewertung im IQWiG Bericht Nr. 150, veröffentlicht am 1. Februar 2013, Vorgangsnummer 2012-11-01-D-042

    2013  

    Institution Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie
    Deutschland / Gemeinsamer Bundesausschuss
    Author's details DGHO - Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie; Gemeinsamer Bundesausschuss ; Die Stellungnahme wurde von Prof. Dr. Bernhard Wörmann in Kooperation mit Prof. Dr. Jan Braess (Krankenhaus der Barmherzigen Brüder, Klinik für Onkologie & Hämatologie, Regensburg), Prof. Dr. Michael Lübbert (Universitätsklinik Freiburg, Abteilung Hämatologie und Onkologie, Freiburg), Prof. Dr. Carsten Müller-Tidow (Universitätsklinikum Münster, Medizinische Klinik und Poliklinik A, Münster), Prof. Dr. Uwe Platzbecker (Universitätsklinikum Carl Gustav Carus an der TU Dresden, Medizinische Klinik und Poliklinik I, Dresden), und Dr. Corinna Strupp (Universitätsklinikum Düsseldorf, Klinik für Hämatologie, Onkologie und klinische Immunologie, Düsseldorf) erarbeitet
    Subject code 610
    Language German
    Size 1 Online-Ressource (7 Seiten)
    Publisher DGHO - Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie
    Publishing place Berlin
    Publishing country Germany
    Document type Book ; Online
    Note Open Access
    HBZ-ID HT020259936
    DOI 10.4126/FRL01-006417373
    Database Repository for Life Sciences

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