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@ARTICLE{Hofmann:181143,
      author       = {W.-K. Hofmann and A. Trumpp$^*$ and C. Müller-Tidow},
      title        = {{T}herapy {R}esistance {M}echanisms in {H}ematological
                      {M}alignancies.},
      journal      = {International journal of cancer},
      volume       = {152},
      number       = {3},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2022-01796},
      pages        = {340-347},
      year         = {2023},
      note         = {2023 Feb 1;152(3):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 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. This article is protected
                      by copyright. All rights reserved.},
      subtyp        = {Review Article},
      keywords     = {Hematological malignancies (Other) / Mechanisms (Other) /
                      Resistance (Other) / Therapy (Other)},
      cin          = {A010 / V960},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / I:(DE-He78)V960-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35962946},
      doi          = {10.1002/ijc.34243},
      url          = {https://inrepo02.dkfz.de/record/181143},
}