Special Issue "Genetics, Biology, and Treatment of Acute Myeloid Leukemia 2.0"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (31 May 2020).
Interests: acute myeloid leukemia; therapy resistance; relapse; retinoic acid; MECOM; non-coding RNAs
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Acute myeloid leukemia (AML) is a highly heterogeneous disease both in terms of its genetic etiology and outcome. In the 1960s, cytogenetic analyses yielded the first insights into the genetic alterations driving its emergence and evolution, and a panel of recurrent chromosome aberrations discovered decades ago still represents one of the main pillars of prognostication. The advent of molecular biology facilitated the discovery and characterization of the fusion genes formed as a consequence of these chromosome rearrangements. In recent years, next-generation sequencing has allowed the establishment of the full inventory of somatically acquired mutations in individuals with AML, as well as the investigation of the evolution of mutational patterns during the course of disease, including treatment, remission, and relapse. In addition to genetic alterations, epigenetic changes and changes in gene expression are of pivotal importance to AML pathogenesis. Together, these studies have identified molecular and genetic alterations that support the diagnosis of AML and facilitate prognostication and disease monitoring. In select cases, they also form the basis for targeted therapies. Indeed, the AML subtype acute promyelocytic leukemia was one of the earliest examples of targeted cancer therapy; all-trans retinoic acid, introduced into the treatment regimen over three decades ago, has impressively improved patient outcome. In the past two years, inhibitors of mutated IDH and FLT3 were approved for use in AML treatment, and several other targeted therapies are under development and hoped to ameliorate the outcome of this aggressive disease in the future.
Another important line of research concerns the role of stem cells in AML. Understanding their roles in disease formation, therapy resistance, and relapse and their interactions with the specific microenvironment of their niche in bone marrow is expected to lead to discoveries that can be exploited therapeutically.
In a recent IJMS Special Issue dedicated to the genetics, biology, and treatment of AML, colleagues contributed valuable articles discussing the genetic hierarchy of AML, the role of measurable residual disease monitoring, relapse of AML after stem cell transplantation, clonal evolution in myelodysplastic syndromes, mouse models of AML, the role of the epigenome in AML with RUNX1-ETO fusions, and therapeutic vulnerabilities in FLT3-mutant AML.
We now welcome additional articles concerning the topics outlined above and/or related to the key words listed below.
Prof. Rotraud Wieser
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Treatment of AML: chemotherapy, stem cell transplantation, novel therapeutics (approved and under development), immunotherapy
- Prognostic significance of genetic and gene expression alterations present at diagnosis of AML
- Kinetics of the molecular response to therapy and its prognostic relevance
- Minimal residual disease
- Molecular and genetic evolution of AML from diagnosis to relapse
- Mechanisms of therapy resistance and ways to overcome them
- AML stem cells and the bone marrow niche
- DNA damage and repair in AML
- Aberrant transcriptional regulation in AML
- mutated/deregulated transcription factors and epigenetic regulators
- Aberrant signaling in AML (PI3K, FLT3, WNT, NOTCH, JAK/STAT, etc.)
- AML-related fusion genes
- microRNAs and other noncoding RNAs in AML
- Therapy-related AML: etiology, molecular, and genetic alterations, treatment
- APL: molecular biology and treatment
- Acquired preleukemic syndromes
- Hereditary syndromes associated with increased risk of AML