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Cancers
Special Issues
Blood Stem Cells in Pre-leukaemia
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Blood Stem Cells in Pre-leukaemia

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (1 June 2021) | Viewed by 8484

Special Issue Editor

Dr. Christopher I. Slape

E-Mail Website
Guest Editor
The University of Queensland Diamantina Institute
Interests: myelodysplasia; acute myeloid leukaemia; acute T cell leukaemia; tumour suppression; cell–cell communication

Special Issue Information

While all cancers pass through an intermediate pre-malignancy phase before reaching the threshold of malignancy, we have more knowledge of this phase in the haematopoietic system than in most other tissues. Pre-malignant conditions in the haematopoietic system include the clinically presenting myelodysplastic syndrome and myeloproliferative neoplasms, the recently identified clonal haematopoiesis of indeterminate potential, the modelled pre-leukemic thymocytes that precede T-cell acute lymphoblastic leukaemia (T-ALL), aplastic anaemia, bone marrow failure conditions and others. These diverse conditions all derive from deficiencies and abnormalities in the haematopoietic stem and progenitor cells, and all carry an increased risk of the development of leukaemia. The ability to identify at-risk populations for leukemic development would appear to be an opportunity to prevent malignant transformation, but, unfortunately, few effective therapies are available for pre-leukaemic states.

This Special Issue of Cancers will include reviews and primary research articles on the abnormal properties of stem and progenitor cells in these different diseases, the mechanisms that can drive the transformation to overt leukaemia, and how these may be targeted or adapted therapeutically.

Dr. Christopher I. Slape
Guest Editor

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 submissions that pass pre-check are 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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.

Keywords

  • pre-leukaemia
  • haematopoietic stem cells
  • haematopoietic progenitor cells
  • myelodysplastic syndrome
  • myeloproliferative neoplasm
  • aplastic anemia
  • clonal haematopoiesis
  • bone marrow failure

Published Papers (3 papers)

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Editorial

Jump to: Research, Review

2 pages, 167 KiB  
Editorial
Pre-Leukemic States: United by Difference
by Christopher I. Slape
Cancers 2021, 13(6), 1382; https://doi.org/10.3390/cancers13061382 - 18 Mar 2021
Viewed by 1058
Abstract
Pre-leukemia is a catch-all term for any haematological condition which predisposes the individual towards developing leukemia [...] Full article
(This article belongs to the Special Issue Blood Stem Cells in Pre-leukaemia)

Research

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15 pages, 3362 KiB  
Article
Cell-Extrinsic Differentiation Block Mediated by EphA3 in Pre-Leukaemic Thymus Contributes to Disease Progression
by Adriana C. Pliego Zamora, Hansini Ranasinghe, Jessica E. Lisle, Chun Ki Ng, Stephen Huang, Racheal Wadlow, Andrew M. Scott, Andrew W. Boyd and Christopher I. Slape
Cancers 2021, 13(15), 3858; https://doi.org/10.3390/cancers13153858 - 31 Jul 2021
Cited by 1 | Viewed by 2069
Abstract
We recently characterised the NUP98-HOXD13 (NHD13) mouse as a model of T-cell pre-leukaemia, featuring thymocytes that can engraft in recipient animals and progress to T-cell acute lymphoblastic leukaemia (T-ALL). However, loss of this engraftment ability by deletion of Lyl1 did not [...] Read more.
We recently characterised the NUP98-HOXD13 (NHD13) mouse as a model of T-cell pre-leukaemia, featuring thymocytes that can engraft in recipient animals and progress to T-cell acute lymphoblastic leukaemia (T-ALL). However, loss of this engraftment ability by deletion of Lyl1 did not result in any loss of leukemogenesis activity. In the present study, we observe that NHD13 thymocytes overexpress EPHA3, and we characterise thymocyte behaviour in NHD13 mice with deletion of EphA3, which show a markedly reduced incidence of T-ALL. Deletion of EphA3 from the NHD13 mice does not prevent the abnormal accumulation or transplantation ability of these thymocytes. However, upon transplantation, these cells are unable to block the normal progression of recipient wild type (WT) progenitor cells through the normal developmental pathway. This is in contrast to the EphA3+/+ NHD13 thymocytes, which block the progression of incoming WT progenitors past the DN1 stage. Therefore, EphA3 is not critical for classical self-renewal, but is essential for mediating an interaction between the abnormally self-renewing cells and healthy progenitors—an interaction that results in a failure of the healthy cells to differentiate normally. We speculate that this may orchestrate a loss of healthy cell competition, which in itself has been demonstrated to be oncogenic, and that this may explain the decrease in T-ALL incidence in the absence of EphA3. We suggest that pre-leukaemic self-renewal in this model is a complex interplay of cell-intrinsic and -extrinsic factors, and that multiple redundant pathways to leukaemogenesis are active. Full article
(This article belongs to the Special Issue Blood Stem Cells in Pre-leukaemia)
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Review

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41 pages, 3681 KiB  
Review
Transcription Factors, R-Loops and Deubiquitinating Enzymes: Emerging Targets in Myelodysplastic Syndromes and Acute Myeloid Leukemia
by Silvia M. L. Barabino, Elisabetta Citterio and Antonella Ellena Ronchi
Cancers 2021, 13(15), 3753; https://doi.org/10.3390/cancers13153753 - 26 Jul 2021
Cited by 2 | Viewed by 4935
Abstract
Myeloid neoplasms encompass a very heterogeneous family of diseases characterized by the failure of the molecular mechanisms that ensure a balanced equilibrium between hematopoietic stem cells (HSCs) self-renewal and the proper production of differentiated cells. The origin of the driver mutations leading to [...] Read more.
Myeloid neoplasms encompass a very heterogeneous family of diseases characterized by the failure of the molecular mechanisms that ensure a balanced equilibrium between hematopoietic stem cells (HSCs) self-renewal and the proper production of differentiated cells. The origin of the driver mutations leading to preleukemia can be traced back to HSC/progenitor cells. Many properties typical to normal HSCs are exploited by leukemic stem cells (LSCs) to their advantage, leading to the emergence of a clonal population that can eventually progress to leukemia with variable latency and evolution. In fact, different subclones might in turn develop from the original malignant clone through accumulation of additional mutations, increasing their competitive fitness. This process ultimately leads to a complex cancer architecture where a mosaic of cellular clones—each carrying a unique set of mutations—coexists. The repertoire of genes whose mutations contribute to the progression toward leukemogenesis is broad. It encompasses genes involved in different cellular processes, including transcriptional regulation, epigenetics (DNA and histones modifications), DNA damage signaling and repair, chromosome segregation and replication (cohesin complex), RNA splicing, and signal transduction. Among these many players, transcription factors, RNA splicing proteins, and deubiquitinating enzymes are emerging as potential targets for therapeutic intervention. Full article
(This article belongs to the Special Issue Blood Stem Cells in Pre-leukaemia)
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