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Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes
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Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes

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 March 2021) | Viewed by 17102

Special Issue Editor

Dr. Thomas Cluzeau

E-Mail Website
Guest Editor
Université Cote d'Azur, Centre Hospitalier Universitaire de Nice, Service d'hématologie clinique, Nice, France
Interests: acute lymphoid leukemia; acute myeloid leukemia; myelodysplastic syndromes

Special Issue Information

Dear Colleagues,

Therapeutic strategies of acute myeloid leukemia and myelodysplastic syndromes improved the five past years. The last past years, treatment were based on anthracycline plus aracytin combinations in fit patients and hypomethylating agents in unfit patients. We observed a wonderful transfer from the bench to the patients. The scope of the special issue is to describe biological studies identifying all the targets and results of clinical trials validating the interest to inhibit these targets. This special issue will focus on bcl-2 inhibitors, TP53 targeting, IDH1 inhibition, IDH2 inhibition, FLT3 inhibitors, CD33 targeting, CD123 targeting and hedgehog pathway inhibition. Several collaborations between scientists, chemists and physicians changed and continue to modify therapeutic strategies of these two hemopathies. Democratization of genomic tools allows to identify new targets and accelerate the transfer to the patients. Personalized treatment become real and conduce an improvement of patient’s outcome and quality of life.

Dr. Cluzeau Thomas
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. 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.

Keywords

  • acute myeloid leukemia
  • myelodysplastic syndromes
  • Bcl-2
  • TP53
  • IDH1
  • IDH2
  • FLT3
  • CD33
  • CD123
  • hedgehog

Published Papers (4 papers)

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Review

9 pages, 243 KiB  
Review
Personalized Medicine for TP53 Mutated Myelodysplastic Syndromes and Acute Myeloid Leukemia
by Thomas Cluzeau, Michael Loschi, Pierre Fenaux, Rami Komrokji and David A. Sallman
Int. J. Mol. Sci. 2021, 22(18), 10105; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810105 - 18 Sep 2021
Cited by 14 | Viewed by 4037
Abstract
Targeting TP53 mutated myelodysplastic syndromes and acute myeloid leukemia remains a significant unmet need. Recently, new drugs have attempted to improve the outcomes of this poor molecular subgroup. The aim of this article is to review all the current knowledge using active agents [...] Read more.
Targeting TP53 mutated myelodysplastic syndromes and acute myeloid leukemia remains a significant unmet need. Recently, new drugs have attempted to improve the outcomes of this poor molecular subgroup. The aim of this article is to review all the current knowledge using active agents including hypomethylating agents with venetoclax, eprenetapopt or magrolimab. We include comprehensive analysis of clinical trials to date evaluating these drugs in TP53 myeloid neoplasms as well as discuss future novel combinations for consideration. Additionally, further understanding of the unique clinicopathologic components of TP53 mutant myeloid neoplasms versus wild-type is critical to guide future study. Importantly, the clinical trajectory of patients is uniquely tied with the clonal burden of TP53, which enables serial TP53 variant allele frequency analysis to be a critical early biomarker in investigational studies. Together, significant optimism is now possible for improving outcomes in this patient population. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes)
16 pages, 413 KiB  
Review
FLT3 Tyrosine Kinase Inhibitors for the Treatment of Fit and Unfit Patients with FLT3-Mutated AML: A Systematic Review
by Michael Loschi, Rinzine Sammut, Edmond Chiche and Thomas Cluzeau
Int. J. Mol. Sci. 2021, 22(11), 5873; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115873 - 30 May 2021
Cited by 9 | Viewed by 4033
Abstract
FLT3-mutated acute myeloid leukemia accounts for around 30% of acute myeloid leukemia (AML). The mutation carried a poor prognosis until the rise of tyrosine kinase inhibitors (TKIs). New potent and specific inhibitors have successfully altered the course of the disease, increasing the complete [...] Read more.
FLT3-mutated acute myeloid leukemia accounts for around 30% of acute myeloid leukemia (AML). The mutation carried a poor prognosis until the rise of tyrosine kinase inhibitors (TKIs). New potent and specific inhibitors have successfully altered the course of the disease, increasing the complete response rate and the survival of patients with FLT3-mutated AML. The aim of this article is to review all the current knowledge on these game-changing drugs as well as the unsolved issues raised by their use for fit and unfit FLT3-mutated AML patients. To this end, we analyzed the results of phase I, II, III clinical trials evaluating FLT3-TKI both in the first-line, relapse monotherapy or in combination referenced in the PubMed, the American Society of Hematology, the European Hematology Association, and the Clinicaltrials.gov databases, as well as basic science reports on TKI resistance from the same databases. The review follows a chronological presentation of the different trials that allowed the development of first- and second-generation TKI and ends with a review of the current lines of evidence on leukemic blasts resistance mechanisms that allow them to escape TKI. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes)
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30 pages, 1179 KiB  
Review
State-of-Art of Cellular Therapy for Acute Leukemia
by Jong-Bok Lee, Daniel Vasic, Hyeonjeong Kang, Karen Kai-Lin Fang and Li Zhang
Int. J. Mol. Sci. 2021, 22(9), 4590; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094590 - 27 Apr 2021
Cited by 13 | Viewed by 3637
Abstract
With recent clinical breakthroughs, immunotherapy has become the fourth pillar of cancer treatment. Particularly, immune cell-based therapies have been envisioned as a promising treatment option with curative potential for leukemia patients. Hence, an increasing number of preclinical and clinical studies focus on various [...] Read more.
With recent clinical breakthroughs, immunotherapy has become the fourth pillar of cancer treatment. Particularly, immune cell-based therapies have been envisioned as a promising treatment option with curative potential for leukemia patients. Hence, an increasing number of preclinical and clinical studies focus on various approaches of immune cell-based therapy for treatment of acute leukemia (AL). However, the use of different immune cell lineages and subsets against different types of leukemia and patient disease statuses challenge the interpretation of the clinical applicability and outcome of immune cell-based therapies. This review aims to provide an overview on recent approaches using various immune cell-based therapies against acute B-, T-, and myeloid leukemias. Further, the apparent limitations observed and potential approaches to overcome these limitations are discussed. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes)
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21 pages, 668 KiB  
Review
Biomarkers of Gemtuzumab Ozogamicin Response for Acute Myeloid Leukemia Treatment
by Laurène Fenwarth, Elise Fournier, Meyling Cheok, Thomas Boyer, Fanny Gonzales, Sylvie Castaigne, Nicolas Boissel, Juliette Lambert, Hervé Dombret, Claude Preudhomme and Nicolas Duployez
Int. J. Mol. Sci. 2020, 21(16), 5626; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21165626 - 06 Aug 2020
Cited by 18 | Viewed by 4346
Abstract
Gemtuzumab ozogamicin (GO, Mylotarg®) consists of a humanized CD33-targeted antibody-drug conjugated to a calicheamicin derivative. Growing evidence of GO efficacy in acute myeloid leukemia (AML), demonstrated by improved outcomes in CD33-positive AML patients across phase I to III clinical trials, led [...] Read more.
Gemtuzumab ozogamicin (GO, Mylotarg®) consists of a humanized CD33-targeted antibody-drug conjugated to a calicheamicin derivative. Growing evidence of GO efficacy in acute myeloid leukemia (AML), demonstrated by improved outcomes in CD33-positive AML patients across phase I to III clinical trials, led to the Food and Drug Administration (FDA) approval on 1 September 2017 in CD33-positive AML patients aged 2 years and older. Discrepancies in GO recipients outcome have raised significant efforts to characterize biomarkers predictive of GO response and have refined the subset of patients that may strongly benefit from GO. Among them, CD33 expression levels, favorable cytogenetics (t(8;21), inv(16)/t(16;16), t(15;17)) and molecular alterations, such as NPM1, FLT3-internal tandem duplications and other signaling mutations, represent well-known candidates. Additionally, in depth analyses including minimal residual disease monitoring, stemness expression (LSC17 score), mutations or single nucleotide polymorphisms in GO pathway genes (CD33, ABCB1) and molecular-derived scores, such as the recently set up CD33_PGx6_Score, represent promising markers to enhance GO response prediction and improve patient management. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Leukemia and Myelodysplastic Syndromes)
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