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Cancers
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Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia
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Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Informatics and Big Data".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 6092

Special Issue Editor

Dr. María Hernández Valladares

E-Mail Website
Guest Editor
Department of Physical Chemistry, University of Granada, 18071 Granada, Spain
Interests: AML heterogeneity; proteomics; metabolomics; PTMs; cohort medicine; personalized medicine

Special Issue Information

Dear Colleagues,

Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are bone marrow and blood cancers with abnormal populations of lymphocytes and myeloblasts, respectively, although both can induce complications at the central nervous system level. While AML is the most common type of leukemia among adults, ALL is most common among children aged 2–10 years. Along with classical induction and consolidation therapies, new targeted drugs and CAR-T cell strategies are becoming part of new theraupetical approaches in relation to both types of cancers. ALL and AML are heterogenous diseases; genetic and epigenetic alterations in cell progenitors cause a dysregulation of multiple and diverse signal transduction pathways. Therefore, we are pleased to invite researchers to contribute to this Special Issue which intends to address the need to find more new drug-able targets than can reach the heterogeneity of leukemic patients. Manuscripts that accommodate omics technologies and their integration, which explore previously published datasets and/or bioinformatics and artificial intelligence strategies to find out common or alternative drug-able routes, are also of interest in this Issue. Provocative insights from past and current research to consider new drug-able features will be appreciated.

In this Special Issue, original research articles, short communications, opinions, and reviews are welcome.

I look forward to receiving your contributions.

Dr. María Hernández Valladares
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

  • ALL
  • AML
  • drug
  • therapy
  • omics
  • heterogeneity
  • survival
  • bioinformatics
  • artificial intelligence
  • personalized medicine

Published Papers (4 papers)

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Editorial

Jump to: Research, Review

5 pages, 363 KiB  
Editorial
Multi-Omic Approaches to Classify, Predict, and Treat Acute Leukemias
by Maria Hernandez-Valladares
Cancers 2023, 15(4), 1049; https://doi.org/10.3390/cancers15041049 - 7 Feb 2023
Viewed by 1331
Abstract
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, in which nearly 5% of the cases are diagnosed before the first year of age [...] Full article
(This article belongs to the Special Issue Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia)
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Research

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24 pages, 5297 KiB  
Article
High Mitochondrial Protein Expression as a Potential Predictor of Relapse Risk in Acute Myeloid Leukemia Patients with the Monocytic FAB Subtypes M4 and M5
by Frode Selheim, Elise Aasebø, Øystein Bruserud and Maria Hernandez-Valladares
Cancers 2024, 16(1), 8; https://doi.org/10.3390/cancers16010008 - 19 Dec 2023
Viewed by 1245
Abstract
AML is a highly aggressive and heterogeneous form of hematological cancer. Proteomics-based stratification of patients into more refined subgroups may contribute to a more precise characterization of the patient-derived AML cells. Here, we reanalyzed liquid chromatography-tandem mass spectrometry (LC-MS/MS) generated proteomic and phosphoproteomic [...] Read more.
AML is a highly aggressive and heterogeneous form of hematological cancer. Proteomics-based stratification of patients into more refined subgroups may contribute to a more precise characterization of the patient-derived AML cells. Here, we reanalyzed liquid chromatography-tandem mass spectrometry (LC-MS/MS) generated proteomic and phosphoproteomic data from 26 FAB-M4/M5 patients. The patients achieved complete hematological remission after induction therapy. Twelve of them later developed chemoresistant relapse (RELAPSE), and 14 patients were relapse-free (REL_FREE) long-term survivors. We considered not only the RELAPSE and REL_FREE characteristics but also integrated the French-American-British (FAB) classification, along with considering the presence of nucleophosmin 1 (NPM1) mutation and cytogenetically normal AML. We found a significant number of differentially enriched proteins (911) and phosphoproteins (257) between the various FAB subtypes in RELAPSE patients. Patients with the myeloblastic M1/M2 subtype showed higher levels of RNA processing-related routes and lower levels of signaling related to terms like translation and degranulation when compared with the M4/M5 subtype. Moreover, we found that a high abundance of proteins associated with mitochondrial translation and oxidative phosphorylation, particularly observed in the RELAPSE M4/M5 NPM1 mutated subgroup, distinguishes relapsing from non-relapsing AML patient cells with the FAB subtype M4/M5. Thus, the discovery of subtype-specific biomarkers through proteomic profiling may complement the existing classification system for AML and potentially aid in selecting personalized treatment strategies for individual patients. Full article
(This article belongs to the Special Issue Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia)
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24 pages, 2623 KiB  
Article
CD22 Exon 12 Deletion as an Independent Predictor of Poor Treatment Outcomes in B-ALL
by Sanjive Qazi and Fatih M. Uckun
Cancers 2023, 15(5), 1599; https://doi.org/10.3390/cancers15051599 - 4 Mar 2023
Viewed by 1377
Abstract
We previously reported a splicing defect (CD22ΔE12) associated with the deletion of exon 12 of the inhibitory co-receptor CD22 (Siglec-2) in leukemia cells from patients with CD19+ B-precursor acute lymphoblastic leukemia (B-ALL). CD22ΔE12 causes a truncating frameshift mutation and yields a dysfunctional [...] Read more.
We previously reported a splicing defect (CD22ΔE12) associated with the deletion of exon 12 of the inhibitory co-receptor CD22 (Siglec-2) in leukemia cells from patients with CD19+ B-precursor acute lymphoblastic leukemia (B-ALL). CD22ΔE12 causes a truncating frameshift mutation and yields a dysfunctional CD22 protein that lacks most of the cytoplasmic domain required for its inhibitory function, and it is associated with aggressive in vivo growth of human B-ALL cells in mouse xenograft models. Although CD22ΔE12 with selective reduction of CD22 exon 12 (CD22E12) levels was detected in a high percentage of newly diagnosed as well as relapsed B-ALL patients, its clinical significance remains unknown. We hypothesized that B-ALL patients with very low levels of wildtype CD22 would exhibit a more aggressive disease with a worse prognosis because the missing inhibitory function of the truncated CD22 molecules could not be adequately compensated by competing wildtype CD22. Here, we demonstrate that newly diagnosed B-ALL patients with very low levels of residual wildtype CD22 (“CD22E12low”), as measured by RNAseq-based CD22E12 mRNA levels, have significantly worse leukemia-free survival (LFS) as well as overall survival (OS) than other B-ALL patients. CD22E12low status was identified as a poor prognostic indicator in both univariate and multivariate Cox proportional hazards models. CD22E12low status at presentation shows clinical potential as a poor prognostic biomarker that may guide the early allocation of risk-adjusted, patient-tailored treatment regimens and refine risk classification in high-risk B-ALL. Full article
(This article belongs to the Special Issue Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia)
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Review

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21 pages, 1889 KiB  
Review
Casein Kinase 2 (CK2): A Possible Therapeutic Target in Acute Myeloid Leukemia
by Øystein Bruserud and Håkon Reikvam
Cancers 2023, 15(14), 3711; https://doi.org/10.3390/cancers15143711 - 21 Jul 2023
Cited by 3 | Viewed by 1521
Abstract
The protein kinase CK2 (also known as casein kinase 2) is one of the main contributors to the human phosphoproteome. It is regarded as a possible therapeutic strategy in several malignant diseases, including acute myeloid leukemia (AML), which is an aggressive bone marrow [...] Read more.
The protein kinase CK2 (also known as casein kinase 2) is one of the main contributors to the human phosphoproteome. It is regarded as a possible therapeutic strategy in several malignant diseases, including acute myeloid leukemia (AML), which is an aggressive bone marrow malignancy. CK2 is an important regulator of intracellular signaling in AML cells, especially PI3K–Akt, Jak–Stat, NFκB, Wnt, and DNA repair signaling. High CK2 levels in AML cells at the first time of diagnosis are associated with decreased survival (i.e., increased risk of chemoresistant leukemia relapse) for patients receiving intensive and potentially curative antileukemic therapy. However, it is not known whether these high CK2 levels can be used as an independent prognostic biomarker because this has not been investigated in multivariate analyses. Several CK2 inhibitors have been developed, but CX-4945/silmitasertib is best characterized. This drug has antiproliferative and proapoptotic effects in primary human AML cells. The preliminary results from studies of silmitasertib in the treatment of other malignancies suggest that gastrointestinal and bone marrow toxicities are relatively common. However, clinical AML studies are not available. Taken together, the available experimental and clinical evidence suggests that the possible use of CK2 inhibition in the treatment of AML should be further investigated. Full article
(This article belongs to the Special Issue Novel Insights in Acute Lymphoblastic and Myeloblastic Leukemia)
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