International Journal of Molecular Sciences

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Dear Colleagues,

Hematological malignancies comprise a wide range of relatively rare cancers. Aggressive types of hematological malignancies entail devastating outcomes, and their treatment includes many challenges. In recent decades, the molecular and genetic investigation of the pathogenesis of hematological malignancies has resulted in unprecedented advances in the landscape of the therapeutics of hematological cancers. The advent of novel types of therapies, such as targeted therapies, immunotherapies and cellular therapies, has revolutionized the field of hemato-oncology, offering long-term remission or even curing patients with highly aggressive and refractory malignancies. However, despite this massive progress, there are still hematological malignancies that remain uncured, and significant research should be undertaken to unravel the key pathways towards treatment.

This Special Issue aims to collect the latest original and review articles on investigating the molecular, genetic and immunological pathways that contribute to the pathogenesis of hematological malignancies or can serve as predictive, preventive and prognostic disease markers. In addition, this Special Issue welcomes research and review articles covering cutting-edge knowledge on novel therapeutics of hematological malignancies.

Dr. Stella Bouziana
Guest Editor

Manuscript Submission Information

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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.

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Keywords

hematological malignancies
molecular pathways
genetics
immunopathogenesis
biomarkers
novel therapies

Published Papers (2 papers)

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Research

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18 pages, 3185 KiB

Open AccessArticle

Metabolic Profiling as an Approach to Differentiate T-Cell Acute Lymphoblastic Leukemia Cell Lines Belonging to the Same Genetic Subgroup

by Husam B. R. Alabed, Roberto Maria Pellegrino, Sandra Buratta, Anair Graciela Lema Fernandez, Roberta La Starza, Lorena Urbanelli, Cristina Mecucci, Carla Emiliani and Paolo Gorello

Int. J. Mol. Sci. 2024, 25(7), 3921; https://doi.org/10.3390/ijms25073921 - 31 Mar 2024

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Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive tumor mainly affecting children and adolescents. It is driven by multiple genetic mutations that together define the leukemic phenotype. Interestingly, based on genetic alterations and/or deregulated expression, at least six genetic subgroups have been recognized. The TAL/LMO subgroup is one of the most represented genetic subgroups, characterizing 30–45% of pediatric T-ALL cases. The study of lipid and metabolic profiles is increasingly recognized as a valuable tool for comprehending the development and progression of tumors. In this study, metabolic and lipidomic analysis via LC/MS have been carried out on four T-ALL cell lines belonging to the TAL/LMO subgroup (Jurkat, Molt-4, Molt-16, and CCRF-CEM) to identify new potential metabolic biomarkers and to provide a subclassification of T-ALL cell lines belonging to the same subgroup. A total of 343 metabolites were annotated, including 126 polar metabolites and 217 lipid molecules. The statistical analysis, for both metabolic and lipid profiles, shows significant differences and similarities among the four cell lines. The Molt-4 cell line is the most distant cell line and CCRF-CEM shows a high activity in specific pathways when compared to the other cell lines, while Molt-16 and Jurkat show a similar metabolic profile. Additionally, this study highlighted the pathways that differ in each cell line and the possible enzymes involved using bioinformatic tools, capable of predicting the pathways involved by studying the differences in the metabolic profiles. This experiment offers an approach to differentiate T-ALL cell lines and could open the way to verify and confirm the obtained results directly in patients. Full article

(This article belongs to the Special Issue Hematological Malignancies: Molecular Mechanisms and Therapy)

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9 pages, 4225 KiB

Open AccessCase Report

ETV6::ABL1-Positive Myeloid Neoplasm: A Case of a Durable Response to Imatinib Mesylate without Additional or Previous Treatment

by Maria Teresa Bochicchio, Giovanni Marconi, Carmen Baldazzi, Lorenza Bandini, Francesca Ruggieri, Alessandro Lucchesi, Claudio Agostinelli, Elena Sabattini, Agnese Orsatti, Anna Ferrari, Giorgia Capirossi, Chiara Servili, Andrea Ghelli Luserna di Rorà, Giovanni Martinelli, Giorgia Simonetti and Gianantonio Rosti

Int. J. Mol. Sci. 2024, 25(1), 118; https://doi.org/10.3390/ijms25010118 (registering DOI) - 21 Dec 2023

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Abstract

ETV6::ABL1 rearranged neoplasms are rare hematological diseases. To date, about 80 cases have been reported, including myeloid and lymphoid leukemias. The ETV6 gene codes for an ETS family transcription factor and several fusion partners have been described. When translocated, ETV6 causes the constitutive activation of the partner genes. Here, we report the case of a 54-year-old woman with a cryptic insertion of the 3′ region of ABL1 in the ETV6 gene. The patient was first diagnosed with idiopathic hypereosinophilic syndrome, according to the clinical history, conventional cytogenetics, standard molecular analyses and pathologist description. Next generation sequencing of diagnosis samples unexpectedly detected both ETV6::ABL1 type A and B fusion transcripts, which were then confirmed by FISH. The diagnosis was Myeloid/Lymphoid neoplasm with ETV6::ABL1 fusion, and the patient received imatinib mesylate treatment. In a follow-up after more than one year, the patient still maintained the molecular and complete hematological responses. This case highlights the importance of timely and proper diagnostics and prompt tyrosine kinase inhibitor treatment. Full article

(This article belongs to the Special Issue Hematological Malignancies: Molecular Mechanisms and Therapy)

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