Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Hematological Malignancies: Molecular Mechanisms and Therapy

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

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 (20 August 2024) | Viewed by 9352

Share This Special Issue

Special Issue Editor

Dr. Stella Bouziana

E-Mail Website
Guest Editor

Department of Haematology, King's College Hospital, London WC2R 2LS, UK
Interests: hematological malignancies; cellular therapies; immunotherapies; CAR T-cell therapies; hematopoietic stem cell transplantation; plasma cell dyscrasias; acute leukemias
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

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

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

hematological malignancies
molecular pathways
genetics
immunopathogenesis
biomarkers
novel therapies

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (10 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review, Other

11 pages, 869 KiB

Open AccessArticle

Immune Checkpoint Inhibitor Therapy and Associations with Clonal Hematopoiesis

by Abhay Singh, Nuria Mencia Trinchant, Rahul Mishra, Kirti Arora, Smit Mehta, Teodora Kuzmanovic, Maedeh Zokaei Nikoo, Inderpreet Singh, Amanda C. Przespolewski, Mahesh Swaminathan, Marc S. Ernstoff, Grace K. Dy, Lunbiao Yan, Eti Sinha, Shruti Sharma, Duane C. Hassane, Elizabeth A. Griffiths, Eunice Wang, Monica L. Guzman and Swapna Thota

Int. J. Mol. Sci. 2024, 25(20), 11049; https://doi.org/10.3390/ijms252011049 - 15 Oct 2024

Viewed by 283

Abstract

Cancer cohorts are now known to be associated with increased rates of clonal hematopoiesis (CH). We sort to characterize the hematopoietic compartment of patients with melanoma and non-small cell lung cancer (NSCLC) given our recent population level analysis reporting evolving rates of secondary leukemias. The advent of immune checkpoint blockade (ICB) has dramatically changed our understanding of cancer biology and has altered the standards of care for patients. However, the impact of ICB on hematopoietic myeloid clonal expansion remains to be determined. We studied if exposure to ICB therapy affects hematopoietic clonal architecture and if their evolution contributed to altered hematopoiesis. Blood samples from patients with melanoma and NSCLC (n = 142) demonstrated a high prevalence of CH. Serial samples (or post ICB exposure samples; n = 25) were evaluated in melanoma and NSCLC patients. Error-corrected sequencing of a targeted panel of genes recurrently mutated in CH was performed on peripheral blood genomic DNA. In serial sample analysis, we observed that mutations in DNMT3A and TET2 increased in size with longer ICB exposures in the melanoma cohort. We also noted that patients with larger size DNMT3A mutations with further post ICB clone size expansion had longer durations of ICB exposure. All serial samples in this cohort showed a statistically significant change in VAF from baseline. In the serial sample analysis of NSCLC patients, we observed similar epigenetic expansion, although not statistically significant. Our study generates a hypothesis for two important questions: (a) Can DNMT3A or TET2 CH serve as predictors of a response to ICB therapy and serve as a novel biomarker of response to ICB therapy? (b) As ICB-exposed patients continue to live longer, the myeloid clonal expansion may portend an increased risk for subsequent myeloid malignancy development. Until now, the selective pressure of ICB/T-cell activating therapies on hematopoietic stem cells were less known and we report preliminary evidence of clonal expansion in epigenetic modifier genes (also referred to as inflammatory CH genes). Full article

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

► Show Figures

Figure 1

11 pages, 2273 KiB

Open AccessArticle

Biallelic Loss of 7q34 (TRB) and 9p21.3 (CDKN2A/2B) in Adult Ph-Negative Acute T-Lymphoblastic Leukemia

by Natalya Risinskaya, Abdulpatakh Abdulpatakhov, Yulia Chabaeva, Olga Aleshina, Maria Gladysheva, Elena Nikulina, Ivan Bolshakov, Anna Yushkova, Olga Dubova, Anastasia Vasileva, Tatiana Obukhova, Hunan Julhakyan, Nikolay Kapranov, Irina Galtseva, Sergey Kulikov, Andrey Sudarikov and Elena Parovichnikova

Int. J. Mol. Sci. 2024, 25(19), 10482; https://doi.org/10.3390/ijms251910482 - 29 Sep 2024

Viewed by 500

Abstract

Tumor cells of acute lymphoblastic leukemia (ALL) may have various genetic abnormalities. Some of them lead to a complete loss of certain genes. Our aim was to reveal biallelic deletions of genes in Ph–negative T-ALL. Chromosomal microarray analysis (CMA) was performed for 47 patients with de novo Ph–negative T-ALL, who received treatment according to RALL-2016m clinical protocol at the National Medical Research Center for Hematology (Moscow, Russia) from 2017 to 2023. Out of forty-seven patients, only three had normal molecular karyotype. The other 44 patients had multiple gains, losses, and copy neutral losses of heterozygosity. Biallelic losses were found in 14 patients (30%). In ten patients (21%), a biallelic deletion of 9p21.3 involved a different number of genes, however CDKN2A gene loss was noted in all ten cases. For seven patients (15%), a biallelic deletion of 7q34 was found, including two genes—PRSS1, PRSS2 located within the T-cell receptor beta (TRB) locus. A clonal rearrangement of the TRB gene was revealed in 6 out of 7 cases with 7q34 biallelic loss. Both biallelic deletions can be considered favorable prognostic factors, with an association with 9p21 being statistically significant (p = 0.01) and a trend for 7q34 (p = 0.12) being observed. Full article

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

► Show Figures

Figure 1

17 pages, 4202 KiB

Open AccessArticle

Mycovirus-Containing Aspergillus flavus Alters Transcription Factors in Normal and Acute Lymphoblastic Leukemia Cells

by Cameron K. Tebbi, Jiyu Yan, Eva Sahakian, Melanie Mediavilla-Varela, Javier Pinilla-Ibarz, Saumil Patel, George E. Rottinghaus, Rachel Y. Liu and Clare Dennison

Int. J. Mol. Sci. 2024, 25(19), 10361; https://doi.org/10.3390/ijms251910361 - 26 Sep 2024

Viewed by 419

Abstract

Transcription factors control genes to maintain normal hemopoiesis, and dysregulation of some factors can lead to acute lymphoblastic leukemia (ALL). Mycoviruses are known to alter the genetics of their fungal host. The present study evaluates the effects of the products of a mycovirus-containing Aspergillus flavus (MCAF), isolated from the home of a patient with ALL, on certain transcription factors of normal and ALL cell lines. Our published studies have shown that ALL patients have antibodies to MCAF, and that exposure of the mononuclear leukocytes of patients in complete remission to its products, unlike controls, results in the re-development of genetic and cell surface phenotypes characteristic of ALL. For the present study, normal, pre-B, and B-cell leukemia cell lines were exposed to the culture of MCAF. Pre- and post-exposure levels of PAX5, Ikaros, and NF-κB were assessed. Exposure to MCAF resulted in apoptosis, cell cycle changes, and complete downregulation of all transcription factors in normal cell lines. In acute leukemia cell lines, cellular apoptosis and alterations in the cell cycle were also noted; however, while there was downregulation of all tested transcription factors, residual levels were retained. The noted alterations in the transcription factors caused by MCAF are novel findings. The possible role of MCAF in leukemogenesis needs to be further investigated. Mycovirus-containing Aspergillus flavus was initially isolated from a leukemia patient’s home. Our prior published studies have illuminated intriguing associations of this organism with leukemia. Unlike controls, patients diagnosed with acute lymphoblastic leukemia (ALL) harbor antibodies to this organism. Furthermore, the exposure of mononuclear cells from patients with ALL in complete remission to the products of this organism reproduced genetic and cell phenotypes characteristic of ALL. These findings underscore the potential role of environmental factors in leukemogenesis and hint at novel avenues for therapeutic intervention and preventive strategies. Full article

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

► Show Figures

Figure 1

31 pages, 8294 KiB

Open AccessArticle

The Role of Mutated Calreticulin in the Pathogenesis of BCR-ABL1-Negative Myeloproliferative Neoplasms

by Roberta Vadeikienė, Baltramiejus Jakštys, Danguolė Laukaitienė, Saulius Šatkauskas, Elona Juozaitytė and Rasa Ugenskienė

Int. J. Mol. Sci. 2024, 25(18), 9873; https://doi.org/10.3390/ijms25189873 - 12 Sep 2024

Viewed by 671

Abstract

Myeloproliferative neoplasms (MPNs) are characterized by increased proliferation of myeloid lineages in the bone marrow. Calreticulin (CALR) 52 bp deletion and CALR 5 bp insertion have been identified in essential thrombocythemia (ET) and primary myelofibrosis (PMF). There is not much data on the crosstalk between mutated CALR and MPN-related signaling pathways, such as JAK/STAT, PI3K/Akt/mTOR, and Hedgehog. Calreticulin, a multifunctional protein, takes part in many cellular processes. Nevertheless, there is little data on how mutated CALR affects the oxidative stress response and oxidative stress-induced DNA damage, apoptosis, and cell cycle progression. We aimed to investigate the role of the CALR 52 bp deletion and 5 bp insertion in the pathogenesis of MPN, including signaling pathway activation and functional analysis in CALR-mutated cells. Our data indicate that the JAK/STAT and PI3K/Akt/mTOR pathways are activated in CALR-mutated cells, and this activation does not necessarily depend on the CALR and MPL interaction. Moreover, it was found that CALR mutations impair calreticulin function, leading to reduced responses to oxidative stress and DNA damage. It was revealed that the accumulation of G2/M-CALR-mutated cells indicates that oxidative stress-induced DNA damage is difficult to repair. Taken together, this study contributes to a deeper understanding of the specific molecular mechanisms underlying CALR-mutated MPNs. Full article

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

► Show Figures

Figure 1

15 pages, 2710 KiB

Open AccessArticle

Loss of Heterozygosity and Mutations in the RAS-ERK Pathway Genes in Tumor Cells of Various Loci in Multiple Myeloma

by Maiia Soloveva, Maksim Solovev, Natalya Risinskaya, Elena Nikulina, Igor Yakutik, Bella Biderman, Tatiana Obukhova, Yulia Chabaeva, Sergej Kulikov, Andrey Sudarikov and Larisa Mendeleeva

Int. J. Mol. Sci. 2024, 25(17), 9426; https://doi.org/10.3390/ijms25179426 - 30 Aug 2024

Viewed by 633

Abstract

Multiple myeloma (MM) is a disease characterized by spatiotemporal heterogeneity of tumor clones. Different genetic aberrations can be observed simultaneously in tumor cells from different loci, and as the disease progresses, new subclones may appear. The role of liquid biopsy, which is based on the analysis of tumor DNA circulating in the blood plasma, continues to be explored in MM. Here, we present an analysis of the STR profiles and mutation status of the KRAS, NRAS, and BRAF genes, evaluated in plasma free circulating tumor DNA (ctDNA), CD138+ bone marrow cells, and plasmacytomas. The prospective single-center study included 97 patients, with a median age of 55 years. Of these, 94 had newly diagnosed symptomatic MM, and three had primary plasma cell leukemia. It should be noted that if mutations were detected only in ctDNA, “non-classical” codons were more often affected. A variety of adverse laboratory and clinical factors have been associated with the detection of rare KRAS or NRAS gene mutations in bone marrow or ctDNA, suggesting that these mutations may be factors of an unfavorable prognosis for MM. Liquid biopsy studies provide undeniable fundamental information about tumor heterogeneity and clonal evolution in MM. Moreover, we focus on using liquid biopsy to identify new high-risk factors for MM. Full article

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

► Show Figures

Figure 1

20 pages, 4784 KiB

Open AccessArticle

An Optimized Peptide Antagonist of CXCR4 Limits Survival of BCR–ABL1-Transformed Cells in Philadelphia-Chromosome-Positive B-Cell Acute Lymphoblastic Leukemia

by Johanna Pohl, Angela Litz, Omar El Ayoubi, Armando Rodríguez-Alfonso, Ludger Ständker, Mirja Harms, Jan Münch, Hassan Jumaa and Moumita Datta

Int. J. Mol. Sci. 2024, 25(15), 8306; https://doi.org/10.3390/ijms25158306 - 30 Jul 2024

Viewed by 824

Abstract

Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph⁺ ALL) is characterized by reciprocal chromosomal translocation between chromosome 9 and 22, leading to the expression of constitutively active oncogenic BCR–ABL1 fusion protein. CXC chemokine receptor 4 (CXCR4) is essential for the survival of BCR–ABL1-transformed mouse pre-B cells, as the deletion of CXCR4 induces death in these cells. To investigate whether CXCR4 inhibition also effectively blocks BCR–ABL1-transformed cell growth in vitro, in this study, we explored an array of peptide-based inhibitors of CXCR4. The inhibitors were optimized derivatives of EPI-X4, an endogenous peptide antagonist of CXCR4. We observed that among all the candidates, EPI-X4 JM#170 (referred to as JM#170) effectively induced cell death in BCR–ABL1-transformed mouse B cells but had little effect on untransformed wild-type B cells. Importantly, AMD3100, a small molecule inhibitor of CXCR4, did not show this effect. Treatment with JM#170 induced transient JNK phosphorylation in BCR–ABL1-transformed cells, which in turn activated the intrinsic apoptotic pathway by inducing cJun, Bim, and Bax gene expressions. Combinatorial treatment of JM#170 with ABL1 kinase inhibitor Imatinib exerted a stronger killing effect on BCR–ABL1-transformed cells even at a lower dose of Imatinib. Surprisingly, JM#170 actively killed Sup-B15 cells, a BCR–ABL1⁺ human ALL cell line, but had no effect on the BCR–ABL1⁻ 697 cell line. This suggests that the inhibitory effect of JM#170 is specific for BCR–ABL1⁺ ALL. Taken together, JM#170 emerges as a potent novel drug against Ph⁺ ALL. Full article

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

► Show Figures

Figure 1

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

Cited by 1 | Viewed by 1254

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)

► Show Figures

Figure 1

Review

Jump to: Research, Other

27 pages, 1356 KiB

Open AccessReview

Haploidentical HSCT in the Treatment of Pediatric Hematological Disorders

by Anna Marszołek, Maria Leśniak, Anna Sekunda, Aleksander Siwek, Zuzanna Skiba, Monika Lejman and Joanna Zawitkowska

Int. J. Mol. Sci. 2024, 25(12), 6380; https://doi.org/10.3390/ijms25126380 - 9 Jun 2024

Viewed by 1296

Abstract

Allogeneic hematopoietic stem cell transplantation has become a treatment option for otherwise non-curative conditions, both malignant and benign, affecting children and adults. Nevertheless, the latest research has been focusing extensively on transplantation from related and unrelated haploidentical donors, suitable for patients requiring emergent hematopoietic stem cell transplantation (HSCT) in the absence of an HLA-matched donor. Haploidentical HSCT (haplo-HSCT) can be an effective treatment for non-malignant pediatric disorders, such as primary immunodeficiencies or hemoglobinopathies, by enabling a much quicker selection of the appropriate donor for virtually all patients, low incidence of graft-versus-host disease (GVHD), and transplant-related mortality (TRM). Moreover, the outcomes of haplo-HSCT among children with hematological malignancies have improved radically. The most demanding tasks for clinicians are minimizing T-cell-mediated alloreactivity as well as early GVHD prevention. As a result, several T-cell depletion approaches, such as ex vivo T-cell depletion (TCD), and T-cell replete approaches, such as a combination of anti-thymocyte globulin (ATG), post-transplantation cyclophosphamide (PTCy), cyclosporine/tacrolimus, mycophenolate mofetil, or methotrexate, have been taken up. As more research is needed to establish the most beneficial form of therapy, haplo-HSCT is currently considered an alternative donor strategy for pediatric and adult patients with complications like viral and bacterial infections, invasive fungal disease, and GVHD. Full article

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

► Show Figures

Figure 1

Other

Jump to: Research, Review

14 pages, 1156 KiB

Open AccessOpinion

The Current Landscape of Secondary Malignancies after CAR T-Cell Therapies: How Could Malignancies Be Prevented?

by Stella Bouziana and Dimitrios Bouzianas

Int. J. Mol. Sci. 2024, 25(17), 9518; https://doi.org/10.3390/ijms25179518 - 1 Sep 2024

Cited by 1 | Viewed by 910

Abstract

Chimeric antigen receptor (CAR) T-cell therapies have revolutionised the field of haematological malignancies by achieving impressive remission rates in patients with highly refractory haematological malignancies, improving overall survival. To date, six commercial anti-CD19 and anti-BCMA CAR T-cell products have been approved by the Food and Drug Administration (FDA) for the treatment of relapsed/refractory B-cell haematological malignancies and multiple myeloma. The indications for CAR T-cell therapies are gradually expanding, with these therapies being investigated in a variety of diseases, including non-malignant ones. Despite the great success, there are several challenges surrounding CAR T-cell therapies, such as non-durable responses and high-grade toxicities. In addition, a new safety concern was added by the FDA on 28 November 2023 following reports of T-cell malignancies in patients previously treated with either anti-CD19 or anti-BCMA autologous CAR T-cell therapies both in clinical trials and in the real-world setting. Since then, several reports have been published presenting the incidence and analysing the risks of other secondary malignancies after CAR T-cell therapies. In this opinion article, the current landscape of secondary malignancies after CAR T-cell therapies is presented, along with a proposed strategy for future research aiming at potentially diminishing or abrogating the risk of developing secondary malignancies after CAR T-cell therapies. Full article

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

► Show Figures

Figure 1

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 - 21 Dec 2023

Cited by 1 | Viewed by 1078

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)

► Show Figures

Journal Menu

Journal Browser

Hematological Malignancies: Molecular Mechanisms and Therapy

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (10 papers)

Research

Review

Other

Further Information

Guidelines

MDPI Initiatives

Follow MDPI