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New Biomarkers and Therapeutics in Hematological Neoplasias
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New Biomarkers and Therapeutics in Hematological Neoplasias

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (10 July 2024) | Viewed by 4320

Special Issue Editor

Dr. Ana Cristina Gonçalves

E-Mail Website
Guest Editor
Faculdade de Medicina, Universidade de Coimbra, Coimbra, Portugal
Interests: hematological neoplasias
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hematologic neoplasias are a broad category of cancers of the hematopoietic system, including leukemias, lymphomas, multiple myeloma, myeloproliferative neoplasias, and myelodysplastic syndromes. Among the new cancer cases estimated to be diagnosed in the US in 2021, about 10% are expected to be leukemias, lymphomas, and myelomas, with leukemia in the top 10 of more lethal cancers worldwide.

The advances in molecular oncology provide new knowledge in the mechanisms of carcinogenesis, the genomic and proteomic landscape of cancer, cancer metabolism, immune evasion, drug resistance, and relapse, among others. This information also helps to identify new molecular drug targets and biomarkers for diagnosis, prognosis, patient monitoring, and therapy response, which could be applied in clinical settings. In the last decades, targeted therapies and cancer biomarkers have significantly improved patients' survival and quality of life with hematological and solid neoplasias. Cancer biomarkers comprise several biological molecules such as proteins, nucleic acids, and metabolites and have several biological sources like plasma, circulating tumor cells, extracellular vesicles, tumor-educated platelets, etc.

This Special Issue aims to publish current research related to the discovery of novel biomarkers and molecular drug targets in hematological malignancies. Original research articles and review articles covering these knowledge fields are strongly invited, including: genetic and epigenetic alterations; cellular and molecular mechanisms; genomic, proteomic, and metabolic profiles; biomarkers of diagnosis, prognosis, monitoring, and therapy response; risk factors; and preclinical studies.

Dr. Ana Cristina Gonçalves
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.

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Published Papers (3 papers)

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Editorial

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5 pages, 189 KiB  
Editorial
Advancements in Biomarkers and Molecular Targets in Hematological Neoplasias
by Ana Cristina Gonçalves, Raquel Alves and Ana Bela Sarmento-Ribeiro
Int. J. Mol. Sci. 2024, 25(12), 6570; https://doi.org/10.3390/ijms25126570 - 14 Jun 2024
Viewed by 977
Abstract
Hematological neoplasias are among the most common cancers worldwide, and the number of new cases has been on the rise since 1990, reaching 1 [...] Full article
(This article belongs to the Special Issue New Biomarkers and Therapeutics in Hematological Neoplasias)

Research

Jump to: Editorial

15 pages, 4051 KiB  
Article
NK Cell Degranulation Triggered by Rituximab Identifies Potential Markers of Subpopulations with Enhanced Cytotoxicity toward Malignant B Cells
by Marta Wlodarczyk, Anna Torun, Abdessamad Zerrouqi and Beata Pyrzynska
Int. J. Mol. Sci. 2024, 25(16), 8980; https://doi.org/10.3390/ijms25168980 - 18 Aug 2024
Viewed by 1226
Abstract
A promising strategy in cancer immunotherapy is to restore or enhance the cytotoxicity of NK cells, among others, by activating the mechanism of antibody-dependent cellular cytotoxicity (ADCC). Monoclonal antibodies targeting tumor antigens, such as rituximab (targeting CD20), induce NK cell-mediated ADCC and have [...] Read more.
A promising strategy in cancer immunotherapy is to restore or enhance the cytotoxicity of NK cells, among others, by activating the mechanism of antibody-dependent cellular cytotoxicity (ADCC). Monoclonal antibodies targeting tumor antigens, such as rituximab (targeting CD20), induce NK cell-mediated ADCC and have been used to treat B cell malignancies, such as non-Hodgkin lymphoma, but not always successfully. The aim of this study was to analyze the gene expression profile of the NK cells involved in the cytolytic response stimulated by rituximab. NK cells were co-cultured with rituximab-opsonized Raji cells. Sorting into responder and non-responder groups was based on the presence of CD107a, which is a degranulation marker. RNA-seq results showed that the KIT and TNFSF4 genes were strongly down-regulated in the degranulating population of NK cells (responders); this was further confirmed by qRT-PCR. Both genes encode surface proteins with cellular signaling abilities, namely c-KIT and the OX40 ligand. Consistent with our findings, c-KIT was previously reported to correlate inversely with cytokine production by activated NK cells. The significance of these findings for cancer immunotherapy seems essential, as the pharmacological inhibition of c-KIT and OX40L, or gene ablation, could be further tested for the enhancement of the anti-tumor activity of NK cells in response to rituximab. Full article
(This article belongs to the Special Issue New Biomarkers and Therapeutics in Hematological Neoplasias)
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16 pages, 959 KiB  
Article
Enhanced Expression of Glycolytic Enzymes and Succinate Dehydrogenase Complex Flavoprotein Subunit A by Mesothelin Promotes Glycolysis and Mitochondrial Respiration in Myeloblasts of Acute Myeloid Leukemia
by Yunseon Jang, Jeong Suk Koh, Jung-Hyun Park, Suyoung Choi, Pham Thi Thuy Duong, Bu Yeon Heo, Sang Woo Lee, Jung Yeon Kim, Myung-Won Lee, Seok-Hwan Kim and Ik-Chan Song
Int. J. Mol. Sci. 2024, 25(4), 2140; https://doi.org/10.3390/ijms25042140 - 10 Feb 2024
Viewed by 1626
Abstract
Acute myeloid leukemia (AML) is an aggressive malignancy characterized by rapid growth and uncontrolled proliferation of undifferentiated myeloid cells. Metabolic reprogramming is commonly observed in the bone marrow of AML patients, as leukemia cells require increased ATP supply to support disease progression. In [...] Read more.
Acute myeloid leukemia (AML) is an aggressive malignancy characterized by rapid growth and uncontrolled proliferation of undifferentiated myeloid cells. Metabolic reprogramming is commonly observed in the bone marrow of AML patients, as leukemia cells require increased ATP supply to support disease progression. In this study, we examined the potential role of mesothelin as a metabolic modulator in myeloid cells in AML. Mesothelin is a well-known marker of solid tumors that promotes cancer cell proliferation and survival. We initially analyzed alterations in mesothelin expression in the myeloblast subpopulations, defined as SSC-Alow/CD45dim, obtained from the bone marrow of AML patients using flow cytometry. Our results showed overexpression of mesothelin in 34.8% of AML patients. Subsequently, metabolic changes in leukemia cells were evaluated by comparing the oxygen consumption rates (OCR) of bone marrow samples derived from adult AML patients. Notably, a higher OCR was observed in the mesothelin-positive compared to the mesothelin-low and non-expressing groups. Treatment with recombinant human mesothelin protein enhanced OCR and increased the mRNA expression of glycolytic enzymes and mitochondrial complex II in KG1α AML cells. Notably, siRNA targeting mesothelin in KG1α cells led to the reduction of glycolysis-related gene expression but had no effect on the mitochondrial complex gene. The collective results demonstrate that mesothelin induces metabolic changes in leukemia cells, facilitating the acquisition of a rapid supply of ATP for proliferation in AML. Therefore, the targeting of mesothelin presents a potentially promising approach to mitigating the progression of AML through the inhibition of glycolysis and mitochondrial respiration in myeloid cells. Full article
(This article belongs to the Special Issue New Biomarkers and Therapeutics in Hematological Neoplasias)
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