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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: 30 June 2024 | Viewed by 682

Special Issue Editor

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

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Research

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
Int. J. Mol. Sci. 2024, 25(4), 2140; https://doi.org/10.3390/ijms25042140 - 10 Feb 2024
Viewed by 457
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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