Molecular Mechanisms of Leukemias

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 20 February 2026 | Viewed by 771

Special Issue Editors


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Guest Editor
Department of Physical Chemistry, University of Granada, Granada, Spain
Interests: mass spectrometry; proteomics; PTMs; metabolomics; leukemia; rare diseases; precision medicine; personalized medicine
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Proteomics Unit of University of Bergen (PROBE), University of Bergen, Bergen, Norway
Interests: pathology of acute myeloid leukemia

Special Issue Information

Dear Colleagues,

Leukemia, a malignancy impacting the blood and hematopoietic organs—including the bone marrow, lymph nodes, and spleen—is characterized by an aberrant proliferation of immature or partially mature white blood cells within the bone marrow. This condition is broadly categorized into four principal types: acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML).

In recent years, rapid progress has been made in researching the biological mechanisms behind leukemia and its treatment strategies. Not only has the development of new treatment methods significantly improved survival rates for patients, it has also greatly improved their quality of life. Therefore, this Special Issue will bring together the latest research results and important discoveries from scholars in the field of leukemia and provide valuable guidance for the diagnosis, treatment, and prognosis of leukemia.

Dr. María Hernández Valladares
Prof. Dr. Frode Selheim
Guest Editors

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Keywords

  • acute lymphoblastic leukemia (ALL)
  • chronic lymphocytic leukemia (CLL)
  • acute myelogenous leukemia (AML)
  • chronic myelogenous leukemia (CML)

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Published Papers (1 paper)

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Review

38 pages, 1281 KB  
Review
NUP214 in Acute Myeloid Leukemia
by Øystein Bruserud and Håkon Reikvam
Cells 2025, 14(18), 1461; https://doi.org/10.3390/cells14181461 - 18 Sep 2025
Viewed by 570
Abstract
Nucleoporin 214 (NUP214) is a component of the nucleopore molecular complex, but in addition to this role in nucleocytoplasmic transport it is also involved in the regulation of gene transcription/translation, intracellular signaling, cell cycle progression and programmed cell death. Several uncommon translocations associated [...] Read more.
Nucleoporin 214 (NUP214) is a component of the nucleopore molecular complex, but in addition to this role in nucleocytoplasmic transport it is also involved in the regulation of gene transcription/translation, intracellular signaling, cell cycle progression and programmed cell death. Several uncommon translocations associated with acute myeloid leukemia (AML) involve the NUP214 gene, and the corresponding fusion proteins are involved in leukemic transformation. First, the t(6;9) translocation encodes the DEK-NUP214 fusion protein; this translocation is seen in 1–2% of AML patients and is associated with an adverse prognosis that is improved by allogeneic stem cell transplantation. Second, the SET-NUP214 fusion gene is less common in AML and is formed either by del(9)(q34.11q34.13) or a balanced t(9;9)(q34;q34). This AML variant shows several biological similarities with the DEK-NUP214 variant, but the possible prognostic impact of this fusion protein is not known. Finally, the NUP214-ABL1 and especially the NUP214-SQSTM1 fusions are very uncommon, and only a few case reports have been published. In this article, we review the functions of the genes/proteins formed by these fusion genes, the available studies of molecular mechanisms and biological functions for each fusion protein, the characteristics of the corresponding AML cells, the clinical characteristics of these patients and the possible prognostic impact of the fusion genes/proteins. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Leukemias)
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