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Cells
Special Issues
Molecular and Cellular Mechanisms of Lymphomas
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Molecular and Cellular Mechanisms of Lymphomas

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1404

Special Issue Editor

Dr. Pier Paolo Piccaluga

E-Mail Website1 Website2
Guest Editor
Department of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum Università di Bologna, 40126 Bologna, Italy
Interests: leukemia; lymphoma; targeted therapy; molecular diagnostics; high throughput genomics; transcriptomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent improvements in our knowledge of the molecular pathogenesis of malignant lymphoma offer new rational basis for innovative targeted therapies. However, there is still a consistent gap between the identification of pathways as potential targets and the development of effective therapeutic strategies in this field.

This Special Issue aims to provide new concepts concerning the molecular pathogenesis, genetics, molecular diagnosis and cell metabolism of human lymphomas. New experimental findings (molecular diagnosis, molecular and cellular mechanisms ) in addition to review articles will be considered.

The objective is to eventually favor the translation of genomic and cellular findings into concrete benefits for lymphoma patients.

Dr. Pier Paolo Piccaluga
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • lymphoma
  • pathogenes and lymphomas
  • molecular pathogenesis
  • molecular diagnosis
  • cellular or gene-targeted therapy
  • cell metabolism

Published Papers (1 paper)

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Research

21 pages, 7244 KiB  
Article
In Doxorubicin-Adapted Hodgkin Lymphoma Cells, Acquiring Multidrug Resistance and Improved Immunosuppressive Abilities, Doxorubicin Activity Was Enhanced by Chloroquine and GW4869
by Naike Casagrande, Cinzia Borghese, Michele Avanzo and Donatella Aldinucci
Cells 2023, 12(23), 2732; https://doi.org/10.3390/cells12232732 - 29 Nov 2023
Viewed by 1153
Abstract
Classical Hodgkin lymphoma (cHL) is a highly curable disease (70–80%), even though long-term toxicities, drug resistance, and predicting clinical responses to therapy are major challenges in cHL treatment. To solve these problems, we characterized two cHL cell lines with acquired resistance to doxorubicin, [...] Read more.
Classical Hodgkin lymphoma (cHL) is a highly curable disease (70–80%), even though long-term toxicities, drug resistance, and predicting clinical responses to therapy are major challenges in cHL treatment. To solve these problems, we characterized two cHL cell lines with acquired resistance to doxorubicin, KM-H2dx and HDLM-2dx (HRSdx), generated from KM-H2 and HDLM-2 cells, respectively. HRSdx cells developed cross-resistance to vinblastine, bendamustin, cisplatin, dacarbazine, gemcitabine, brentuximab vedotin (BV), and γ-radiation. Both HDLM-2 and HDLM-2dx cells had intrinsic resistance to BV but not to the drug MMAE. HDLM-2dx acquired cross-resistance to caelyx. HRSdx cells had in common decreased CD71, CD80, CD54, cyt-ROS, HLA-DR, DDR1, and CD44; increased Bcl-2, CD58, COX2, CD26, CCR5, and invasive capability; increased CCL5, TARC, PGE2, and TGF-β; and the capability of hijacking monocytes. In HRSdx cells less sensitive to DNA damage and oxidative stress, the efflux drug transporters MDR1 and MRP1 were not up-regulated, and doxorubicin accumulated in the cytoplasm rather than in the nucleus. Both the autophagy inhibitor chloroquine and extracellular vesicle (EV) release inhibitor GW4869 enhanced doxorubicin activity and counteracted doxorubicin resistance. In conclusion, this study identifies common modulated antigens in HRSdx cells, the associated cross-resistance patterns, and new potential therapeutic options to enhance doxorubicin activity and overcome resistance. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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