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Cells
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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: closed (31 December 2024) | Viewed by 9731

Special Issue Editor

Prof. Dr. Pier Paolo Piccaluga

E-Mail Website
Guest Editor
Biobank of Research, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Department of Medical and Surgical Sciences (DIMEC), Bologna University, 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.

Prof. 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

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Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 5075 KiB  
Article
The Oncoprotein Fra-2 Drives the Activation of Human Endogenous Retrovirus Env Expression in Adult T-Cell Leukemia/Lymphoma (ATLL) Patients
by Julie Tram, Laetitia Marty, Célima Mourouvin, Magali Abrantes, Ilham Jaafari, Raymond Césaire, Philippe Hélias, Benoit Barbeau, Jean-Michel Mesnard, Véronique Baccini, Laurent Chaloin and Jean-Marie Jr. Peloponese
Cells 2024, 13(18), 1517; https://doi.org/10.3390/cells13181517 - 10 Sep 2024
Viewed by 1450
Abstract
Human endogenous retroviruses (HERVs) are retroviral sequences integrated into 8% of the human genome resulting from ancient exogenous retroviral infections. Unlike endogenous retroviruses of other mammalian species, HERVs are mostly replication and retro-transposition defective, and their transcription is strictly regulated by epigenetic mechanisms [...] Read more.
Human endogenous retroviruses (HERVs) are retroviral sequences integrated into 8% of the human genome resulting from ancient exogenous retroviral infections. Unlike endogenous retroviruses of other mammalian species, HERVs are mostly replication and retro-transposition defective, and their transcription is strictly regulated by epigenetic mechanisms in normal cells. A significant addition to the growing body of research reveals that HERVs’ aberrant activation is often associated with offsetting diseases like autoimmunity, neurodegenerative diseases, cancers, and chemoresistance. Adult T-cell leukemia/lymphoma (ATLL) is a very aggressive and chemoresistant leukemia caused by the human T-cell leukemia virus type 1 (HTLV-1). The prognosis of ATLL remains poor despite several new agents being approved in the last few years. In the present study, we compare the expression of HERV genes in CD8+-depleted PBMCs from HTLV-1 asymptomatic carriers and patients with acute ATLL. Herein, we show that HERVs are highly upregulated in acute ATLL. Our results further demonstrate that the oncoprotein Fra-2 binds the LTR region and activates the transcription of several HERV families, including HERV-H and HERV-K families. This raises the exciting possibility that upregulated HERV expression could be a key factor in ATLL development and the observed chemoresistance, potentially leading to new therapeutic strategies and significantly impacting the field of oncology and virology. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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14 pages, 3123 KiB  
Article
SATB1 and p16 Expression and Prognostic Value in Croatian Hodgkin Lymphoma Patients: A Unicentric Study
by Lučana Vicelić Čutura, Milan Vujčić, Davor Galušić, Viktor Blaslov, Marija Petrić, Antonija Miljak, Mirela Lozić, Benjamin Benzon, Katarina Vukojević, Toni Bubić, Nenad Kunac, Danijela Zjačić Puljiz, Ivana Kristina Delić Jukić, Marinela Križanac and Bernarda Lozić
Cells 2024, 13(16), 1323; https://doi.org/10.3390/cells13161323 - 8 Aug 2024
Viewed by 1211
Abstract
Hodgkin lymphoma (HL) is a rare lymphoid neoplasm in which Hodgkin/Reed–Stenberg (HRS) cells are admixed with a population of non-neoplastic inflammatory cells and fibrosis. Dysregulated expressions of cell cycle regulators and transcription factors have been proven as one of the hallmarks of HL. [...] Read more.
Hodgkin lymphoma (HL) is a rare lymphoid neoplasm in which Hodgkin/Reed–Stenberg (HRS) cells are admixed with a population of non-neoplastic inflammatory cells and fibrosis. Dysregulated expressions of cell cycle regulators and transcription factors have been proven as one of the hallmarks of HL. In that context, SATB1 and p16 have been reported as potential regulators of HL progression and survival. However, to date, no studies have assessed the expression levels of SATB1 and p16 in HL in Croatian patients or their prognostic values. Therefore, we investigated the expression pattern of SATB1 and p16 in paraffin-embedded lymph node biopsies using standard immunohistochemistry. We found that 21% of the patients stained positive for SATB1, while 15% of the patients displayed positive staining for p16. Furthermore, we aimed to understand the prognostic value of each protein through the analysis of the overall survival (OS) and progression-free survival (PFS). SATB1 showed a significantly positive correlation with better OS and PFS, while p16 expression had no impact. Interestingly, when patients were stratified by a combination of the two studied markers, we found that patients in the SATB1+/p16- group tended to have the best prognosis in HL, according to statistical significance. In conclusion, SATB1 and p16 might be potentially useful as diagnostic and prognostic markers for HL. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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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
Cited by 2 | Viewed by 2058
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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Review

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17 pages, 1432 KiB  
Review
The CD39/CD73/Adenosine and NAD/CD38/CD203a/CD73 Axis in Cutaneous T-Cell Lymphomas
by Liyun Lin, Gabriele Roccuzzo, Yuliya Yakymiv, Sara Marchisio, Erika Ortolan, Ada Funaro, Rebecca Senetta, Valentina Pala, Martine Bagot, Adèle de Masson, Maxime Battistella, Emmanuella Guenova, Simone Ribero and Pietro Quaglino
Cells 2025, 14(4), 309; https://doi.org/10.3390/cells14040309 - 19 Feb 2025
Viewed by 481
Abstract
Cutaneous T-cell lymphoma (CTCL), characterized by malignant T-cell proliferation primarily in the skin, includes subtypes such as mycosis fungoides (MF) and Sézary syndrome (SS). The tumor microenvironment (TME) is central to their pathogenesis, with flow cytometry and histology being the gold standards for [...] Read more.
Cutaneous T-cell lymphoma (CTCL), characterized by malignant T-cell proliferation primarily in the skin, includes subtypes such as mycosis fungoides (MF) and Sézary syndrome (SS). The tumor microenvironment (TME) is central to their pathogenesis, with flow cytometry and histology being the gold standards for detecting malignant T cells within the TME. Alongside emerging molecular markers, particularly clonality analysis, these tools are indispensable for accurate diagnosis and treatment planning. Of note, adenosine signaling within the TME has been shown to suppress immune responses, affecting various cell types. The expression of CD39, CD73, and CD38, enzymes involved in adenosine production, can be elevated in MF and SS, contributing to immune suppression. Conversely, the expression of CD26, part of the adenosine deaminase/CD26 complex, that degrades adenosine, is often lost by circulating tumoral cells. Flow cytometry has demonstrated increased levels of CD39 and CD73 on Sézary cells, correlating with disease progression and prognosis, while CD38 shows a variable expression, with its prognostic significance remaining under investigation. Understanding these markers’ roles in the complexity of TME-mediated immune evasion mechanisms might enhance diagnostic precision and offer new therapeutic targets in CTCL. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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18 pages, 2529 KiB  
Review
3D-Q-FISH/Telomere/TRF2 Nanotechnology Identifies a Progressively Disturbed Telomere/Shelterin/Lamin AC Complex as the Common Pathogenic, Molecular/Spatial Denominator of Classical Hodgkin Lymphoma
by Hans Knecht, Tina Petrogiannis-Haliotis, Sherif Louis and Sabine Mai
Cells 2024, 13(21), 1748; https://doi.org/10.3390/cells13211748 - 23 Oct 2024
Viewed by 1279
Abstract
The bi- or multinucleated Reed–Sternberg cell (RS) is the diagnostic cornerstone of Epstein–Barr Virus (EBV)-positive and EBV-negative classical Hodgkin lymphoma (cHL). cHL is a germinal center (GC)-derived B-cell disease. Hodgkin cells (H) are the mononuclear precursors of RS. An experimental model has to [...] Read more.
The bi- or multinucleated Reed–Sternberg cell (RS) is the diagnostic cornerstone of Epstein–Barr Virus (EBV)-positive and EBV-negative classical Hodgkin lymphoma (cHL). cHL is a germinal center (GC)-derived B-cell disease. Hodgkin cells (H) are the mononuclear precursors of RS. An experimental model has to fulfill three conditions to qualify as common pathogenic denominator: (i) to be of GC-derived B-cell origin, (ii) to be EBV-negative to avoid EBV latency III expression and (iii) to support permanent EBV-encoded oncogenic latent membrane protein (LMP1) expression upon induction. These conditions are unified in the EBV-, diffuse large B-Cell lymphoma (DLBCL) cell line BJAB-tTA-LMP1. 3D reconstructive nanotechnology revealed spatial, quantitative and qualitative disturbance of telomere/shelterin interactions in mononuclear H-like cells, with further progression during transition to RS-like cells, including progressive complexity of the karyotype with every mitotic cycle, due to BBF (breakage/bridge/fusion) events. The findings of this model were confirmed in diagnostic patient samples and correlate with clinical outcomes. Moreover, in vitro, significant disturbance of the lamin AC/telomere interaction progressively occurred. In summary, our research over the past three decades identified cHL as the first lymphoid malignancy driven by a disturbed telomere/shelterin/lamin AC interaction, generating the diagnostic RS. Our findings may act as trailblazer for tailored therapies in refractory cHL. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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21 pages, 2462 KiB  
Review
Tumour Microenvironment: The General Principles of Pathogenesis and Implications in Diffuse Large B Cell Lymphoma
by Stanislavs Sinkarevs, Boriss Strumfs, Svetlana Volkova and Ilze Strumfa
Cells 2024, 13(12), 1057; https://doi.org/10.3390/cells13121057 - 18 Jun 2024
Cited by 1 | Viewed by 2457
Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma worldwide, constituting around 30–40% of all cases. Almost 60% of patients develop relapse of refractory DLBCL. Among the reasons for the therapy failure, tumour microenvironment (TME) components could be [...] Read more.
Diffuse large B cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma worldwide, constituting around 30–40% of all cases. Almost 60% of patients develop relapse of refractory DLBCL. Among the reasons for the therapy failure, tumour microenvironment (TME) components could be involved, including tumour-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), tumour-associated neutrophils (TANs), cancer-associated fibroblasts (CAFs), and different subtypes of cytotoxic CD8+ cells and T regulatory cells, which show complex interactions with tumour cells. Understanding of the TME can provide new therapeutic options for patients with DLBCL and improve their prognosis and overall survival. This review provides essentials of the latest understanding of tumour microenvironment elements and discusses their role in tumour progression and immune suppression mechanisms which result in poor prognosis for patients with DLBCL. In addition, we point out important markers for the diagnostic purposes and highlight novel therapeutic targets. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Lymphomas)
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