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Cancers
Special Issues
Oncogenesis of Lymphoma
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Oncogenesis of Lymphoma

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 2385

Special Issue Editors

Dr. Annunziata Gloghini

E-Mail Website
Guest Editor
Department of Diagnostic Innovation, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy
Interests: immunohistochemistry; in situ molecular techniques; brightfield in situ hybridization; virologic characterization; EBV; HHV8/KSHV; HPV; tumor microenvironment; Hodgkin’s lymphoma; HIV-associated lymphomas
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giancarlo Pruneri

E-Mail Website
Guest Editor
Department of Diagnostic Innovation, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy
Interests: molecular pathology; lymphoma pathology; breast cancer; molecular tumor; genomic research

Special Issue Information

Dear Colleagues,

Advances in the fields of molecular genetics, immunology and virology have clarified the mechanisms involved in lymphomagenesis. Human lymphomas have been found to be heterogeneous, not only pathologically but also in terms of pathogenetic pathways, cellular derivation and the tumor microenvironment. Traditionally, some types of lymphomas, such as follicular lymphomas and mantle cell lymphomas, are consistently correlated with genetic abnormalities involving BCL2 and BCL1, respectively. It is well known that the molecular pathway in Burkitt lymphoma involves activation of MYC, inactivation of p53 and infection by EBV. Furthermore, in diffuse large B-cell lymphomas (DLBCL), molecular studies have shown rearrangements in BCL2, BCL6 and MYC genes. Recent studies with NGS and mutational profiling have identified clinically significant genetic subgroups. Four major genetic subgroups have been demonstrated in DLBCL. They are based on 1) mutations in MYD88 and CD79B, 2) BCL6 fusions and NOTCH2 mutations, 3) NOTCH1 mutations and 4) EZH2 mutations/BCL2 rearrangement. A new concept, viral cooperation, has been revealed in lymphomagenesis by molecular virologic studies on primary effusion lymphomas (PELs). In immune-deficient/dysregulated patients, PEL tumor cells, in addition to consistent infection by KSHV/HHV8, are also commonly infected by EBV. Finally, recent insights from genetics, epigenetics and knowledge in the cellular microenvironment have led to the refinement of diagnostic definition and, hopefully, appropriate therapy.

Dr. Annunziata Gloghini
Prof. Dr. Giancarlo Pruneri
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 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

  • lymphomagenesis
  • molecular genetics
  • immunology
  • molecular virology
  • KSHV/HHV8
  • EBV
  • HIV
  • pathogenetic pathways
  • genotypic subgroups
  • tumor microenvironment
  • follicular lymphoma
  • mantle cell lymphoma
  • diffuse large B-cell lymphoma
  • targeted therapy
  • drug target

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Published Papers (3 papers)

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Research

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24 pages, 18716 KiB  
Article
Multi-Omic Data Integration Suggests Putative Microbial Drivers of Aetiopathogenesis in Mycosis Fungoides
by Philipp Licht and Volker Mailänder
Cancers 2024, 16(23), 3947; https://doi.org/10.3390/cancers16233947 - 25 Nov 2024
Viewed by 423
Abstract
Background: Mycosis fungoides (MF) represents the most prevalent entity of cutaneous T cell lymphoma (CTCL). The MF aetiopathogenesis is incompletely understood, due to significant transcriptomic heterogeneity and conflicting views on whether oncologic transformation originates in early thymocytes or mature effector memory T cells. [...] Read more.
Background: Mycosis fungoides (MF) represents the most prevalent entity of cutaneous T cell lymphoma (CTCL). The MF aetiopathogenesis is incompletely understood, due to significant transcriptomic heterogeneity and conflicting views on whether oncologic transformation originates in early thymocytes or mature effector memory T cells. Recently, using clinical specimens, our group showed that the skin microbiome aggravates disease course, mainly driven by an outgrowing, pathogenic S. aureus strain carrying the virulence factor spa, which was shown by others to activate the T cell signalling pathway NF-κB. Methods: To explore the role of the skin microbiome in MF aetiopathogenesis, we here performed RNA sequencing, multi-omic data integration of the skin microbiome and skin transcriptome using Multi-Omic Factor Analysis (MOFA), virome profiling, and T cell receptor (TCR) sequencing in 10 MF patients from our previous study group. Results: We observed that inter-patient transcriptional heterogeneity may be largely attributed to differential activation of T cell signalling pathways. Notably, the MOFA model resolved the heterogenous activation pattern of T cell signalling after denoising the transcriptome from microbial influence. The MOFA model suggested that the outgrowing S. aureus strain evoked signalling by non-canonical NF-κB and IL-1B, which in turn may have fuelled the aggravated disease course. Further, the MOFA model indicated aberrant pathways of early thymopoiesis alongside enrichment of antiviral innate immunity. In line with this, viral prevalence, particularly of Epstein–Barr virus (EBV), trended higher in both lesional skin and the blood compared to nonlesional skin. Additionally, TCRs in both MF skin lesions and the blood were significantly more likely to recognize EBV peptides involved in latent infection. Conclusions: First, our findings suggest that S. aureus with its virulence factor spa fuels MF progression through non-canonical NF-κB and IL-1B signalling. Second, our data provide insights into the potential role of viruses in MF aetiology. Last, we propose a model of microbiome-driven MF aetiopathogenesis: Thymocytes undergo initial oncologic transformation, potentially caused by viruses. After maturation and skin infiltration, an outgrowing, pathogenic S. aureus strain evokes activation and maturation into effector memory T cells, resulting in aggressive disease. Further studies are warranted to verify and extend our data, which are based on computational analyses. Full article
(This article belongs to the Special Issue Oncogenesis of Lymphoma)
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Review

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14 pages, 610 KiB  
Review
Increased c-MYC Expression Associated with Active IGH Locus Rearrangement: An Emerging Role for c-MYC in Chronic Lymphocytic Leukemia
by Kenza Guiyedi, Milène Parquet, Said Aoufouchi, Jasmine Chauzeix, David Rizzo, Israa Al Jamal, Jean Feuillard, Nathalie Gachard and Sophie Peron
Cancers 2024, 16(22), 3749; https://doi.org/10.3390/cancers16223749 - 6 Nov 2024
Viewed by 655
Abstract
This review examines the pivotal role of c-MYC in Chronic Lymphocytic Leukemia (CLL), focusing on how its overexpression leads to increased genetic instability, thereby accelerating disease progression. MYC, a major oncogene, encodes a transcription factor that regulates essential cellular processes, including cell [...] Read more.
This review examines the pivotal role of c-MYC in Chronic Lymphocytic Leukemia (CLL), focusing on how its overexpression leads to increased genetic instability, thereby accelerating disease progression. MYC, a major oncogene, encodes a transcription factor that regulates essential cellular processes, including cell cycle control, proliferation, and apoptosis. In CLL cases enriched with unmutated immunoglobulin heavy chain variable (IGHV) genes, MYC is significantly overexpressed and associated with active rearrangements in the IGH immunoglobulin heavy chain locus. This overexpression results in substantial DNA damage, including double-strand breaks, chromosomal translocations, and an increase in abnormal repair events. Consequently, c-MYC plays a dual role in CLL: it promotes aggressive cell proliferation while concurrently driving genomic instability through its involvement in genetic recombination. This dynamic contributes not only to CLL progression but also to the overall aggressiveness of the disease. Additionally, the review suggests that c-MYC’s influence on genetic rearrangements makes it an attractive target for therapeutic strategies aimed at mitigating CLL malignancy. These findings underscore c-MYC’s critical importance in advancing CLL progression, highlighting the need for further research to explore its potential as a target in future treatment approaches. Full article
(This article belongs to the Special Issue Oncogenesis of Lymphoma)
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19 pages, 2151 KiB  
Review
Molecular Mechanisms of Kaposi Sarcoma-Associated Herpesvirus (HHV8)-Related Lymphomagenesis
by Caroline J. Yu and Blossom Damania
Cancers 2024, 16(21), 3693; https://doi.org/10.3390/cancers16213693 - 31 Oct 2024
Viewed by 792
Abstract
Approximately 15–20% of cancers are caused by viruses. Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is an oncogenic virus that is the etiologic agent of not only Kaposi sarcoma but also the lymphoproliferative disorders, primary effusion lymphoma (PEL) and [...] Read more.
Approximately 15–20% of cancers are caused by viruses. Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is an oncogenic virus that is the etiologic agent of not only Kaposi sarcoma but also the lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). KSHV can infect a broad tropism of cells, including B lymphocytes, wherein KSHV encodes specific viral proteins that can transform the cell. KSHV infection precedes the progression of PEL and MCD. KSHV establishes lifelong infection and has two phases of its lifecycle: latent and lytic. During the latent phase, viral genomes are maintained episomally with limited gene expression. Upon sporadic reactivation, the virus enters its replicative lytic phase to produce infectious virions. KSHV relies on its viral products to modulate host factors to evade immune detection or to co-opt their function for KSHV persistence. These manipulations dysregulate normal cell pathways to ensure cell survival and inhibit antiviral immune responses, which in turn, contribute to KSHV-associated malignancies. Here, we highlight the known molecular mechanisms of KSHV that promote lymphomagenesis and how these findings identify potential therapeutic targets for KSHV-associated lymphomas. Full article
(This article belongs to the Special Issue Oncogenesis of Lymphoma)
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