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Cancers
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Molecular Advances in Diffuse Large B-Cell Lymphoma
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Molecular Advances in Diffuse Large B-Cell Lymphoma

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 25294

Special Issue Editors

Dr. Socorro María Rodríguez-Pinilla

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Guest Editor
Pathology Department, Hospital Universitario Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Interests: lymphoma; prognosis; molecular background
Special Issues, Collections and Topics in MDPI journals
Dr. Arantza Onaindia

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Guest Editor
Surgical Pathology Department (Hematopathology, Dermatopathology), Hospital Universitario de Araba. 01009 Gasteiz, Araba, Spain
Interests: surgical pathology and hematopathology; molecular pathology; clinical research; translational cancer research; targeted therapeutics; new molecular assays and technologies; personalized medicine
Dr. Paola A. Chabay

E-Mail Website
Guest Editor
Laboratory of Molecular Biology, Pathology Division, Multidisciplinary Institute for Investigation in Pediatric Pathologies (IMIPP-CONICET-GCBA), Ricardo Gutiérrez Children’s Hospital, Gallo 1330, Buenos Aires C1425EFD, Argentina
Interests: EBV-positive DLBCL lymphomas; plasmablastic lymphomas
Special Issues, Collections and Topics in MDPI journals
Dr. Fina Climent

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Guest Editor
Department of Pathology, Hospital Universitari de Bellvitge-IDIBELL, 08907 L'Hospitalet de Llobregat, Barcelona. Spain
Interests: extranodal DLBCL; DLBCL in children

Special Issue Information

Dear Colleagues,

Diffuse large B-cell lymphomas are heterogeneous aggressive lymphomas whose molecular background is still poorly understood. They are biologically and clinically different based on age (children, adults, elderly) of onset, place of development (nodal vs. extranodal), viral relationship, and immunosurveillance. Moreover, genetic subgroups have also been identified, such as high grade B-cell lymphomas with double or triple MYC/BCL2/BCL6 gene rearrangements, 11q Burkitt-like lymphoma, IRF4 translocated, or ALK translocated lymphomas, among others. We are proposing an extended review of new molecular advances in diffuse large B-cell lymphomas, taking into account all these previous features. Moreover, we highlight the existence of new approaches for high-grade B-cell lymphoma identification.

Prof. Dr. Socorro María Rodríguez-Pinilla
Dr. Arantza Onaindia
Dr. Paola A Chabay
Dr. Fina Climent
Guest Editors

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Keywords

  • DLBCL
  • genetics
  • molecular
  • Epstein–Barr virus
  • immunodeficiency
  • IRF4
  • ALK
  • high-grade B-cell lymphomas
  • extranodal DLBCL

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Published Papers (5 papers)

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18 pages, 6058 KiB  
Article
RAS Mediates BET Inhibitor-Endued Repression of Lymphoma Migration and Prognosticates a Novel Proteomics-Based Subgroup of DLBCL through Its Negative Regulator IQGAP3
by Chih-Cheng Chen, Chia-Chen Hsu, Sung-Lin Chen, Po-Han Lin, Ju-Pei Chen, Yi-Ru Pan, Cih-En Huang, Ying-Ju Chen, Yi-Yang Chen, Yu-Ying Wu and Muh-Hwa Yang
Cancers 2021, 13(19), 5024; https://doi.org/10.3390/cancers13195024 - 7 Oct 2021
Cited by 5 | Viewed by 3049
Abstract
Phenotypic heterogeneity and molecular diversity make diffuse large B-cell lymphoma (DLBCL) a challenging disease. We recently illustrated that amoeboid movement plays an indispensable role in DLBCL dissemination and inadvertently identified that the inhibitor of bromodomain and extra-terminal (BET) proteins JQ1 could repress DLBCL [...] Read more.
Phenotypic heterogeneity and molecular diversity make diffuse large B-cell lymphoma (DLBCL) a challenging disease. We recently illustrated that amoeboid movement plays an indispensable role in DLBCL dissemination and inadvertently identified that the inhibitor of bromodomain and extra-terminal (BET) proteins JQ1 could repress DLBCL migration. To explore further, we dissected the impacts of BET inhibition in DLBCL. We found that JQ1 abrogated amoeboid movement of DLBCL cells through both restraining RAS signaling and suppressing MYC-mediated RhoA activity. We also demonstrated that BET inhibition resulted in the upregulation of a GTPase regulatory protein, the IQ motif containing GTPase activating protein 3 (IQGAP3). IQGAP3 similarly exhibited an inhibitory effect on RAS activity in DLBCL cells. Through barcoded mRNA/protein profiling in clinical samples, we identified a specific subgroup of DLBCL tumors with enhanced phosphatidylinositol-3-kinase (PI3K) activity, which led to an inferior survival in these patients. Strikingly, a lower IQGAP3 expression level further portended those with PI3K-activated DLBCL a very dismal outcome. The inhibition of BET and PI3K signaling activity led to effective suppression of DLBCL dissemination in vivo. Our study provides an important insight into the ongoing efforts of targeting BET proteins as a therapeutic approach for DLBCL. Full article
(This article belongs to the Special Issue Molecular Advances in Diffuse Large B-Cell Lymphoma)
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15 pages, 18325 KiB  
Article
Role of Epstein–Barr Virus C Promoter Deletion in Diffuse Large B Cell Lymphoma
by Seiyo Mabuchi, Fumiya Hijioka, Takahiro Watanabe, Yusuke Yanagi, Yusuke Okuno, H. M. Abdullah Al Masud, Yoshitaka Sato, Takayuki Murata and Hiroshi Kimura
Cancers 2021, 13(3), 561; https://doi.org/10.3390/cancers13030561 - 1 Feb 2021
Cited by 12 | Viewed by 4374
Abstract
The Epstein–Barr virus (EBV) is the cause of several malignancies, including diffuse large B cell lymphoma (DLBCL). We recently found that EBV genomes in EBV-positive cancer specimens have various deletions (Okuno et al. Nat Microbiol. 2019). Here, we focus on the deletion of [...] Read more.
The Epstein–Barr virus (EBV) is the cause of several malignancies, including diffuse large B cell lymphoma (DLBCL). We recently found that EBV genomes in EBV-positive cancer specimens have various deletions (Okuno et al. Nat Microbiol. 2019). Here, we focus on the deletion of C promoter (Cp), which transcribes EBV nuclear antigen (EBNA) genes in type III latency. The Cp deletion found in a DLBCL patient (332 bp) was introduced into EBV-BAC of the B95-8 strain. Interestingly, the dCp virus transformed B cells more efficiently than WT and revertant strains. Deletion of Cp also promoted tumor formation and severe pathogenicity in a mouse xenograft model. RNA sequencing and qRT–PCR analyses revealed that Cp transcription was undetectable in the dCp cells. Instead, transcription from the W promoter (Wp), an alternative promoter for EBNA, was activated in the dCp mutant. We also found that the expression of latent membrane protein 2A (LMP2A) was somehow induced in the dCp mutant. Double knockout of Cp and LMP2A indicated that LMP2A is crucial for B cell transformation, but the increased transformation induced by Cp deletion cannot be explained by LMP2A alone. We also tested the effect of an anti-apoptotic viral BCL2 homolog, BHRF1, because its expression was reportedly induced more efficiently by that of Wp. However, increased growth transformation via Cp deletion was not due to the BHRF1 gene. Taken together, the results indicated that deletion of a specific region in Cp increased in vitro transformation and the rate of progression of EBV-positive lymphoproliferative disorders in vivo. Our data suggest that genomic alteration not only of the host but also the virus promotes EBV-positive tumor generation and expansion, although the molecular mechanism underlying this phenomenon is still unclear. However, LMP2A and BHRF1 are not involved. Full article
(This article belongs to the Special Issue Molecular Advances in Diffuse Large B-Cell Lymphoma)
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Review

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24 pages, 768 KiB  
Review
Molecular Update and Evolving Classification of Large B-Cell Lymphoma
by Arantza Onaindia, Nancy Santiago-Quispe, Erika Iglesias-Martinez and Cristina Romero-Abrio
Cancers 2021, 13(13), 3352; https://doi.org/10.3390/cancers13133352 - 3 Jul 2021
Cited by 17 | Viewed by 4326
Abstract
Diffuse large B-cell lymphomas (DLBCLs) are aggressive B-cell neoplasms with considerable clinical, biologic, and pathologic diversity. The application of high throughput technologies to the study of lymphomas has yielded abundant molecular data leading to the identification of distinct molecular identities and novel pathogenetic [...] Read more.
Diffuse large B-cell lymphomas (DLBCLs) are aggressive B-cell neoplasms with considerable clinical, biologic, and pathologic diversity. The application of high throughput technologies to the study of lymphomas has yielded abundant molecular data leading to the identification of distinct molecular identities and novel pathogenetic pathways. In light of this new information, newly refined diagnostic criteria have been established in the fourth edition of the World Health Organization (WHO) consensus classification of lymphomas, which was revised in 2016. This article reviews the histopathological and molecular features of the various aggressive B-cell lymphoma subtypes included in the updated classification. Full article
(This article belongs to the Special Issue Molecular Advances in Diffuse Large B-Cell Lymphoma)
22 pages, 8122 KiB  
Review
An Overview on Diffuse Large B-Cell Lymphoma Models: Towards a Functional Genomics Approach
by Natalia Yanguas-Casás, Lucía Pedrosa, Ismael Fernández-Miranda and Margarita Sánchez-Beato
Cancers 2021, 13(12), 2893; https://doi.org/10.3390/cancers13122893 - 9 Jun 2021
Cited by 9 | Viewed by 6073
Abstract
Lymphoma research is a paradigm of the integration of basic and clinical research within the fields of diagnosis and therapy. Clinical, phenotypic, and genetic data are currently used to predict which patients could benefit from standard treatment. However, alternative therapies for patients at [...] Read more.
Lymphoma research is a paradigm of the integration of basic and clinical research within the fields of diagnosis and therapy. Clinical, phenotypic, and genetic data are currently used to predict which patients could benefit from standard treatment. However, alternative therapies for patients at higher risk from refractoriness or relapse are usually empirically proposed, based on trial and error, without considering the genetic complexity of aggressive B-cell lymphomas. This is primarily due to the intricate mosaic of genetic and epigenetic alterations in lymphomas, which are an obstacle to the prediction of which drug will work for any given patient. Matching a patient’s genes to drug sensitivity by directly testing live tissues comprises the “precision medicine” concept. However, in the case of lymphomas, this concept should be expanded beyond genomics, eventually providing better treatment options for patients in need of alternative therapeutic approaches. We provide an overview of the most recent findings in diffuse large B-cell lymphomas genomics, from the classic functional models used to study tumor biology and the response to experimental treatments using cell lines and mouse models, to the most recent approaches with spheroid/organoid models. We also discuss their potential relevance and applicability to daily clinical practice. Full article
(This article belongs to the Special Issue Molecular Advances in Diffuse Large B-Cell Lymphoma)
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15 pages, 901 KiB  
Review
Advances in the Pathogenesis of EBV-Associated Diffuse Large B Cell Lymphoma
by Paola Chabay
Cancers 2021, 13(11), 2717; https://doi.org/10.3390/cancers13112717 - 31 May 2021
Cited by 31 | Viewed by 5784
Abstract
Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin’s lymphoma (NHL) in adults. Epstein–Barr virus (EBV) positive DLBCL of the elderly was defined by the World Health Organization (WHO) in 2008, it was restricted only to patients older than 50 years old, [...] Read more.
Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin’s lymphoma (NHL) in adults. Epstein–Barr virus (EBV) positive DLBCL of the elderly was defined by the World Health Organization (WHO) in 2008, it was restricted only to patients older than 50 years old, and it was attributed to immunesenescence associated with physiological aging. After the description of EBV-associated DLBCL in children and young adults, the WHO redefined the definition, leading to the substitution of the modifier “elderly” with “not otherwise specified” (EBV + DLBCL, NOS) in the updated classification, and it is no more considered provisional. The incidence of EBV + DLBCL, NOS varies around the world, in particular influenced by the percentage of EBV+ cells used as cut-off to define a case as EBV-associated. EBV has effect on the genetic composition of tumor cells, on survival, and at the recruitment of immune cells at the microenvironment. In this review, the role of EBV in the pathogenesis of DLBCL is discussed. Full article
(This article belongs to the Special Issue Molecular Advances in Diffuse Large B-Cell Lymphoma)
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