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Cited by 103Viral-associated cancers and disordersLymphoma Diagnosis and TreatmentCNS Lymphoma Diagnosis and Treatment

Biology and management of primary effusion lymphoma

Shimada, Kazuyuki, Hayakawa, Fumihiko, Kiyoi, Hitoshi·2018·Blood
DOI 10.1182/blood-2018-03-791426
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Abstract

Primary effusion lymphoma (PEL) is a rare B-cell malignancy that most often occurs in immunocompromised patients, such as HIV-infected individuals and patients receiving organ transplantation. The main characteristic of PEL is neoplastic effusions in body cavities without detectable tumor masses. The onset of the disease is associated with latent infection of human herpes virus 8/Kaposi sarcoma–associated herpes virus, and the normal counterpart of tumor cells is B cells with plasmablastic differentiation. A condition of immunodeficiency and a usual absence of CD20 expression lead to the expectation of the lack of efficacy of anti-CD20 monoclonal antibody; clinical outcomes of the disease remain extremely poor, with an overall survival at 1 year of ∼30%. Although recent progress in antiretroviral therapy has improved outcomes of HIV-infected patients, its benefit is still limited in patients with PEL. Furthermore, the usual high expression of programmed death ligand 1 in tumor cells, one of the most important immune-checkpoint molecules, results in the immune escape of tumor cells from the host immune defense, which could be the underlying mechanism of poor treatment efficacy. Molecular-targeted therapies for the activating pathways in PEL, including NF-κB, JAK/STAT, and phosphatidylinositol 3-kinase/AKT, have emerged to treat this intractable disease. A combination of immunological recovery from immune deficiency, overcoming the immune escape, and the development of more effective drugs will be vital for improving the outcomes of PEL patients in the future.

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Crossref · 10.1182/blood-2018-03-791426

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  • Avadomide is chemically similar to pomalidomide and accordingly has similar substrate specificity and potency of degradation.

    “Avadomide (previously known as CC-122) is chemically similar to pomalidomide (FIG. 1c), and accordingly, has similar substrate specificity and potency of degradation113.”

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  • CC-90009 targets GSPT1 and GSPT2, which are essential regulators of translation termination.

    “CC-90009 differs from the other thalidomide analogues in that it targets the substrates G1 to S phase transition protein 1 homologue (GSPT1) and GSPT2, which are also known as eukaryotic peptide chain release factor GTP-binding subunits ERF3A and ERF3B, respectively, reflecting their roles as essential regulators of translation termination113,121.”

    From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [113]

  • Induced overexpression of one substrate reduced the degradation of other substrates and induced drug resistance in cellular models.

    “Indeed, induced overexpression of one substrate reduced the degradation of other substrates and induced drug resistance in cellular models113.”

    From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [113]

  • Targeted mass spectrometry analyses have revealed the importance of competition among both substrates and E3 ubiquitin ligase complexes in determining neosubstrate abundance during thalidomide analogue therapy.

    “Such analyses have revealed the importance of competition among both substrates and E3 ubiquitin ligase complexes in determining neosubstrate abundance during thalidomide analogue therapy.”

    From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [113]

  • In a quantitative multiplex mass spectrometry-based assay, a stereotyped order of polysubstrate degradation was identified for various thalidomide analogues, suggesting that substrates with higher affinity and/or greater abundance can outcompete others.

    “In a study using a quantitative multiplex mass spectrometry-based assay to quantitate multiple substrate proteins, a stereotyped order of polysubstrate degradation was identified for various thalidomide analogues113, suggesting that substrates with higher affinity and/or greater abundance can outcompete others.”

    From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [113]

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Authors
Shimada, K., Hayakawa, F., & Kiyoi, H.
Affiliations
Nagoya University (JP)
ORCID
Venue
Blood
Publisher
American Society of Hematology
Published
2018-11-01
Volume
132
Issue
18
Pages
1879-1888
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
DOI
10.1182/blood-2018-03-791426
OpenAlex
W2888846757
Cited by
103
References
100
Citations by year
2026: 3 · 2025: 9 · 2024: 12 · 2023: 15 · 2022: 14 · 2021: 25 · 2020: 18 · 2019: 5
FWCI
1.25
Type
journal article
Language
en
Open access
closed
Locations
  • Blood (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Mashhad University of Medical Sciences
  • Japan Society for the Promotion of Science (17K09922, 17K09921)
Topics
  • Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
  • Health Sciences › Medicine › Neurology › CNS Lymphoma Diagnosis and Treatment
Keywords
primary effusion lymphoma, Kaposi's sarcoma-associated herpesvirus, HIV infection, immunocompromised patients, organ transplantation, CD20-negative lymphoma, anti-CD20 monoclonal antibody, tumor immune evasion, NF-κB signaling, JAK/STAT signaling, PI3K/Akt signaling, targeted therapy, antiretroviral therapy
MeSH terms
Animals, Cytogenetics, Humans, Immunophenotyping, Disease Management, Lymphoma, Primary Effusion, Transcriptome

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