ReviewCold Spring Harbor perspectives in medicine2021
Mouse Models in the Study of Mature B-Cell Malignancies.
Review in Cold Spring Harbor perspectives in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Next-generation models for lymphoid malignancies: the rise of 3D culture systems in translational hematology.British journal of cancer · 2026Review
- Host heterogeneity shapes clonal selection and organotropism in an extranodal lymphoma mouse model.Cell death & disease · 2026Article
- Enhanced antibody responses in CD19-Cre mice.Scientific reports · 2025Article
- Lymphoma dissemination is a pathological hallmark for malignant progression of B-cell lymphoma.Frontiers in immunology · 2023Article
- Human B Lymphomas Reveal Their Secrets Through Genetic Mouse Models.Frontiers in immunology · 2021Review
- Mouse Models of Germinal Center Derived B-Cell Lymphomas.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Over the past two decades, genomic analyses of several B-cell lymphoma entities have identified a large number of genes that are recurrently mutated, suggesting that their aberrant function promotes lymphomagenesis. For many of those genes, the specific role in normal B-cell development is unknown; moreover, whether and how their deregulated activity contributes to lymphoma initiation and/or maintenance is often difficult to determine. Genetically engineered mouse models that faithfully mimic lymphoma-associated genetic alterations represent valuable tools for elucidating the pathogenic roles of candidate oncogenes and tumor suppressors in vivo, as well as for the preclinical testing of novel therapeutic principles in an intact microenvironment. Here we summarize what has been learned about the mechanisms of oncogenic transformation from accurately modeling the most common and well-characterized genetic alterations identified in mature B-cell malignancies. This information is expected to guide the design of improved molecular diagnostics and mechanism-based therapeutic approaches for these diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.