Evidence map›Paper›PMID 30874354›Full record

ReviewImmunological reviews2019

Germinal center-derived lymphomas: The darkest side of humoral immunity.

Coraline Mlynarczyk, Lorena Fontán, Ari Melnick

Abstract readReview
In one paragraph

Review in Immunological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

119 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  5. CCL19bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
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  9. Rethinking the microenvironment's role in chemical-induced malignancy.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Review
  10. Review
  11. Article
  12. HemaSphere · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

59 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Coraline MlynarczykDepartment of Medicine, Division of Hematology & Medical Oncology, Weill Cornell Medicine, New York City, New York.ORCID 0000-0002-6750-0240
Lorena FontánDepartment of Medicine, Division of Hematology & Medical Oncology, Weill Cornell Medicine, New York City, New York.ORCID 0000-0002-1021-3654
Ari MelnickDepartment of Medicine, Division of Hematology & Medical Oncology, Weill Cornell Medicine, New York City, New York.ORCID 0000-0002-8074-2287

Funding

Translating Stress Response Targeted Therapy for B-Cell LymphomasP50CA192937 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI DALLA-FAVERA, RICCARDO, ZELENETZ, ANDREW D. · 2016 to 2020
$10.9M
Targeting Epigenetic Circuits in B-Cell LymphomasR35CA220499 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2018 to 2024
$7.2M
NCI NIH HHS P50 CA192937NCI NIH HHS R35 CA220499
6 · The paper itself

Abstract

One of the unusual features of germinal center (GC) B cells is that they manifest many hallmarks of cancer cells. Accordingly, most B-cell neoplasms originate from the GC reaction, and characteristically display abundant point mutations, structural genomic lesions, and clonal diversity from the genetic and epigenetic standpoints. The dominant biological theme of GC-derived lymphomas is mutation of genes involved in epigenetic regulation and immune receptor signaling, which come into play at critical transitional stages of the GC reaction. Hence, mechanistic studies of these mutations reveal fundamental insight into the biology of the normal and malignant GC B cell. The BCL6 transcription factor plays a central role in establishing the GC phenotype in B cells, and most lymphomas are dependent on BCL6 to maintain survival, proliferation, and perhaps immune evasion. Many lymphoma mutations have the commonality of enhancing the oncogenic functions of BCL6, or overcoming some of its tumor suppressive effects. Herein, we discuss how unique features of the GC reaction create vulnerabilities that select for particular lymphoma mutations. We examine the interplay between epigenetic programming, metabolism, signaling, and immune regulatory mechanisms in lymphoma, and discuss how these are leading to novel precision therapy strategies to treat lymphoma patients.

Indexed as

AnimalsB-LymphocytesEpigenesis, GeneticGene Expression Regulation, LeukemicGerminal CenterHumansImmunity, HumoralImmunomodulationLymphomaProto-Oncogene Proteins c-bcl-6Receptors, Antigen, B-CellSignal TransductionProto-Oncogene Proteins c-bcl-6Receptors, Antigen, B-Cellepigenetic deregulationgerminal centerimmune surveillancelymphomagenesisprecision therapysignal transduction

Identifiers

PMID30874354
PMCPMC6518944

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.