Evidence map›Paper›PMID 22546857›Full record

ArticleThe Journal of clinical investigation2012

CD19 is a major B cell receptor-independent activator of MYC-driven B-lymphomagenesis.

Elaine Y Chung, James N Psathas, Duonan Yu, Yimei Li, Mitchell J Weiss, Andrei Thomas-Tikhonenko

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.5field-weighted citation impact, top 4% of its field
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

60 citing papers in PubMed, 95 citations in OpenAlex.

  1. Tumor-associated CD19Nature communications · 2026
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  8. Phase I Study of Niraparib in Combination with Radium-223 for the Treatment of Metastatic Castrate-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  9. Review
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  18. Review
  19. The use of tafasitamab in diffuse large B-cell lymphoma.Therapeutic advances in hematology · 2021
    Review
  20. Article
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

6 authors at 3 institutions in 1 country.

Elaine Y ChungDivision of Cancer Pathobiology, Department of Pathology and Laboratory Medicine, The Children’s Hospital of Philadelphia, Philadelphia 19104-4399, Pennsylvania, USA.
James N Psathas
Duonan Yu
Yimei Li
Mitchell J Weiss
Andrei Thomas-Tikhonenko
Cancer Genetics (United States) · USChildren's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

HEMATOLOGY CLINICAL RESEARCH TRAINING PROGRAMT32HL007439 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE F BRASS, PETER S KLEIN · 1985 to 2026
$17.1M
Training In Tumor VirologyT32CA115299 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2006 to 2021
$4.7M
Interplay between Pax5 and Myc in B-lymphomagenesisR01CA102709 · NCI · UNIVERSITY OF PENNSYLVANIA · PI THOMAS-TIKHONENKO, ANDREI · 2003 to 2006
$1.2M
NCI NIH HHS R01 CA102709NCI NIH HHS T32 CA115299NHLBI NIH HHS T32 HL007439
6 · The paper itself

Abstract

PAX5, a B cell-specific transcription factor, is overexpressed through chromosomal translocations in a subset of B cell lymphomas. Previously, we had shown that activation of immunoreceptor tyrosine-based activation motif (ITAM) proteins and B cell receptor (BCR) signaling by PAX5 contributes to B-lymphomagenesis. However, the effect of PAX5 on other oncogenic transcription factor-controlled pathways is unknown. Using a MYC-induced murine lymphoma model as well as MYC-transformed human B cell lines, we found that PAX5 controls c-MYC protein stability and steady-state levels. This promoter-independent, posttranslational mechanism of c-MYC regulation was independent of ITAM/BCR activity. Instead it was controlled by another PAX5 target, CD19, through the PI3K-AKT-GSK3β axis. Consequently, MYC levels in B cells from CD19-deficient mice were sharply reduced. Conversely, reexpression of CD19 in murine lymphomas with spontaneous silencing of PAX5 boosted MYC levels, expression of its key target genes, cell proliferation in vitro, and overall tumor growth in vivo. In human B-lymphomas, CD19 mRNA levels were found to correlate with those of MYC-activated genes. They also negatively correlated with the overall survival of patients with lymphoma in the same way that MYC levels do. Thus, CD19 is a major BCR-independent regulator of MYC-driven neoplastic growth in B cell neoplasms.

Indexed as

AnimalsAntigens, CD19B-LymphocytesCell Line, TransformedGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansLymphoma, B-CellMiceNeoplasms, ExperimentalPAX5 Transcription FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptors, Antigen, B-CellAntigens, CD19Glycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseMyc protein, mousePax5 protein, mousePAX5 Transcription FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptors, Antigen, B-CellRNA, MessengerRNA, Neoplasm

Identifiers

PMID22546857
PMCPMC3366393
OpenAlexW2127013298

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.