Evidence map›Paper›PMID 15753301›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

The protooncogene MYC can break B cell tolerance.

Yosef Refaeli, Kenneth A Field, Brian C Turner, Andreas Trumpp, J Michael Bishop

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. A role for IRF8 in B cell anergy.Journal of immunology (Baltimore, Md. : 1950) · 2013
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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

5 authors at 3 institutions in 1 country.

Yosef RefaeliThe G. W. Hooper Foundation and Department of Microbiology and Immunology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA. refaeliy@njc.org
Kenneth A Field
Brian C Turner
Andreas Trumpp
J Michael Bishop
National Jewish Health · USUniversity of Colorado Cancer Center · USUniversity of Colorado Denver · US

Funding

NCI NIH HHS CA 4438
6 · The paper itself

Abstract

The protooncogene MYC has been implicated in both the proliferation and programmed cell death of lymphoid cells, and in the genesis of lymphoid tumors. Here, we report that overexpression of MYC, as found in many lymphomas, can break immune tolerance. Mice that would otherwise be tolerant to a transgenic autoantigen mounted an immune response to the antigen if MYC was vigorously expressed in the B cell lineage. The responsive B cells converted to an activated phenotype and produced copious amounts of autoantibody that engendered immune complex disease of the kidney. MYC was required to both establish and maintain the breach of tolerance. These effects may be due to the ability of MYC to serve as a surrogate for cytokines. We found that the gene could mimic the effects of cytokines on both B cell proliferation and survival and, indeed, was required for those effects. These findings demonstrate a critical role for MYC in the response of B cells to antigen and expand the potential contributions of MYC to the genesis of lymphomas.

Indexed as

AnimalsAutoantibodiesB-LymphocytesCell DivisionCytokinesImmune ToleranceMiceMice, TransgenicProto-Oncogene Proteins c-mycReceptors, Antigen, B-CellTime FactorsAutoantibodiesCytokinesMyc protein, mouseProto-Oncogene Proteins c-mycReceptors, Antigen, B-Cell

Identifiers

PMID15753301
PMCPMC552974
OpenAlexW2097034929

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.