Evidence map›Paper›PMID 20956327›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

B-cell activating factor and v-Myc myelocytomatosis viral oncogene homolog (c-Myc) influence progression of chronic lymphocytic leukemia.

Weizhou Zhang, Arnon P Kater, George F Widhopf, Han-Yu Chuang, Thomas Enzler, Danelle F James, Maxim Poustovoitov, Ping-Hui Tseng, Siegfried Janz, Carl Hoh and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 78 citations in OpenAlex.

  1. Unique and redundant roles of mouse BCMA, TACI, BAFF, APRIL, and IL-6 in supporting antibody-producing cells in different tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  20. Small molecules targeting c-Myc oncogene: promising anti-cancer therapeutics.International journal of biological sciences · 2014
    Review
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

13 authors at 6 institutions in 6 countries.

Weizhou ZhangLaboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, Moores Cancer Center, University of California at San Diego, La Jolla, CA 92093, USA.
Arnon P Kater
George F Widhopf
Han-Yu Chuang
Thomas Enzler
Danelle F James
Maxim Poustovoitov
Ping-Hui Tseng
Siegfried Janz
Carl Hoh
Harvey Herschman
Michael Karin
Thomas J Kipps
University of California, Los Angeles · USMoores Cancer CenterAcademic Medical Center · NLNational Yang Ming Chiao Tung University · TWStanford Medicine · USUniversity of Iowa · US

Funding

REGULATION OF NFKB AND IKK BY PROINFLAMMATORY STIMULIR01AI043477 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL · 1998 to 2017
$7.4M
NIAID NIH HHS R01 AI043477
6 · The paper itself

Abstract

Mice bearing a v-Myc myelocytomatosis viral oncogene homolog (c-Myc) transgene controlled by an Ig-alpha heavy-chain enhancer (iMyc(Cα) mice) rarely develop lymphomas but instead have increased rates of memory B-cell turnover and impaired antibody responses to antigen. We found that male progeny of iMyc(Cα) mice mated with mice transgenic (Tg) for CD257 (B-cell activating factor, BAFF) developed CD5(+) B-cell leukemia resembling human chronic lymphocytic leukemia (CLL), which also displays a male gender bias. Surprisingly, leukemic cells of Myc/Baff Tg mice expressed higher levels of c-Myc than did B cells of iMyc(Cα) mice. We found that CLL cells of many patients with progressive disease also expressed high amounts of c-MYC, particularly CLL cells whose survival depends on nurse-like cells (NLC), which express high-levels of BAFF. We find that BAFF could enhance CLL-cell expression of c-MYC via activation the canonical IκB kinase (IKK)/NF-κB pathway. Inhibition of the IKK/NF-κB pathway in mouse or human leukemia cells blocked the capacity of BAFF to induce c-MYC or promote leukemia-cell survival and significantly impaired disease progression in Myc/Baff Tg mice. This study reveals an important relationship between BAFF and c-MYC in CLL which may affect disease development and progression, and suggests that inhibitors of the canonical NF-κB pathway may be effective in treatment of patients with this disease.

Indexed as

Genes, mycAnimalsB-Cell Activating FactorB-LymphocytesFemaleGene Expression Regulation, LeukemicHumansImmunologic MemoryLeukemia, Lymphocytic, Chronic, B-CellMaleMiceMice, TransgenicNF-kappa BProto-Oncogene Proteins c-mycB-Cell Activating FactorMYC protein, humanMyc protein, mouseNF-kappa BProto-Oncogene Proteins c-mycTnfsf13b protein, mouse

Identifiers

PMID20956327
PMCPMC2973856
OpenAlexW2156834005

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.