Evidence map›Paper›PMID 16751281›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

The role of NF-{kappa}B-1 and NF-{kappa}B-2-mediated resistance to apoptosis in lymphomas.

Leon Bernal-Mizrachi, Christine M Lovly, Lee Ratner

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Article
  7. FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025
    Review
  8. Article
  9. Review
  10. Jozimine AInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Targeted In Vivo Delivery of NF-κB Decoy Inhibitor Augments Sensitivity of B Cell Lymphoma to Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article

5 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 at 2 institutions in 1 country.

Leon Bernal-MizrachiDivision of Molecular Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Christine M Lovly
Lee Ratner
Molecular Oncology (United States) · USWashington University in St. Louis · US

Funding

PROLIFERATIVE EFFECTS OF HTLV1R01CA063417 · NCI · WASHINGTON UNIVERSITY · PI RATNER, LEE · 1995 to 2017
$3.7M
Chemo/Antiretroviral therapy for HTLV-1 ATLLR01CA105218 · NCI · WASHINGTON UNIVERSITY · PI RATNER, LEE · 2003 to 2005
$681k
NCI NIH HHS CA10073NCI NIH HHS CA105218NCI NIH HHS CA63417NCI NIH HHS R01 CA063417NCI NIH HHS R01 CA105218
6 · The paper itself

Abstract

The NF-kappaB pathways have been implicated in tumorigenesis in several lymphoid malignancies, including non-Hodgkin's and Hodgkin's lymphomas. However, the antiapoptotic functions and the mechanism responsible for signaling through each NF-kappaB pathway remain to be elucidated. In the current study, lymphoma cell lines with constitutively active NF-kappaB were found to be resistant to inducers of the extrinsic and intrinsic apoptosis pathways. Resistance to cell death resulted from blocks early and late in the apoptosis cascade. Several NF-kappaB target genes were overexpressed in these cell lines, including Bcl-xL, Fas-associated death domain-like IL-1beta-converting enzyme inhibitor protein, cellular inhibitor of apoptosis, and X inhibitor of apoptosis. Inhibition of the canonical or noncanonical NF-kappaB pathways with small interfering RNAs or adenovirus expressing a stable form of inhibitor of NF-kappaB (IkappaB) enhanced sensitivity to apoptosis inducers and resulted in lower levels of Bcl-xL or Fas-associated death domain-like IL-1beta-converting enzyme inhibitor protein, cellular inhibitor of apoptosis, and X inhibitor of apoptosis. These findings demonstrate an important role of both NF-kappaB pathways in mediating resistance to apoptosis and distinctive antiapoptotic downstream target gene profiles responsible for this effect.

Indexed as

AdenoviridaeApoptosisbcl-X ProteinCASP8 and FADD-Like Apoptosis Regulating ProteinCell Line, TumorHumansI-kappa B ProteinsInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsLymphomaNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitProtein IsoformsRNA, Small InterferingSignal TransductionBCL2L1 protein, humanbcl-X ProteinCASP8 and FADD-Like Apoptosis Regulating ProteinCFLAR protein, humanI-kappa B ProteinsInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsNF-KappaB Inhibitor alphaNF-kappa B p50 SubunitNFKB1 protein, humanNFKBIA protein, humanProtein IsoformsRNA, Small Interfering

Identifiers

PMID16751281
PMCPMC1482593
OpenAlexW2005798625

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.