Evidence map›Paper›PMID 22440007›Full record

ReviewClinical lymphoma, myeloma & leukemia2012

TRAF6 activation in multiple myeloma: a potential therapeutic target.

Hong Liu, Samantha Tamashiro, Stavroula Baritaki, Manuel Penichet, Youhua Yu, Haiming Chen, James Berenson, Benjamin Bonavida

Abstract readReview
In one paragraph

Review in Clinical lymphoma, myeloma & leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Novel Biomarkers for Diagnosis and Monitoring of Immune Thrombocytopenia.International journal of molecular sciences · 2023
    Review
  6. Article
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  10. Review
  11. Article
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  15. Review
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  18. Cinchonine induces apoptosis of HeLa and A549 cells through targeting TRAF6.Journal of experimental & clinical cancer research : CR · 2017
    Article
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Hong LiuDepartment of Microbiology, Immunology, and Molecular Genetics, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Samantha Tamashiro
Stavroula Baritaki
Manuel Penichet
Youhua Yu
Haiming Chen
James Berenson
Benjamin Bonavida
University of California, Los Angeles · USChinese Academy of Medical Sciences & Peking Union Medical College · CNInstitute for Myeloma & Bone Cancer Research · US

Funding

Anti-TfR IgG3-Av: A New Drug Against Multiple MyelomaR01CA107023 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PENICHET, MANUEL L · 2005 to 2009
$1.7M
NCI NIH HHS R01 CA107023
6 · The paper itself

Abstract

Multiple myeloma (MM) is an incurable B-lymphocyte malignancy. New therapeutic options have become available during the past several years; however nearly all patients acquire resistance to currently available therapeutic agents. Mechanisms contributing to the pathogenesis and chemoresistance of MM include genetic abnormalities, chromosomal translocations, gene mutations, the interaction between MM cells and the bone marrow microenvironment, and defects in the apoptotic signaling pathways. Survival signaling pathways associated with the pathogenesis of MM and bone marrow stromal cells play crucial roles in promoting growth, survival, adhesion, immortalization, angiogenesis, and drug resistance. The receptor activator of nuclear factor-kappa B/receptor activator of nuclear factor-kappa B ligand/tumor necrosis factor receptor-associated factor (RANK/RANKL-TRAF6) signal pathway mediates osteolytic bone lesions through the activation of the NF-κB and Janus kinase/signal transducer and activator of transcription (JNK) pathways in osteoclast precursor cells and thus contributes to the main clinical manifestations of bone disease. TRAF6 has also been identified as a ligase for Akt ubiquitination and membrane recruitment and its phosphorylation on growth factor stimulation. The inhibition of TRAF6 by silencing RNA or by decoy peptides decreases MM tumor cell proliferation and increases apoptosis as well as bone resorption. Some proteasome inhibitors and benzoxadiazole derivatives showed inhibitory effects on the activity and function of TRAF6. Overall, we propose that TRAF6 may be considered as a potential therapeutic target for the treatment of MM.

Indexed as

AnimalsBone ResorptionDrug Resistance, NeoplasmGene ExpressionHumansMolecular Targeted TherapyMultiple MyelomaSignal TransductionTNF Receptor-Associated Factor 6TNF Receptor-Associated Factor 6

Identifiers

PMID22440007
PMCPMC3799862
OpenAlexW2004758487

What OpenQuestion holds

Textmetadata
LicenceTDM
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.