Evidence map›Paper›PMID 20454508›Full record

ArticleNeoplasia (New York, N.Y.)2010

The rGel/BLyS fusion toxin inhibits diffuse large B-cell lymphoma growth in vitro and in vivo.

Mi-Ae Lyu, Deepak Rai, Kwang Seok Ahn, Bokyung Sung, Lawrence H Cheung, John W Marks, Bharat B Aggarwal, Ricardo C T Aguiar, Varsha Gandhi, Michael G Rosenblum

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Toxic proteins application in cancer therapy.Molecular biology reports · 2021
    Review
  5. Advances on Tumor-Targeting Delivery of Cytotoxic Proteins.ACS pharmacology & translational science · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 1 country.

Mi-Ae LyuImmunopharmacology and Targeted Therapy Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Deepak Rai
Kwang Seok Ahn
Bokyung Sung
Lawrence H Cheung
John W Marks
Bharat B Aggarwal
Ricardo C T Aguiar
Varsha Gandhi
Michael G Rosenblum
The University of Texas MD Anderson Cancer Center · USTarget (United States) · USThe University of Texas Health Science Center · USThe University of Texas Health Science Center at San Antonio · US

Funding

UT M.D. Anderson Cancer Center Lymphoma SPOREP50CA136411 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KWAK, LARRY W · 2009 to 2011
$1.5M
NCI NIH HHS CA136411NCI NIH HHS P50 CA136411
6 · The paper itself

Abstract

Diffuse large B-cell lymphoma (DLBCL) is an aggressive subtype of B-cell non-Hodgkin lymphoma (NHL) and accounts for 30%to 40%of NHL. Molecules targeting nuclear factor-kappaB (NF-kappaB) are expected to be of therapeutic value in those tumors where NF-kappaB seems to play a unique survival role such as activated B-cell (ABC)-subtype DLBCL. We previously generated a rGel/BLyS fusion toxin for receptor-mediated delivery of the rGel toxin specifically to malignant B cells. In this study, we examined this fusion toxin for its ability to suppress DLBCL growth in vitro and in vivo. rGel/BLyS was specifically cytotoxic to DLBCL lines expressing all three BLyS receptors and constitutively active NF-kappaB. Treatment with rGel/BLyS induced down-regulation of the phosphorylation of inhibitory subunit of NF-kappaB (IkappaB-alpha), inhibition of NF-kappaB DNA-binding activity, and accumulation of IkappaB-alpha. In agreement with these results, we additionally found that rGel/BLyS downregulated levels of several NF-kappaB targets including Bcl-xL, Mcl-1, survivin, and x-chromosome linked inhibitor-of-apoptosis. Treatment also induced up-regulation of Bax and apoptosis through caspase-3 activation and poly ADP-ribose polymerase cleavage. Importantly, rGel/BLyS significantly inhibited tumor growth (P < .05) in a DLBCL xenograft model. Thus, our results indicate that rGel/BLyS is an excellent candidate for the treatment of aggressive NHLs that are both dependent on NF-kappaB and are resistant to conventional chemotherapeutic regimens.

Indexed as

AnimalsAntineoplastic AgentsApoptosisB-Cell Activating FactorBlotting, WesternCell Line, TumorCell ProliferationCell SeparationDrug Delivery SystemsElectrophoretic Mobility Shift AssayFlow CytometryFluorescent Antibody TechniqueHumansI-kappa B ProteinsIn Situ Nick-End LabelingLymphoma, Large B-Cell, DiffuseAntineoplastic AgentsB-Cell Activating FactorGEL protein, Gelonium multiflorumI kappa B beta proteinI-kappa B ProteinsNF-kappa BRecombinant Fusion ProteinsRibosome Inactivating Proteins, Type 1Toxins, Biological

Identifiers

PMID20454508
PMCPMC2864474
OpenAlexW1237125621

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.