Evidence map›Paper›PMID 18176602›Full record

ReviewOncogene2008

Obstacles to effective Toll-like receptor agonist therapy for hematologic malignancies.

D E Spaner, R Foley, J Galipeau, J Bramson

Abstract readEvaluation StudyReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Maltose-binding protein isolated from Escherichia coli induces Toll-like receptor 2-mediated viability in U937 cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011
    Article
  7. Article
  8. Article
  9. 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

4 authors at 3 institutions in 1 country.

D E SpanerDivision of Molecular and Cellular Biology, Research Institute, Sunnybrook and Women's College Health Sciences Center, Toronto, Canada. david.spaner@swri.ca
R Foley
J Galipeau
J Bramson
McMaster University · CAMcGill University · CASunnybrook Health Science Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has long been noted that products of microorganisms have clinical activity against hematologic malignancies. Recent advances suggest that Toll-like receptors (TLRs) activated by ligands in the microbial preparations might account for some of this activity, and that defined TLR agonists might improve the clinical efficacy of this approach. A potentially important mechanism of action of TLR agonists is their ability to cause tumor cells to differentiate into a 'tolerized' state in which they become highly sensitive to cytotoxic effector cells and chemotherapeutic drugs. TLR agonists as single agents have strong activity against cutaneous leukemias and lymphomas but are not as effective against systemic disease. A possible reason for this discrepancy is the hypoxic internal tumor microenvironment, which promotes glycolytic metabolism, and the presence of suppressive cytokines, prostaglandins and nucleosides that prevent strong TLR signaling in cancer cells. Accordingly, concomitant use of agents to counter this intrinsic microenvironmental inhibition, together with TLR agonists, may prove to be an effective treatment strategy for the hematologic malignancies.

Indexed as

Antineoplastic AgentsBacterial ToxinsCombined Modality TherapyHematologic NeoplasmsHumansInfectionsModels, BiologicalSignal TransductionToll-Like ReceptorsTreatment FailureTreatment OutcomeAntineoplastic AgentsBacterial ToxinsToll-Like Receptors

Identifiers

PMID18176602
OpenAlexW1990113015

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.