Evidence map›Paper›PMID 19055946›Full record

ReviewAdvances in cancer research2008

IFN inducibility of major histocompatibility antigens in tumors.

Barbara Seliger, Francisco Ruiz-Cabello, Federico Garrido

Abstract readReview
In one paragraph

Review in Advances in cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
23.9field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 94 citations in OpenAlex.

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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 2 countries.

Barbara SeligerMartin Luther University Halle-Wittenberg, Institute of Medical Immunology, Halle, Germany.
Francisco Ruiz-Cabello
Federico Garrido
Universidad de Granada · ESMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferons represent a protein family with pleiotropic functions including immunomodulatory, cytostatic, and cytotoxic activities. Based on these effects, interferons are involved in innate as well as adaptive immunity, thereby shaping the tumor host immune responses. These cytokines, alone or in combination, have been successfully implemented for the treatment of some malignancies. However, it has been recently demonstrated that tumor cells could be resistant to interferon treatment, which may be associated with an escape of tumor cells from immune surveillance. Therefore, the aim of this chapter is to summarize the frequency of impaired interferon signal transduction, their underlying molecular mechanisms, and their clinical relevance.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntigens, NeoplasmBase SequenceHumansInterferon-alphaInterferon-gammaMajor Histocompatibility ComplexModels, BiologicalModels, GeneticMolecular Sequence DataNeoplasmsPromoter Regions, GeneticSignal TransductionT-LymphocytesAntigens, NeoplasmInterferon-alphaInterferon-gamma

Identifiers

PMID19055946
PMCPMC7125809
OpenAlexW1571428739

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.