Evidence map›Paper›PMID 33941535›Full record

ArticleCancer immunology research2021

Reversing Imatinib's Immunosuppressive Effects by Modulating Type I IFN Signaling.

David A Largaespada

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Cancer immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 93% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

David A LargaespadaMasonic Cancer Center, University of Minnesota, Minneapolis, Minnesota. larga002@umn.edu.
University of Minnesota Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal pathway inhibition is a well-validated approach for treating cancers driven by activated kinases such as KIT. However, kinase inhibitors may make tumor cells less responsive to tumor immune surveillance and less sensitive to immunotherapies. In this issue, Liu and colleagues report that, in a mouse model, inhibition of oncogenic KIT in gastrointestinal stromal tumors reduces type I interferon (IFN) production and signaling, and the effectiveness of the immune system in controlling tumor growth. They were able to partially overcome the immunosuppressive effects of KIT inhibition using agonists of the type I IFN response, pointing the way toward intelligently combining kinase inhibitors and immune modulators for therapy.

Indexed as

Gastrointestinal Stromal TumorsProto-Oncogene Proteins c-kitAnimalsImatinib MesylateMiceSignal TransductionImatinib MesylateProto-Oncogene Proteins c-kit

Identifiers

PMID33941535
OpenAlexW3159600144

What Socratic 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 Socratic graph.