Evidence map›Paper›PMID 42683051›Full record

ReviewExploration of targeted anti-tumor therapy2026

Mitochondrial checkpoint for interferon responses in macrophages.

Andreas O Mieland, Oliver H Krämer

Abstract readReview
In one paragraph

Review in Exploration of targeted anti-tumor therapy, 2026. 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
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.

No citing paper in PubMed yet.

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

2 authors.

Andreas O MielandInstitute of Toxicology, University Medical Center of Johannes Gutenberg University, 55131 Mainz, Germany.ORCID https://orcid.org/0000-0002-8672-0708
Oliver H KrämerInstitute of Toxicology, University Medical Center of Johannes Gutenberg University, 55131 Mainz, Germany.ORCID https://orcid.org/0000-0003-3973-045X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A functional immune system is a key antagonist of cancer cell growth. Cytokines such as interferons (IFNs) promote the onset of inflammation, turn cells into an anti-viral state, and shape the dynamic tumor-immune cell interactome. Recent work illustrates how type I IFNs contribute to the resolution of inflammatory conditions. This involves macrophage-mediated efferocytosis for the clearance of apoptotic cells and the intrinsic capacity of type I IFNs to restrict their own autocrine signaling loops via the IFN-stimulated gene 15 (ISG15) protein. We discuss how this may affect tumor cells and how acetylation-dependent processes can affect the phosphorylation-dependent signaling cascades that augment IFN-dependent gene expression.

Indexed as

acetylationefferocytosisgene expressionhistone deacetylase (HDAC)interferonISG15JAK-STATmacrophage

Identifiers

PMID42683051
PMCPMC13530846

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.