Evidence map›Paper›PMID 36216730›Full record

ReviewTrends in cancer2023

How cancer cells make and respond to interferon-I.

HyeonJoo Cheon, Yuxin Wang, Samantha M Wightman, Mark W Jackson, George R Stark

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
18.4field-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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.

  1. Pooled it
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  15. Natural and Engineered Cytokines as Cancer Therapeutics.Annual review of cancer biology · 2026
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42 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

HyeonJoo CheonDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI, USA.
Yuxin WangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Samantha M WightmanDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Mark W JacksonDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
George R StarkDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: starkg@ccf.org.
Cleveland Clinic Lerner College of Medicine · USUniversity School · USWayne State University · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA · 1994 to 2020
$35.6M
Targeting Oncostatin M-Receptor to Suppress Metastasis and Therapy FailureR01CA252224 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 2021 to 2025
$2.0M
PD-L1 inhibition promotes type I interferon responses, enhancing chemotherapy-induced cytotoxicity in cancer cellsR21CA252387 · NCI · WAYNE STATE UNIVERSITY · PI CHEON, HYEONJOO · 2021 to 2022
$414k
p53 mutation induces constitutive expression of interferon beta, enhancing the resistance of cancer cells to DNA damageR03CA215941 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI CHEON, HYEONJOO · 2017 to 2018
$159k
NCI NIH HHS P01 CA062220NCI NIH HHS R01 CA252224NCI NIH HHS R03 CA215941NCI NIH HHS R21 CA252387
6 · The paper itself

Abstract

Acute exposure of cancer cells to high concentrations of type I interferon (IFN-I) drives growth arrest and apoptosis, whereas chronic exposure to low concentrations provides important prosurvival advantages. Tyrosine-phosphorylated IFN-stimulated gene (ISG) factor 3 (ISGF3) drives acute deleterious responses to IFN-I, whereas unphosphorylated (U-)ISGF3, lacking tyrosine phosphorylation, drives essential constitutive prosurvival mechanisms. Surprisingly, programmed cell death-ligand 1 (PD-L1), often expressed on the surfaces of tumor cells and well recognized for its importance in inactivating cytotoxic T cells, also has important cell-intrinsic protumor activities, including dampening acute responses to cytotoxic high levels of IFN-I and sustaining the expression of the low levels that benefit tumors. More thorough understanding of the newly recognized complex roles of IFN-I in cancer may lead to the identification of novel therapeutic strategies.

Indexed as

InterferonsNeoplasmsHumansInterferon-Stimulated Gene Factor 3Interferon-Stimulated Gene Factor 3, gamma SubunitSignal TransductionTyrosineInterferonsInterferon-Stimulated Gene Factor 3Interferon-Stimulated Gene Factor 3, gamma SubunitTyrosineDNA damageinterferonPD-L1STAT2triple-negative breast cancer

Identifiers

PMID36216730
PMCPMC9797472
OpenAlexW4303575274

What OpenQuestion holds

Textmetadata
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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.