Evidence map›Paper›PMID 24675568›Full record

ArticleCancers2014

The Role of STAT3 in Non-Small Cell Lung Cancer.

Daijiro Harada, Nagio Takigawa, Katsuyuki Kiura

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06502249 (Modulatory Effect of Prodigiosin or Pioglitazone on Tumor Immune Microenvironment and the Crosstalk to Immune-Checkpoint Protein), which is not on this map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
7.3field-weighted citation impact, top 2% 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.

NCT06502249 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Modulatory Effect of Prodigiosin or Pioglitazone on Tumor Immune Microenvironment and the Crosstalk to Immune-Checkpoint Protein(s)

TypeobservationalSponsorAin Shams UniversityRan2026 to 2028Enrolled60ConditionsLung Cancer, NSCLC
3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 190 citations in OpenAlex.

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50 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

3 authors at 3 institutions in 1 country.

Daijiro HaradaDepartment of Thoracic Oncology, NHO Shikoku Cancer Center, 160 Minami-Umemoto-cho, Matsuyama 791-0280, Japan. h401068@yahoo.co.jp.
Nagio TakigawaDepartment of General Internal Medicine 4, Kawasaki Medical School, 2-1-80 Nakasange, Kita-ku, Okayama 700-8505, Japan. ntakigaw@gmail.com.
Katsuyuki KiuraDepartment of Allergy and Respiratory Medicine, Okayama University Hospital, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan. kkiura@md.okayama-u.ac.jp.
Kawasaki Medical School · JPOkayama University Hospital · JPShikoku Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent phosphorylation of signal transducer and activator of transcription 3 (STAT3) has been demonstrated in 22%~65% of non-small cell lung cancers (NSCLC). STAT3 activation is mediated by receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and MET, cytokine receptors, such as IL-6, and non-receptor kinases, such as Src. Overexpression of total or phosphorylated STAT3 in resected NSCLC leads to poor prognosis. In a preclinical study, overexpression of STAT3 was correlated with chemoresistance and radioresistance in NSCLC cells. Here, we review the role of STAT3 and the mechanisms of treatment resistance in malignant diseases, especially NSCLC. As STAT3 is a critical mediator of the oncogenic effects of EGFR mutations, we discuss STAT3 pathways in EGFR-mutated NSCLC, referring to mechanisms of EGFR tyrosine kinase inhibitor resistance.

Identifiers

PMID24675568
PMCPMC4074799
OpenAlexW2092338119

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.