Evidence map›Paper›PMID 15298723›Full record

ReviewCancer science2004

ETS transcription factors: possible targets for cancer therapy.

Tsuneyuki Oikawa

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 182 citations in OpenAlex.

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  20. Lumefantrine, an antimalarial drug, reverses radiation and temozolomide resistance in glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article

26 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

1 author at 1 institution in 1 country.

Tsuneyuki OikawaDepartment of Cell Genetics, Sasaki Institute, Chiyoda-ku, Tokyo 101-0062, Japan. oikawa@sasaki.or.jp
Sasaki Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ets family (ETS) transcription factors, characterized by an evolutionally conserved Ets domain, play important roles in cell development, cell differentiation, cell proliferation, apoptosis and tissue remodeling. Most of them are downstream nuclear targets of Ras-MAP kinase signaling, and the deregulation of ETS genes results in the malignant transformation of cells. Several ETS genes are rearranged in human leukemia and Ewing tumors to produce chimeric oncoproteins. Furthermore, the aberrant expression of several ETS genes is often observed in various types of human malignant tumors. Considering that some ETS transcription factors are involved in malignant transformation and tumor progression, including invasion, metastasis and neo-angiogenesis through the activation of cancer-related genes, they could be potential molecular targets for selective cancer therapy.

Indexed as

Cell Transformation, NeoplasticHumansLeukemiaLymphomaNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsNeovascularization, PathologicPrognosisProto-Oncogene ProteinsProto-Oncogene Proteins c-etsSignal TransductionTranscription FactorsProto-Oncogene ProteinsProto-Oncogene Proteins c-etsTranscription Factors

Identifiers

PMID15298723
PMCPMC11159856
OpenAlexW2056372829

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.