Evidence map›Paper›PMID 11948426›Full record

ArticleOncogene2002

Frequent and histological type-specific inactivation of 14-3-3sigma in human lung cancers.

Hirotaka Osada, Yoshio Tatematsu, Yasushi Yatabe, Taku Nakagawa, Hiroyuki Konishi, Tomoko Harano, Ekmel Tezel, Minoru Takada, Takashi Takahashi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.6field-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

47 citing papers in PubMed, 145 citations in OpenAlex.

  1. Article
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  12. 14-3-3 isoforms bind directly exon B of the 5'-UTR of human surfactant protein A2 mRNA.American journal of physiology. Lung cellular and molecular physiology · 2015
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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

9 authors at 1 institution in 1 country.

Hirotaka OsadaDivision of Molecular Oncology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. hosada@aichi-cc.jp
Yoshio Tatematsu
Yasushi Yatabe
Taku Nakagawa
Hiroyuki Konishi
Tomoko Harano
Ekmel Tezel
Minoru Takada
Takashi Takahashi
Aichi Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One isoform of the 14-3-3 family, 14-3-3sigma, plays a crucial role in the G2 checkpoint by sequestering Cdc2-cyclinB1 in the cytoplasm, and the expression of 14-3-3sigma is frequently lost in breast cancers. This loss of expression is thought to cause a G2 checkpoint defect, resulting in chromosomal aberrations. Since lung cancers frequently carry numerous chromosomal aberrations, we examined the DNA methylation status and expression level of the 14-3-3sigma gene in 37 lung cancer cell lines and 30 primary lung tumor specimens. We found that small cell lung cancer (SCLC) cell lines frequently showed DNA hypermethylation (9 of 13 lines, 69%), and subsequent silencing of the 14-3-3sigma gene. Among non-small cell lung cancers (NSCLC), large cell lung cancer cell lines showed frequent hypermethylation and silencing of 14-3-3sigma (4 or 7 lines, 57%). In contrast, in other NSCLC cell lines, hypermethylation occurred very rarely (1 of 17 lines, 6%). All eight primary SCLC specimens examined also showed a loss or significant reduction in 14-3-3sigma expression in vivo, while a loss or reduction of 14-3-3sigma expression was very rare in primary NSCLC specimens (1 of 22 tissues, 5%). This is the first description that indicates lung cancers frequently show significant inactivation of the 14-3-3sigma gene mainly due to DNA hypermethylation in SCLC, but rarely in NSCLC, suggesting involvement of the 14-3-3sigma gene in lung tumorigenesis in a histological type-specific manner.

Indexed as

Biomarkers, TumorExonucleasesGene Expression Regulation, NeoplasticGene SilencingNeoplasm Proteins14-3-3 ProteinsCarcinoma, Non-Small-Cell LungCarcinoma, Small CellDNA MethylationDNA, NeoplasmExoribonucleasesHumansLung NeoplasmsProtein BiosynthesisProteinsRNA, Neoplasm14-3-3 ProteinsBiomarkers, TumorDNA, NeoplasmExonucleasesExoribonucleasesNeoplasm ProteinsProteinsRNA, NeoplasmSFN protein, human

Identifiers

PMID11948426
OpenAlexW2330398072

What OpenQuestion holds

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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.