Evidence map›Paper›PMID 26705127›Full record

ArticleMedical molecular morphology2016

Increased phosphorylation of ERK1/2 is associated with worse chemotherapeutic outcome and a poor prognosis in advanced lung adenocarcinoma.

Ichiro Tsujino, Yoko Nakanishi, Hisato Hiranuma, Tetsuo Shimizu, Yukari Hirotani, Sumie Ohni, Yasushi Ouchi, Noriaki Takahashi, Norimichi Nemoto, Shu Hashimoto

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In one paragraph

Article in Medical molecular morphology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Oncogene KRAS activates fatty acid synthase, resulting in specific ERK and lipid signatures associated with lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  6. Article
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

10 authors.

Ichiro TsujinoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan. tsujino.ichiro@nihon-u.ac.jp.
Yoko NakanishiDivision of Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Hisato HiranumaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Tetsuo ShimizuDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Yukari HirotaniDivision of Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Sumie OhniDivision of Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Yasushi OuchiDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Noriaki TakahashiDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Norimichi NemotoDivision of Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.
Shu HashimotoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Ohyaguchikamimachi, Itabashi-ku, Tokyo, 173-8610, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive activation of extracellular signal-regulated kinase (ERK)1/2 pathway, that is activated by various stimuli including growth factors and oncogenic driver mutations, is observed in various cancers. However, the difference of the activated levels of the pathway is still unclear in clinical significances. The aim of this study was to investigate the effect of different ERK1/2 pathway activation, assessed by the expression levels of phosphorylated (p) ERK1/2, on the prognosis of advanced lung adenocarcinoma patients. Paraffin-embedded lung biopsy samples were obtained from 85 lung adenocarcinoma patients. Correlation between pERK1/2 expression levels that were assessed by immunohistochemistry (IHC) analysis and oncogenic driver mutation status, clinicopathological factors, outcome from standard anticancer therapies, and prognosis was investigated. Varying levels of pERK1/2 expression were observed in 68 (80.0 %) patients. The overall survival was significantly reduced in patients with higher pERK1/2 expression in comparison to those with lower expression levels (P = 0.03). In particular, higher pERK1/2 expression levels correlated with worse performance status and worse clinical outcome. Thus, the IHC analysis of pERK1/2 expression levels may predict patient prognosis in advanced lung adenocarcinoma. Inhibition of ERK1/2 pathway activated by various signals may improve the effects of standard chemotherapies and the clinical condition of patients with advanced cancer.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAdultAgedAged, 80 and overAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesFemaleHumansImmunohistochemistryLung NeoplasmsMaleMiddle AgedMutationNeoplasm StagingPhosphorylationAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesChemotherapyEGFRKRASLung adenocarcinomapERK1/2Prognosis

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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.