Evidence map›Paper›PMID 24632612›Full record

ArticleOncogene2015

Heterogeneity in ERK activity as visualized by in vivo FRET imaging of mammary tumor cells developed in MMTV-Neu mice.

Y Kumagai, H Naoki, E Nakasyo, Y Kamioka, E Kiyokawa, M Matsuda

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. ERK Activity Imaging During Migration of Living Cells In Vitro and In Vivo.International journal of molecular sciences · 2019
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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

6 authors at 3 institutions in 1 country.

Y KumagaiDepartment of Bioimaging and Cell Signaling, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
H NaokiInnovative Techno-Hub for Integrated Medical Bio-Imaging, Kyoto University, Kyoto, Japan.
E NakasyoLife & Industrial Products Development Department 1, R&D Division, Olympus Corporation, Hachioji, Japan.
Y Kamioka1] Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Kyoto, Japan [2] Imaging Platform for Spatio-Temporal Information, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
E KiyokawaDepartment of Oncologic Pathology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa, Japan.
M Matsuda1] Department of Bioimaging and Cell Signaling, Graduate School of Biostudies, Kyoto University, Kyoto, Japan [2] Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JPKanazawa Medical University · JPOlympus (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human epidermal growth factor receptor2/Neu, which is overexpressed in about 30% of human breast cancers, transduces growth signals in large part via the Ras-Raf-MEK-ERK pathway. Nevertheless, it is a matter of controversy whether high ERK activity in breast cancer tissues correlates with better or worse prognosis, leaving the role of ERK activity in the progression of breast cancers unresolved. To address this issue, we live-imaged ERK activity in mammary tumors developed in mouse mammary tumor virus-Neu transgenic mice, which had been crossed with transgenic mice expressing a Förster resonance energy transfer biosensor for ERK. Observation of the tumor by two-photon microscopy revealed significant heterogeneity in ERK activity among the mammary tumor cells. The level of ERK activity in each cell was stable up to several hours, implying a robust mechanism that maintained the ERK activity within a limited range. By sorting the mammary tumor cells on the basis of their ERK activity, we found that ERK(high) cells less efficiently generated tumorspheres in vitro and tumors in vivo than did ERK(low) cells. In agreement with this finding, the expressions of the cancer stem cell markers CD49f, CD24 and CD61 were decreased in ERK(high) cells. These observations suggest that high ERK activity may suppress the self-renewal of mammary cancer stem cells.

Indexed as

Fluorescence Resonance Energy TransferAnimalsAntineoplastic AgentsBenzamidesComputer SystemsDiphenylamineExtracellular Signal-Regulated MAP KinasesFemaleGenes, erbB-2Mammary Neoplasms, ExperimentalMammary Tumor Virus, MouseMiceMice, TransgenicMolecular ImagingNeoplasm MetastasisProtein Kinase InhibitorsAntineoplastic AgentsBenzamidesDiphenylamineExtracellular Signal-Regulated MAP KinasesmirdametinibProtein Kinase Inhibitors

Identifiers

PMID24632612
OpenAlexW2085198453

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.