Evidence map›Paper›PMID 27186512›Full record

ReviewTranslational lung cancer research2016

The role of epithelial to mesenchymal transition in resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer.

Kristine Raaby Jakobsen, Christina Demuth, Boe Sandahl Sorensen, Anders Lade Nielsen

Open access · hybridAbstract readReview
In one paragraph

Review in Translational lung cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
8.2field-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.

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

71 citing papers in PubMed, 102 citations in OpenAlex.

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  19. SOS2 regulates the threshold of mutantbioRxiv : the preprint server for biology · 2023
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11 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

4 authors at 2 institutions in 1 country.

Kristine Raaby Jakobsen1 Department of Biomedicine, Aarhus University, Aarhus, Denmark ; 2 Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Christina Demuth1 Department of Biomedicine, Aarhus University, Aarhus, Denmark ; 2 Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Boe Sandahl Sorensen1 Department of Biomedicine, Aarhus University, Aarhus, Denmark ; 2 Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Anders Lade Nielsen1 Department of Biomedicine, Aarhus University, Aarhus, Denmark ; 2 Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Aarhus University · DKAarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of the epidermal growth factor receptor (EGFR) is an important strategy when treating non-small cell lung cancer (NSCLC) patients. However, intrinsic resistance or development of resistance during the course of treatment constitutes a major challenge. The knowledge on EGFR-directed tyrosine kinase inhibitors (TKIs) and their biological effect keeps increasing. Within the group of patients with EGFR mutations some benefit to a much higher degree than others, and for patients lacking EGFR mutations a subset experience an effect. Up to 70% of patients with EGFR mutations and 10-20% of patients without EGFR mutations initially respond to the EGFR-TKI erlotinib, but there is a severe absence of good prognostic markers. Despite initial effect, all patients acquire resistance to EGFR-TKIs. Multiple mechanisms have implications in resistance development, but much is still to be explored. Epithelial to mesenchymal transition (EMT) is a transcriptionally regulated phenotypic shift rendering cells more invasive and migratory. Within the EMT process lays a need for external or internal stimuli to give rise to changes in central signaling pathways. Expression of mesenchymal markers correlates to a bad prognosis and an inferior response to EGFR-TKIs in NSCLC due to the contribution to a resistant phenotype. A deeper understanding of the role of EMT in NSCLC and especially in EGFR-TKI resistance-development constitute one opportunity to improve the benefit of TKI treatment for the individual patient. Many scientific studies have linked the EMT process to EGFR-TKI resistance in NSCLC and our aim is to review the role of EMT in both intrinsic and acquired resistance to EGFR-TKIs.

Indexed as

Epidermal growth factor receptor (EGFR)epithelial to mesenchymal transition (EMT)non-small cell lung cancer (NSCLC)tyrosine kinase inhibitor (TKI)

Identifiers

PMID27186512
PMCPMC4858579
OpenAlexW2344820605

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.