Evidence map›Paper›PMID 28855609›Full record

ArticleScientific reports2017

Primary patient-derived lung adenocarcinoma cell culture challenges the association of cancer stem cells with epithelial-to-mesenchymal transition.

Verena Tiran, Joerg Lindenmann, Luka Brcic, Ellen Heitzer, Stefanie Stanzer, Nassim Ghaffari Tabrizi-Wizsy, Elvira Stacher, Herbert Stoeger, Helmut H Popper, Marija Balic and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Verena TiranDivision of Oncology, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria.
Joerg LindenmannDivision of Thoracic and Hyperbaric Surgery, Medical University of Graz, A-8036, Graz, Austria.
Luka BrcicInstitute of Pathology, Medical University of Graz, A-8036, Graz, Austria.ORCID 0000-0002-9098-8416
Ellen HeitzerInstitute of Human Genetics, Medical University of Graz, A-8010, Graz, Austria.ORCID 0000-0002-8815-7859
Stefanie StanzerDivision of Oncology, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria.
Nassim Ghaffari Tabrizi-WizsySFL Chicken CAM Lab, Institute of Pathophysiology and Immunology, Medical University of Graz, A-8010, Graz, Austria.ORCID 0000-0001-6696-8717
Elvira StacherInstitute of Pathology, Medical University of Graz, A-8036, Graz, Austria.
Herbert StoegerDivision of Oncology, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria.
Helmut H PopperInstitute of Pathology, Medical University of Graz, A-8036, Graz, Austria.ORCID 0000-0003-4970-1265
Marija BalicDivision of Oncology, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria. marija.balic@medunigraz.at.
Nadia DandachiDivision of Oncology, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria. nadia.dandachi@medunigraz.at.
Medical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cancer stem cell (CSC) and epithelial-to-mesenchymal transition (EMT) models have been closely associated and used to describe both the formation of metastasis and therapy resistance. We established a primary lung cell culture from a patient in a clinically rare and unique situation of primary resistant disease. This culture consisted of two biologically profoundly distinct adenocarcinoma cell subpopulations, which differed phenotypically and genotypically. One subpopulation initiated and sustained in spheroid cell culture (LT22s) whereas the other subpopulation was only capable of growth and proliferation under adherent conditions (LT22a). In contrast to our expectations, LT22s were strongly associated with the epithelial phenotype, and expressed additionally CSC markers ALDH1 and CD133, whereas the LT22a was characterized as mesenchymal with lack of CSC markers. The LT22s cells also demonstrated an invasive behavior and mimicked gland formation. Finally, LT22s were more resistant to Cisplatin than LT22a cells. We demonstrate a primary lung adenocarcinoma cell culture derived from a patient with resistant disease, with epithelial aggressive subpopulation of cells associated with stem cell features and therapy resistance. Our findings challenge the current model associating CSC and disease resistance mainly to mesenchymal cells and may have important clinical implications.

Indexed as

Epithelial-Mesenchymal TransitionAC133 AntigenAdenocarcinomaAdultAldehyde Dehydrogenase 1 FamilyAnimalsBiomarkers, TumorChickensCisplatinDrug Resistance, NeoplasmFemaleHumansIsoenzymesLung NeoplasmsMaleMiceAC133 AntigenAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanALDH1A1 protein, mouseBiomarkers, TumorCisplatinIsoenzymesRetinal Dehydrogenase

Identifiers

PMID28855609
PMCPMC5577216
OpenAlexW2750114219

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.