Evidence map›Paper›PMID 25034785›Full record

ArticleCell death and differentiation2014

Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer.

A Zeuner, F Francescangeli, P Contavalli, G Zapparelli, T Apuzzo, A Eramo, M Baiocchi, M L De Angelis, M Biffoni, G Sette and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.8field-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

63 citing papers in PubMed, 112 citations in OpenAlex.

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  18. [Lung Cancer Stem-like Cells and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022
    Review
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  20. Article

3 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

13 authors at 1 institution in 1 country.

A ZeunerDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
F FrancescangeliDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
P ContavalliDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
G ZapparelliDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
T ApuzzoDepartment of Surgical and Oncological Sciences, University of Palermo, Palermo 90128, Italy.
A EramoDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
M BaiocchiDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
M L De AngelisDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
M BiffoniDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome 00161, Italy.
G SetteRegina Elena National Cancer Institute, Rome, Italy.
M TodaroDepartment of Surgical and Oncological Sciences, University of Palermo, Palermo 90128, Italy.
G StassiDepartment of Surgical and Oncological Sciences, University of Palermo, Palermo 90128, Italy.
R De MariaRegina Elena National Cancer Institute, Rome, Italy.
Istituto Superiore di Sanità · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL. In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC.

Indexed as

AnimalsAntineoplastic Agentsbcl-X ProteinBiphenyl CompoundsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell SurvivalFemaleHumansLung NeoplasmsMice, Inbred NODMice, SCIDNeoplastic Stem CellsNitrophenolsPiperazinesABT-737Antineoplastic AgentsBCL2L1 protein, humanbcl-X ProteinBiphenyl CompoundsNitrophenolsPiperazinesSulfonamides

Identifiers

PMID25034785
PMCPMC4227145
OpenAlexW2050093720

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.