Evidence map›Paper›PMID 33761896›Full record

ArticleBMC cancer2021

EML4-ALK induces cellular senescence in mortal normal human cells and promotes anchorage-independent growth in hTERT-transduced normal human cells.

Akihiko Miyanaga, Masaru Matsumoto, Jessica A Beck, Izumi Horikawa, Takahiro Oike, Hirokazu Okayama, Hiromi Tanaka, Sandra S Burkett, Ana I Robles, Mohammed Khan and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 8 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

15 authors at 6 institutions in 2 countries.

Akihiko MiyanagaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Masaru MatsumotoLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Jessica A BeckLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Izumi HorikawaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Takahiro OikeLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Hirokazu OkayamaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Hiromi TanakaMedical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Sandra S BurkettMolecular Cytogenetic Core Facility, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD, USA.
Ana I RoblesLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Mohammed KhanLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Delphine LissaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA.
Masahiro SeikeDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Akihiko GemmaDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Hiroyuki ManoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.
Curtis C HarrisLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 3068A, Bethesda, MD, 20892, USA. harrisc@mail.nih.gov.
Center for Cancer Research · USNippon Medical School · JPNational Cancer Institute · USCancer Genetics (United States) · USIndiana University – Purdue University Indianapolis · USNational Institutes of Health · US

Funding

p53, Aging, and CancerZIABC011496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2013 to 2025
$21.1M
NCI NIH HHS Intramural funds
6 · The paper itself

Abstract

backgroundChromosomal inversions involving anaplastic lymphoma kinase (ALK) and echinoderm microtubule associated protein like 4 (EML4) generate a fusion protein EML4-ALK in non-small cell lung cancer (NSCLC). The understanding of EML4-ALK function can be improved by a functional study using normal human cells.

methodsHere we for the first time conduct such study to examine the effects of EML4-ALK on cell proliferation, cellular senescence, DNA damage, gene expression profiles and transformed phenotypes.

resultsThe lentiviral expression of EML4-ALK in mortal, normal human fibroblasts caused, through its constitutive ALK kinase activity, an early induction of cellular senescence with accumulated DNA damage, upregulation of p16

conclusionsOur data indicate that the expression of hTERT is critical for EML4-ALK to manifest its in vitro transforming activity in human cells. This study provides the isogenic pairs of human cells with and without EML4-ALK expression.

Indexed as

AnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungCell LineCell ProliferationCellular SenescenceDisease Models, AnimalDNA DamageEpithelial CellsFemaleFibroblastsGene Expression Regulation, NeoplasticGenetic VectorsHumansLentivirusLung NeoplasmsEML4-ALK fusion protein, humanOncogene Proteins, FusionTelomeraseTERT protein, humanAnchorage-independent growthDNA damageEML4-ALKhTERTLung cancerSenescence

Identifiers

PMID33761896
PMCPMC7992817
OpenAlexW3112271019

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.