Evidence map›Paper›PMID 29738110›Full record

ArticleMolecular oncology2018

Genotoxic stress induces Sca-1-expressing metastatic mammary cancer cells.

Jianlin Gong, Benjamin J Lang, Desheng Weng, Takanori Eguchi, Ayesha Murshid, Thiago J Borges, Sachin Doshi, Baizheng Song, Mary A Stevenson, Stuart K Calderwood

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

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 17 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

10 authors at 2 institutions in 1 country.

Jianlin GongDepartment of Medicine, Boston University Medical Center, MA, USA.
Benjamin J LangDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-2205-8591
Desheng WengDepartment of Medicine, Boston University Medical Center, MA, USA.
Takanori EguchiDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Ayesha MurshidDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Thiago J BorgesDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Sachin DoshiDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Baizheng SongDepartment of Medicine, Boston University Medical Center, MA, USA.
Mary A StevensonDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Stuart K CalderwoodDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USBoston University · US

Funding

TRANSMEMBRANE SIGNAL MODULATION BY HYPERTHERMIAR01CA047407 · NCI · DANA-FARBER CANCER INSTITUTE · PI CALDERWOOD, STUART KEITH · 1988 to 2014
$4.3M
Extracellular Hsp70 and hyperthermia in tumor therapyR01CA119045 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH · 2007 to 2016
$3.1M
Complex Role of HSF1 in Breast CancerR01CA176326 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH, SHERMAN, MICHAEL Y · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA047407NCI NIH HHS R01 CA119045NCI NIH HHS R01 CA176326
6 · The paper itself

Abstract

We describe a cell damage-induced phenotype in mammary carcinoma cells involving acquisition of enhanced migratory and metastatic properties. Induction of this state by radiation required increased activity of the Ptgs2 gene product cyclooxygenase 2 (Cox2), secretion of its bioactive lipid product prostaglandin E2 (PGE2), and the activity of the PGE2 receptor EP4. Although largely transient, decaying to low levels in a few days to a week, this phenotype was cumulative with damage and levels of cell markers Sca-1 and ALDH1 increased with treatment dose. The Sca-1

Indexed as

Aldehyde Dehydrogenase 1 FamilyAnimalsAntigens, LyCell Line, TumorCell MovementDNA DamageFemaleGene Expression Regulation, NeoplasticIsoenzymesMammary Neoplasms, AnimalMembrane ProteinsMiceMice, Inbred C57BLNeoplasm MetastasisRetinal DehydrogenaseAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, mouseAntigens, LyIsoenzymesLy6a protein, mouseMembrane ProteinsRetinal Dehydrogenasegenotoxic stressradiation bystander effectradiation therapyresponses to cancer therapySca-1

Identifiers

PMID29738110
PMCPMC6068352
OpenAlexW2802345016

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.