Evidence map›Paper›PMID 27354473›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2017

Tumor-Derived CCL2 Mediates Resistance to Radiotherapy in Pancreatic Ductal Adenocarcinoma.

Anusha Kalbasi, Chad Komar, Graham M Tooker, Mingen Liu, Jae W Lee, Whitney L Gladney, Edgar Ben-Josef, Gregory L Beatty

Open access · greenAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
191citing papers in PubMed, 2 pooled it
11.0field-weighted citation impact, top 1% 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

191 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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131 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

8 authors at 1 institution in 1 country.

Anusha KalbasiAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Chad KomarAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Graham M TookerAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Mingen LiuAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Jae W LeeAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Whitney L GladneyAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Edgar Ben-JosefAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania.
Gregory L BeattyAbramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania. gregory.beatty@uphs.upenn.edu.
University of Pennsylvania · US

Funding

Targeting the liver for immunotherapy in pancreatic cancerR01CA197916 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Gregory L Beatty · 2016 to 2026
$3.7M
CD40 Pathway in Pancreatic AdenocarcinomaK08CA138907 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BEATTY, GREGORY L · 2011 to 2015
$812k
Pro- and anti-phagocytic signals on pancreatic cancer regulate tumor macrophagesF30CA196124 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LIU, MINGEN · 2015 to 2017
$126k
A role for macrophage phenotype in regulating metastasis in pancreatic carcinomaF30CA196106 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LEE, JAE WON · 2015 to 2016
$95k
NCI NIH HHS F30 CA196106NCI NIH HHS F30 CA196124NCI NIH HHS K08 CA138907NCI NIH HHS R01 CA197916
6 · The paper itself

Abstract

purposeLocal tumor growth is a major cause of morbidity and mortality in nearly 30% of patients with pancreatic ductal adenocarcinoma (PDAC). Radiotherapy is commonly used for local disease control in PDAC, but its efficacy is limited. We studied the impact of selectively intervening on radiotherapy-induced inflammation as an approach to overcome resistance to radiotherapy in PDAC. EXPERIMENTAL

designPDAC cell lines derived from primary pancreatic tumors arising spontaneously in Kras

resultsAblative radiotherapy alone had minimal impact on PDAC growth but led to a significant increase in CCL2 production by tumor cells and recruitment of Ly6C

conclusionsPDAC responds to radiotherapy by producing CCL2, which recruits Ly6C

Indexed as

AnimalsBiomarkersCarcinoma, Pancreatic DuctalCell Line, TumorChemokine CCL2ChemotaxisCytokinesDisease Models, AnimalImmunophenotypingInflammation MediatorsMacrophagesMiceModels, BiologicalMonocytesRadiation ToleranceTumor BurdenBiomarkersChemokine CCL2CytokinesInflammation Mediators

Identifiers

PMID27354473
PMCPMC5195913
OpenAlexW2471840718

What OpenQuestion holds

Textmetadata
LicenceTDM
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.