Evidence map›Paper›PMID 24908682›Full record

ReviewCarcinogenesis2014

Stromal reengineering to treat pancreas cancer.

Ingunn M Stromnes, Kathleen E DelGiorno, Philip D Greenberg, Sunil R Hingorani

Open access · bronzeAbstract readReview
In one paragraph

Review in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

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13 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

4 authors at 3 institutions in 1 country.

Ingunn M StromnesClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Department of Immunology, University of Washington, Seattle, WA 98195, USA.
Kathleen E DelGiornoClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Philip D GreenbergClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Department of Immunology, University of Washington, Seattle, WA 98195, USA, Department of Medicine, Division of Medical Oncology, University of Washington School of Medicine, Seattle, WA 98195, USA and.
Sunil R HingoraniClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Department of Medicine, Division of Medical Oncology, University of Washington School of Medicine, Seattle, WA 98195, USA and Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA srh@fhcrc.org.
Fred Hutch Cancer Center · USUniversity of Washington · USUniversity of Washington Medical Center · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
VIRUS-MEDIATED MYELOSUPPRESSIONP01CA018029 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Geoffrey Roger HILL · 1985 to 2026
$128.4M
OVERCOMING STROMAL BARRIERS TO THERAPEUTICS IN PANCREAS CANCERR01CA161112 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Sunil R Hingorani · 2011 to 2026
$7.6M
Mechanisms of Murine Turmor Eradication by ImmunotherapyR01CA033084 · NCI · UNIVERSITY OF WASHINGTON · PI GREENBERG, PHILIP D · 1986 to 2017
$5.8M
MECHANISMS OF MURINE TUMOR ERADICATION BY IMMUNOTHERAPYR37CA033084 · NCI · UNIVERSITY OF WASHINGTON · PI GREENBERG, PHILIP D · 1991 to 2006
$3.5M
Genetic progression of pancreatic mucinous cystic neoplasms to invasive carcinomaR01CA129357 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HINGORANI, SUNIL R · 2009 to 2013
$1.8M
Dissecting the roles of stellate cells in pancreas cancer progressionR21CA152249 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HINGORANI, SUNIL R, PROVENZANO, PAOLO · 2010 to 2011
$414k
NCI NIH HHS CA015704NCI NIH HHS CA129357NCI NIH HHS CA152249NCI NIH HHS CA161112NCI NIH HHS CA18029NCI NIH HHS CA33084NCI NIH HHS P01 CA018029NCI NIH HHS R01 CA033084NCI NIH HHS R01 CA161112
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma co-opts multiple cellular and extracellular mechanisms to create a complex cancer organ with an unusual proclivity for metastasis and resistance to therapy. Cell-autonomous events are essential for the initiation and maintenance of pancreatic ductal adenocarcinoma, but recent studies have implicated critical non-cell autonomous processes within the robust desmoplastic stroma that promote disease pathogenesis and resistance. Thus, non-malignant cells and associated factors are culprits in tumor growth, immunosuppression and invasion. However, even this increasing awareness of non-cell autonomous contributions to disease progression is tempered by the conflicting roles stromal elements can play. A greater understanding of stromal complexity and complicity has been aided in part by studies in highly faithful genetically engineered mouse models of pancreatic ductal adenocarcinoma. Insights gleaned from such studies are spurring the development of therapies designed to reengineer the pancreas cancer stroma and render it permissive to agents targeting cell-autonomous events or to reinstate immunosurveillance. Integrating conventional and immunological treatments in the context of stromal targeting may provide the key to a durable clinical impact on this formidable disease.

Indexed as

Tissue EngineeringAnimalsExtracellular MatrixHumansMicePancreatic NeoplasmsStromal Cells

Identifiers

PMID24908682
PMCPMC4076816
OpenAlexW2127329148

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.