Evidence map›Paper›PMID 36074156›Full record

ArticleEuropean journal of nuclear medicine and molecular imaging2022

Functional biomarkers derived from computed tomography and magnetic resonance imaging differentiate PDAC subgroups and reveal gemcitabine-induced hypo-vascularization.

Irina Heid, Marija Trajkovic-Arsic, Fabian Lohöfer, Georgios Kaissis, Felix N Harder, Moritz Mayer, Geoffrey J Topping, Friderike Jungmann, Barbara Crone, Moritz Wildgruber and 9 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in European journal of nuclear medicine and molecular imaging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 53% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 3 countries.

Irina HeidSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany. Irina.Heid@tum.de.
Marija Trajkovic-ArsicDivision of Solid Tumor Translational Oncology, German Cancer Consortium (DKTK, partner site Essen) and German Cancer Research Center, DKFZ, Heidelberg, Germany.
Fabian LohöferSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Georgios KaissisSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Felix N HarderSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Moritz MayerSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Geoffrey J ToppingSchool of Medicine, Department of Nuclear Medicine, Technical University of Munich, Munich, Germany.
Friderike JungmannSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Barbara CroneInstitute of Inorganic and Analytical Chemistry, University of Muenster, Muenster, Germany.
Moritz WildgruberInstitute of Clinical Radiology, University Hospital Muenster, Muenster, Germany.
Uwe KarstInstitute of Inorganic and Analytical Chemistry, University of Muenster, Muenster, Germany.
Lucia LiottaSchool of Medicine, Clinic and Policlinic of Internal Medicine II, Technical University of Munich, Munich, Germany.
Hana AlgülComprehensive Cancer Center München, Chair for Tumor Metabolism, Klinikum rechts der Isar, Technical University of Munich, Munich, Bavaria, Germany.
Hsi-Yu YenSchool of Medicine, Institute of Pathology, Technical University of Munich, Munich, Germany.
Katja SteigerSchool of Medicine, Institute of Pathology, Technical University of Munich, Munich, Germany.
Wilko WeichertSchool of Medicine, Institute of Pathology, Technical University of Munich, Munich, Germany.
Jens T SivekeDivision of Solid Tumor Translational Oncology, German Cancer Consortium (DKTK, partner site Essen) and German Cancer Research Center, DKFZ, Heidelberg, Germany.
Marcus R MakowskiSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany.
Rickmer F BrarenSchool of Medicine, Institute of Diagnostic and Interventional Radiology, Technical University of Munich, Munich, Germany. rbraren@tum.de.
Technical University of Munich · DEDeutschen Konsortium für Translationale Krebsforschung · DEUniversity of Münster · DEArtificial Intelligence in Medicine (Canada) · CAEssen University Hospital · DEGerman Cancer Research Center · DEUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePancreatic ductal adenocarcinoma (PDAC) is a molecularly heterogeneous tumor entity with no clinically established imaging biomarkers. We hypothesize that tumor morphology and physiology, including vascularity and perfusion, show variations that can be detected by differences in contrast agent (CA) accumulation measured non-invasively. This work seeks to establish imaging biomarkers for tumor stratification and therapy response monitoring in PDAC, based on this hypothesis. METHODS AND MATERIALS: Regional CA accumulation in PDAC was correlated with tumor vascularization, stroma content, and tumor cellularity in murine and human subjects. Changes in CA distribution in response to gemcitabine (GEM) were monitored longitudinally with computed tomography (CT) Hounsfield Units ratio (HUr) of tumor to the aorta or with magnetic resonance imaging (MRI) ΔR

resultsTumor cell poor, stroma-rich regions exhibited high CA accumulation both in human (meanHUr 0.64 vs. 0.34, p < 0.001) and mouse PDAC (meanAUC60r 2.0 vs. 1.1, p < 0.001). Compared to the baseline, in vivo CA accumulation decreased specifically in response to GEM treatment in a subset of human (HUr -18%) and mouse (AUC60r -36%) tumors. Ex vivo analyses of mPDAC showed reduced cisplatin delivery (GEM: 0.92 ± 0.5 mg/g, vs. vehicle: 3.1 ± 1.5 mg/g, p = 0.004) and diminished endothelial cell proliferation (GEM: 22.3% vs. vehicle: 30.9%, p = 0.002) upon GEM administration.

conclusionIn PDAC, CA accumulation, which is related to tumor vascularization and perfusion, inversely correlates with tumor cellularity. The standard of care GEM treatment results in decreased CA accumulation, which impedes drug delivery. Further investigation is warranted into potentially detrimental effects of GEM in combinatorial therapy regimens.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsBiomarkersCell Line, TumorCisplatinGemcitabineHumansMagnetic Resonance ImagingMiceNeovascularization, PathologicTomographyTomography, X-Ray ComputedXenograft Model Antitumor AssaysBiomarkersCisplatinGemcitabineCA accumulationCTDCE-MRIGemcitabinePDAC

Identifiers

PMID36074156
PMCPMC9668793
OpenAlexW4294944331

What OpenQuestion holds

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Registered trials

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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.