Evidence map›Paper›PMID 30442938›Full record

ArticleOncogenesis2018

ADAM12 is a circulating marker for stromal activation in pancreatic cancer and predicts response to chemotherapy.

V L Veenstra, H Damhofer, C Waasdorp, L B van Rijssen, M J van de Vijver, F Dijk, H W Wilmink, M G Besselink, O R Busch, D K Chang and 9 more

3 registry-linked trialsOpen access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 8% 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.

NCT02027428 phase3completednot on this map

A Phase III, Randomized, Open-Label, Multi-Center, Safety and Efficacy Study to Evaluate Nab-Paclitaxel (Abraxane®) as Maintenance Treatment After Induction With Nab-Paclitaxel Plus Carboplatin in Subjects With Squamous Cell Non-Small Cell Lung Cancer (NSCLC)

TypeinterventionalSponsorCelgeneRan2014 to 2019Enrolled427ConditionsSquamous Cell Carcinoma, Non-Small-Cell LungArmsAbraxane (Induction), Carboplatin (Induction), Abraxane (Maintenance), Best Supportive Care (Maintenance)
NCT02250326 phase2completednot on this map

A Phase 2, Open-Label, Multi-Center Study to Assess Safety and Efficacy of Second/Third-Line Treatment With NAB®-Paclitaxel (ABI-007) In Combination With Epigenetic Modifying Therapy Of CC-486, Or Immunotherapy of Durvalumab (MEDI4736), Or As Monotherapy In Subjects With Advanced Non-Small Cell Lung Cancer (NSCLC): Abound.2L+

TypeinterventionalSponsorCelgeneRan2015 to 2023Enrolled240ConditionsCarcinoma, Non-Small-Cell LungArmsnab-paclitaxel IV, CC-486, Duravalumab
NCT02670746 terminatednot on this map

Non-interventional Observational Post-authorization Study to Assess Clinical and Patient Reported Outcomes With Nab-paclitaxel in Combination With Gemcitabine in Routine Clinical Practice Treating Pancreatic Cancer (TRUST)

TypeobservationalSponsorCelgeneRan2015 to 2017Enrolled44ConditionsPancreatic Neoplasms
3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  8. Review
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  10. Depletion of slow-cycling PDGFRαNature immunology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Pancreatic cancer in 2021: What you need to know to win.World journal of gastroenterology · 2021
    Review
  17. Hypoxia-inducible factor-dependent ADAM12 expression mediates breast cancer invasion and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Article
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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

19 authors at 7 institutions in 3 countries.

V L VeenstraAmsterdam UMC, University of Amsterdam, LEXOR, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam, Netherlands.
H DamhoferAmsterdam UMC, University of Amsterdam, LEXOR, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam, Netherlands.
C WaasdorpAmsterdam UMC, University of Amsterdam, LEXOR, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam, Netherlands.
L B van RijssenAmsterdam UMC, University of Amsterdam, Department of Surgery, Cancer Center Amsterdam, Amsterdam, Netherlands.
M J van de VijverAmsterdam UMC, University of Amsterdam, Department of Pathology, Cancer Center Amsterdam, Amsterdam, Netherlands.
F DijkAmsterdam UMC, University of Amsterdam, Department of Pathology, Cancer Center Amsterdam, Amsterdam, Netherlands.
H W WilminkAmsterdam UMC, University of Amsterdam, Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam, Netherlands.
M G BesselinkAmsterdam UMC, University of Amsterdam, Department of Surgery, Cancer Center Amsterdam, Amsterdam, Netherlands.
O R BuschAmsterdam UMC, University of Amsterdam, Department of Surgery, Cancer Center Amsterdam, Amsterdam, Netherlands.
D K ChangWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
P J BaileyWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
A V BiankinWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
H M KocherCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
J P MedemaAmsterdam UMC, University of Amsterdam, LEXOR, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam, Netherlands.
J S LiCelgene Corporation, Summit, NJ, USA.
R JiangCelgene Corporation, Summit, NJ, USA.
D W PierceCelgene Corporation, Summit, NJ, USA.
H W M van LaarhovenAmsterdam UMC, University of Amsterdam, Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam, Netherlands.
M F BijlsmaAmsterdam UMC, University of Amsterdam, LEXOR, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam, Netherlands. m.f.bijlsma@amc.uva.nl.
Amsterdam University Medical Centers · NLUniversity of Amsterdam · NLUniversity of Glasgow · GBGlasgow Royal Infirmary · GBOncode Institute · NLQueen Mary University of London · GBUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterized by abundant stroma that harbors tumor-promoting properties. No good biomarkers exist to monitor the effect of stromal targeting therapies or to predict response. We set out to identify such non-invasive markers for PDAC stroma and predict response to therapy. Gene expression datasets, co-culture experiments, xenografts, and patient samples were analyzed. Serum samples were measured from a cohort of 58 resected patients, and 87 metastatic or locally advanced PDAC patients. Baseline and follow-up levels were assessed in 372 additional metastatic PDAC patients who received nab-paclitaxel with gemcitabine (n = 184) or gemcitabine monotherapy (n = 188) in the phase III MPACT trial. Increased levels of ADAM12 were found in PDAC patients compared to healthy controls (p < 0.0001, n = 157 and n = 38). High levels of ADAM12 significantly associated with poor outcome in resected PDAC (HR 2.07, p = 0.04). In the MPACT trial survival was significantly longer for patients who received nab-paclitaxel and had undetectable ADAM12 levels before treatment (OS 12.3 m vs 7.9 m p = 0.0046). Consistently undetectable or decreased ADAM12 levels during treatment significantly associated with longer survival as well (OS 14.4 m and 11.2 m, respectively vs 8.3, p = 0.0054). We conclude that ADAM12 is a blood-borne proxy for stromal activation, the levels of which have prognostic significance and correlate with treatment benefit.

Identifiers

PMID30442938
PMCPMC6237826
OpenAlexW2901460096

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.