Evidence map›Paper›PMID 28524160›Full record

ArticleBritish journal of cancer2017

Stroma-regulated HMGA2 is an independent prognostic marker in PDAC and AAC.

Carina Strell, Karin Jessica Norberg, Artur Mezheyeuski, Jonas Schnittert, Praneeth R Kuninty, Carlos Fernández Moro, Janna Paulsson, Nicolai Aagaard Schultz, Dan Calatayud, Johannes Matthias Löhr and 6 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Significance of High-Mobility Group A Protein 2 Expression in Pancreatic Ductal Adenocarcinoma and Ampullary Adenocarcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

16 authors at 7 institutions in 4 countries.

Carina StrellDepartment of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
Karin Jessica NorbergDepartment of Clinical Intervention and Technology (CLINTEC), Center for Digestive Diseases, Karolinska University Hospital and Division of Surgery, Karolinska Institutet, Stockholm 14186, Sweden.
Artur MezheyeuskiDepartment of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
Jonas SchnittertDepartment of Biomaterials Science and Technology, Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Zuidhorst building, ZH254, Enschede 7500AE, The Netherlands.
Praneeth R KunintyDepartment of Biomaterials Science and Technology, Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Zuidhorst building, ZH254, Enschede 7500AE, The Netherlands.
Carlos Fernández MoroDepartment of Laboratory Medicine (LabMed) Division of Pathology, Karolinska Institutet, Stockholm 14186, Sweden.
Janna PaulssonDepartment of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
Nicolai Aagaard SchultzDepartment of Surgical Gastroenterology and Transplantation, Rigshospitalet, Copenhagen University Hospital, Copenhagen 2100, Denmark.
Dan CalatayudDepartment of Surgical Gastroenterology and Transplantation, Rigshospitalet, Copenhagen University Hospital, Copenhagen 2100, Denmark.
Johannes Matthias LöhrDepartment of Clinical Intervention and Technology (CLINTEC), Center for Digestive Diseases, Karolinska University Hospital and Division of Surgery, Karolinska Institutet, Stockholm 14186, Sweden.
Oliver FringsDepartment of Oncology-Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm 17176, Sweden.
Caroline Sophie VerbekeInstitute of Clinical Medicine, University of Oslo, Postbox 1171 Blindern, Oslo 0318, Norway.
Rainer Lothar HeuchelDepartment of Clinical Intervention and Technology (CLINTEC), Center for Digestive Diseases, Karolinska University Hospital and Division of Surgery, Karolinska Institutet, Stockholm 14186, Sweden.
Jai PrakashDepartment of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
Julia Sidenius JohansenDepartment of Oncology and Medicine, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev 2730, Denmark.
Arne ÖstmanDepartment of Oncology-Pathology, Cancer Center Karolinska (CCK), Karolinska Institutet, Stockholm 17176, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SEUniversity of Twente · NLCopenhagen University Hospital · DKGentofte Hospital · DKScience for Life Laboratory · SEUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe HMGA2 protein has experimentally been linked to EMT and cancer stemness. Recent studies imply that tumour-stroma interactions regulate these features and thereby contribute to tumour aggressiveness.

methodsWe analysed 253 cases of pancreatic ductal adenocarcinoma (PDAC) and 155 cases of ampullary adenocarcinoma (AAC) for HMGA2 expression by IHC. The data were correlated with stroma abundance and supplemented by experimental studies.

resultsHMGA2 acts as an independent prognostic marker associated with a significantly shorter overall survival in both tumour types. Overall, HMGA2-positivity was more frequent in patients with PDAC than with AAC. The HMGA2 status in tumour cells significantly correlated with the abundance of PDGFRβ-defined stroma cells. In vivo co-injection of Panc-1 cancer cells with pancreatic stellate cells increased tumour growth in a manner associated with increased HMGA2 expression. Furthermore, in vitro treatment of Panc-1 with conditioned media from PDGF-BB-activated stellate cells increased their ability to form tumour spheroids.

conclusionsThis study identifies HMGA2 expression in tumour cells as an independent prognostic marker in PDAC and AAC. Correlative data analysis gives novel tissue-based evidence for a heterotypic cross-talk with stroma cells as a possible mechanism for HMGA2 induction, which is further supported by experimental models.

Indexed as

AdenocarcinomaAgedAmpulla of VaterAnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCommon Bile Duct NeoplasmsFemaleHMGA2 ProteinHumansImmunohistochemistryMaleMiceMice, SCIDMiddle AgedMultivariate AnalysisHMGA2 ProteinReceptor, Platelet-Derived Growth Factor beta

Identifiers

PMID28524160
PMCPMC5520204
OpenAlexW2615238397

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.