Evidence map›Paper›PMID 30228296›Full record

ArticleScientific reports2018

Hmga2 is dispensable for pancreatic cancer development, metastasis, and therapy resistance.

Shin-Heng Chiou, Madeleine Dorsch, Eva Kusch, Santiago Naranjo, Margaret M Kozak, Albert C Koong, Monte M Winslow, Barbara M Grüner

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. HMGA2 Expression Predicts Subtype, Survival, and Treatment Outcome in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  10. Evaluation of Serum microRNA Let-7c and Let-7d as Predictive Biomarkers for Metastatic Pancreatic Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    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

8 authors at 4 institutions in 2 countries.

Shin-Heng ChiouDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Madeleine DorschDepartment of Medical Oncology, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Eva KuschDepartment of Medical Oncology, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Santiago NaranjoDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Margaret M KozakDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Albert C KoongDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Monte M WinslowDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA. mwinslow@stanford.edu.
Barbara M GrünerDepartment of Medical Oncology, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Essen, Germany. barbara.gruener@uk-essen.de.ORCID 0000-0003-0974-4826
Stanford University · USEssen University Hospital · DEStanford Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
NCI NIH HHS P30 CA124435
6 · The paper itself

Abstract

Expression of the chromatin-associated protein HMGA2 correlates with progression, metastasis and therapy resistance in pancreatic ductal adenocarcinoma (PDAC). Hmga2 has also been identified as a marker of a transient subpopulation of PDAC cells that has increased metastatic ability. Here, we characterize the requirement for Hmga2 during growth, dissemination, and metastasis of PDAC in vivo using conditional inactivation of Hmga2 in well-established autochthonous mouse models of PDAC. Overall survival, primary tumour burden, presence of disseminated tumour cells in the peritoneal cavity or circulating tumour cells in the blood, and presence and number of metastases were not significantly different between mice with Hmga2-wildtype or Hmga2-deficient tumours. Treatment of mice with Hmga2-wildtype and Hmga2-deficient tumours with gemcitabine did not uncover a significant impact of Hmga2-deficiency on gemcitabine sensitivity. Hmga1 and Hmga2 overlap in their expression in both human and murine PDAC, however knockdown of Hmga1 in Hmga2-deficient cancer cells also did not decrease metastatic ability. Thus, Hmga2 remains a prognostic marker which identifies a metastatic cancer cell state in primary PDAC, however Hmga2 has limited if any direct functional impact on PDAC progression and therapy resistance.

Indexed as

Cell ProliferationDrug Resistance, NeoplasmAdenocarcinomaAnimalsAntimetabolites, AntineoplasticCarcinoma, Pancreatic DuctalDeoxycytidineGemcitabineHMGA2 ProteinHumansMiceMice, KnockoutPancreatic NeoplasmsPrognosisSurvival RateTissue Array AnalysisAntimetabolites, AntineoplasticDeoxycytidineGemcitabineHMGA2 Protein

Identifiers

PMID30228296
PMCPMC6143627
OpenAlexW2891352044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.