Evidence map›Paper›PMID 27219517›Full record

ArticlePloS one2016

Midkine Increases Diagnostic Yield in AFP Negative and NASH-Related Hepatocellular Carcinoma.

Roslyn Vongsuvanh, David van der Poorten, Tristan Iseli, Simone I Strasser, Geoffrey W McCaughan, Jacob George

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 6 pooled it
4.0field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 6 syntheses or guidelines pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Article
  8. Article
  9. Review
  10. Article
  11. Prediagnostic plasma proteomics profile for hepatocellular carcinoma.Journal of the National Cancer Institute · 2024
    Article
  12. RNA Interference based Midkine Gene Therapy for Hepatocellular Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  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

6 authors at 4 institutions in 1 country.

Roslyn VongsuvanhStorr Liver Unit, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Sydney, NSW, Australia.
David van der PoortenStorr Liver Unit, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Sydney, NSW, Australia.
Tristan IseliStorr Liver Unit, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Sydney, NSW, Australia.
Simone I StrasserAW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
Geoffrey W McCaughanAW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
Jacob GeorgeStorr Liver Unit, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Sydney, NSW, Australia.
Royal Prince Alfred Hospital · AUWestmead Institute · AUThe University of Sydney · AUWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledRobust biomarkers for population-level hepatocellular carcinoma (HCC) surveillance are lacking. We compared serum midkine (MDK), dickkopf-1 (DKK1), osteopontin (OPN) and AFP for HCC diagnosis in 86 HCC patients matched to 86 cirrhotics, 86 with chronic liver disease (CLD) and 86 healthy controls (HC). Based on the performance of each biomarker, we assessed a separate longitudinal cohort of 28 HCC patients, at and before cancer diagnosis. Serum levels of MDK and OPN were higher in HCC patients compared to cirrhosis, CLD and HC groups. DKK1 was not different between cases and controls. More than half of HCC patients had normal AFP. In this AFP-negative HCC cohort, 59.18% (n = 29/49) had elevated MDK, applying the optimal cut-off of 0.44 ng/ml. Using AFP ≥ 20 IU/ml or MDK ≥ 0.44 ng/ml, a significantly greater number (76.7%; n = 66/86) of HCC cases were detected. The area under the receiver operating curve for MDK was superior to AFP and OPN in NASH-HCC diagnosis. In the longitudinal cohort, MDK was elevated in 15/28 (54%) of HCC patients at diagnosis, of whom 67% had elevated MDK 6 months prior.

conclusionAFP and MDK have a complementary role in HCC detection. MDK increases the diagnostic yield in AFP-negative HCC and has greater diagnostic performance than AFP, OPN and DKK-1 in the diagnosis of NASH-HCC. Additionally, MDK has a promising role in the pre-clinical diagnosis of HCC.

Indexed as

Agedalpha-FetoproteinsBiomarkers, TumorCarcinoma, HepatocellularCase-Control StudiesCross-Sectional StudiesFemaleHumansIntercellular Signaling Peptides and ProteinsLiver NeoplasmsLongitudinal StudiesMaleMiddle AgedMidkineNerve Growth FactorsNon-alcoholic Fatty Liver DiseaseAFP protein, humanalpha-FetoproteinsBiomarkers, TumorDKK1 protein, humanIntercellular Signaling Peptides and ProteinsMDK protein, humanMidkineNerve Growth FactorsOsteopontin

Identifiers

PMID27219517
PMCPMC4878793
OpenAlexW2405656126

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.