Evidence map›Paper›PMID 18618498›Full record

ArticleCancer2008

Heparanase is overexpressed in lung cancer and correlates inversely with patient survival.

Esti Cohen, Ilana Doweck, Inna Naroditsky, Ofer Ben-Izhak, Ran Kremer, Lael A Best, Israel Vlodavsky, Neta Ilan

Open access · greenAbstract read
In one paragraph

Article in Cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 67 citations in OpenAlex.

  1. Integrated 3D-QSAR and cellular profiling of sulfated and hydrophobic aminoglycoside glycans to modulate heparanase activity.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Article
  2. Article
  3. Article
  4. The Role of KRAS Mutation in Colorectal Cancer-Associated Thrombosis.International journal of molecular sciences · 2023
    Article
  5. Article
  6. Article
  7. The Heparanase Regulatory Network in Health and Disease.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. PI-88 inhibits postoperative recurrence of hepatocellular carcinoma via disrupting the surge of heparanase after liver resection.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Glycosylation alterations in lung and brain cancer.Advances in cancer research · 2015
    Review
  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

8 authors at 3 institutions in 1 country.

Esti CohenCancer and Vascular Biology Research Center, Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Ilana Doweck
Inna Naroditsky
Ofer Ben-Izhak
Ran Kremer
Lael A Best
Israel Vlodavsky
Neta Ilan
Rambam Health Care Campus · ILRappaport Family Institute for Research in the Medical Sciences · ILCarmel Medical Center · IL

Funding

Regulation of heparanase in cancer progressionR01CA106456 · NCI · TECHNION-ISRAEL INSTITUTE OF TECHNOLOGY · PI VLODAVSKY, ISRAEL · 2004 to 2013
$1.7M
NCI NIH HHS R01 CA106456NCI NIH HHS R01-CA106456
6 · The paper itself

Abstract

backgroundHeparanase is an endo-beta-D-glucuronidase that is capable of cleaving heparan sulfate (HS) side chains at a limited number of sites, yielding HS fragments of still appreciable size (approximately 5-7 kDa). Heparanase activity has been detected frequently in several cell types and tissues. Heparanase activity correlates with the metastatic potential of tumor-derived cells, a correlation that has been attributed to enhanced cell dissemination as a consequence of HS cleavage and remodeling of the extracellular matrix barrier.

methodsIn this study, the authors examined heparanase expression in 114 patients with lung cancer by means of immunohistochemistry and correlated clinical-pathologic data with heparanase immunostaining and cellular localization.

resultsHeparanase was overexpressed in 75% of the study patients. Heparanase expression was correlated with lung cancer lymph node status and metastasis classification (P = .04 and P = .01, respectively) and was correlated inversely with patient survival (P = .007). It is noteworthy that this adverse effect depended largely on the cellular localization of heparanase. Thus, whereas cytoplasmic staining of heparanase is associated with a poor prognosis, nuclear heparanase predicts a favorable outcome for patients with lung cancer.

conclusionsThe current findings suggest that heparanase expression and cellular localization are decisive for lung cancer patients' prognosis, most likely because of heparanase-mediated tumor cell dissemination by blood and lymph vessels.

Indexed as

AdenocarcinomaAgedBiomarkers, TumorCell NucleusCytoplasmFemaleGlucuronidaseHeparanaseHumansImmunohistochemistryLung NeoplasmsMaleMiddle AgedNeoplasm MetastasisPrognosisSurvival RateBiomarkers, TumorGlucuronidaseHeparanase

Identifiers

PMID18618498
PMCPMC2625296
OpenAlexW2083242210

What OpenQuestion holds

Textmetadata
LicenceTDM
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.