Evidence map›Paper›PMID 27758044›Full record

ReviewThe FEBS journal2017

Heparanase regulation of cancer, autophagy and inflammation: new mechanisms and targets for therapy.

Ralph D Sanderson, Michael Elkin, Alan C Rapraeger, Neta Ilan, Israel Vlodavsky

Abstract readReview
In one paragraph

Review in The FEBS journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 220 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. International journal of molecular sciences · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. The Pathophysiological Functions of Heparanases: From Evolution, Structural and Tissue-Specific Perspectives.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

55 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Ralph D SandersonDepartment of Pathology, Comprehensive Cancer Center, University of Alabama at Birmingham, AL, USA.
Michael ElkinSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Alan C RapraegerDepartment of Human Oncology, Wisconsin Institutes for Medical Research, Carbone Cancer Center, University of Wisconsin-Madison, WI, USA.
Neta IlanCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Israel VlodavskyCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Hebrew University of Jerusalem · ILUniversity of Alabama at Birmingham · USUniversity of Wisconsin–Madison · US

Funding

Heparanase Regulation of Myeloma Metastasis: Mechanism and TherapyR01CA138340 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERSON, RALPH D · 2009 to 2018
$3.3M
Synstatin Therapy for Multiple MyelomaR01CA139872 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2010 to 2014
$1.9M
Syndecan-1 (CD138) and its synstatins: targeting invasion, survival and angiogenesis in myelomaR01CA212413 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2017 to 2021
$1.8M
NCI NIH HHS R01 CA138340NCI NIH HHS R01 CA139872NCI NIH HHS R01 CA212413
6 · The paper itself

Abstract

Because of its impact on multiple biological pathways, heparanase has emerged as a major regulator of cancer, inflammation and other disease processes. Heparanase accomplishes this by degrading heparan sulfate which regulates the abundance and location of heparin-binding growth factors thereby influencing multiple signaling pathways that control gene expression, syndecan shedding and cell behavior. In addition, heparanase can act via nonenzymatic mechanisms that directly activate signaling at the cell surface. Clinical trials testing heparanase inhibitors as anticancer therapeutics are showing early signs of efficacy in patients further emphasizing the biological importance of this enzyme. This review focuses on recent developments in the field of heparanase regulation of cancer and inflammation, including the impact of heparanase on exosomes and autophagy, and novel mechanisms whereby heparanase regulates tumor metastasis, angiogenesis and chemoresistance. In addition, the ongoing development of heparanase inhibitors and their potential for treating cancer and inflammation are discussed.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsAutophagyClinical Trials as TopicDrug Resistance, NeoplasmEnzyme InhibitorsExosomesGlucuronidaseHeparanaseHeparan SulfateHumansInflammationMolecular Targeted TherapyNeoplasm MetastasisNeoplasmsNeovascularization, PathologicAntineoplastic AgentsEnzyme InhibitorsGlucuronidaseHeparanaseHeparan SulfateSyndecansangiogenesisautophagycancerexosomesheparanaseheparanase inhibitorsheparan sulfateinflammationmetastasisproteoglycan

Identifiers

PMID27758044
PMCPMC5226874
OpenAlexW2539079898

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.