Evidence map›Paper›PMID 29162390›Full record

ReviewTrends in biochemical sciences2018

Opposing Functions of Heparanase-1 and Heparanase-2 in Cancer Progression.

Israel Vlodavsky, Miriam Gross-Cohen, Marina Weissmann, Neta Ilan, Ralph D Sanderson

Open access · greenAbstract readReview
In one paragraph

Review in Trends in biochemical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
8.3field-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

67 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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
  5. Article
  6. Article
  7. Pan-Cancer Single-Nucleus Total RNA Sequencing Using snHH-Seq.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Role of heparanase in pulmonary hypertension.Frontiers in pharmacology · 2023
    Review
  15. Glycan Modulation of Insulin-like Growth Factor-1 Receptor.Angewandte Chemie (International ed. in English) · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Induction of heparanase 2 (Hpa2) expression by stress is mediated by ATF3.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Article

7 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 2 institutions in 2 countries.

Israel VlodavskyTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel. Electronic address: vlodavsk@mail.huji.ac.il.
Miriam Gross-CohenTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Marina WeissmannTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Neta IlanTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.
Ralph D SandersonUniversity of Alabama at Birmingham, Department of Pathology, Birmingham, AL 35294, USA.
Technion – Israel Institute of Technology · ILUniversity of Alabama at Birmingham · 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
Heparanase in Tumor Progression, Metastasis and ChemoresistanceR01CA211752 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERSON, RALPH D · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA138340NCI NIH HHS R01 CA211752
6 · The paper itself

Abstract

Heparanase, the sole heparan sulfate (HS)-degrading endoglycosidase, regulates multiple biological activities that enhance tumor growth, metastasis, angiogenesis, and inflammation. Heparanase accomplishes this by degrading HS and thereby regulating the bioavailability of heparin-binding proteins; priming the tumor microenvironment; mediating tumor-host crosstalk; and inducing gene transcription, signaling pathways, exosome formation, and autophagy that together promote tumor cell performance and chemoresistance. By contrast, heparanase-2, a close homolog of heparanase, lacks enzymatic activity, inhibits heparanase activity, and regulates selected genes that promote normal differentiation, endoplasmic reticulum stress, tumor fibrosis, and apoptosis, together resulting in tumor suppression. The emerging premise is that heparanase is a master regulator of the aggressive phenotype of cancer, while heparanase-2 functions as a tumor suppressor.

Indexed as

AnimalsDisease ProgressionHumansNeoplasmsPolysaccharide-Lyasesheparatinase Iheparatinase IIPolysaccharide-Lyaseschemoresistanceexosomesheparanaseheparanase-2tumor microenvironmenttumor suppressor

Identifiers

PMID29162390
PMCPMC5741533
OpenAlexW2770636902

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.