Evidence map›Paper›PMID 24565907›Full record

ArticleBiochemical pharmacology2014

The potential of heparanase as a therapeutic target in cancer.

Claudio Pisano, Israel Vlodavsky, Neta Ilan, Franco Zunino

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 105 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Claudio PisanoBiogem, Research Institute, Ariano Irpino (AV), Italy.
Israel VlodavskyCancer and Vascular Biology Research Center Rappaport, Faculty of Medicine, Technion, Haifa, Israel.
Neta IlanCancer and Vascular Biology Research Center Rappaport, Faculty of Medicine, Technion, Haifa, Israel.
Franco ZuninoFondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. Electronic address: franco.zunino@istitutotumori.mi.it.
Biogem · ITFondazione IRCCS Istituto Nazionale dei Tumori · IT

Funding

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

Abstract

Heparanase has generated substantial interest as therapeutic target for antitumor therapy, because its activity is implicated in malignant behavior of cancer cells and in tumor progression. Increased heparanase expression was found in numerous tumor types and correlates with poor prognosis. Heparanase, an endoglucuronidase responsible for heparan sulfate cleavage, regulates the structure and function of heparan sulfate proteoglycans, leading to disassembly of the extracellular matrix. The action of heparanase is involved in multiple regulatory events related, among other effects, to augmented bioavailability of growth factors and cytokines. Inhibitors of heparanase suppress tumor growth, angiogenesis and metastasis by modulating growth factor-mediated signaling, ECM barrier function and cell interactions in the tumor microenvironment. Therefore, targeting heparanase has potential implications for anti-tumor, anti-angiogenic and anti-inflammatory therapies. Current approaches for heparanase inhibition include development of chemically modified heparins, small molecule inhibitors and neutralizing antibodies. The available evidence supports the emerging utility of heparanase inhibition as a promising antitumor strategy, specifically in rational combination with other agents. The recent studies with compounds designed to block heparanase (e.g., modified heparins) provide a rational basis for their therapeutic application and optimization.

Indexed as

Disease ProgressionGlucuronidaseHeparanaseHumansInflammationNeoplasmsTumor MicroenvironmentGlucuronidaseHeparanaseAntitumor therapyDrug targetHeparanaseHeparanase inhibitors

Identifiers

PMID24565907
PMCPMC4709407
OpenAlexW2020098579

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.