Evidence map›Paper›PMID 24699306›Full record

ArticleLeukemia2014

Heparanase enhances myeloma progression via CXCL10 downregulation.

U Barash, Y Zohar, G Wildbaum, K Beider, A Nagler, N Karin, N Ilan, I Vlodavsky

Abstract read
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

61 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  5. Engineered chemokines, resistant to cancer-mediated post-transcriptional modifications, as drugs to improve cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. SubvertingBiology · 2024
    Review
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1 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

8 authors at 1 institution in 1 country.

U BarashCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Y ZoharDepartment of Immunology, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
G WildbaumDepartment of Immunology, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
K BeiderDivision of Hematology and Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel Aviv University, Tel Hashomer, Israel.
A NaglerDivision of Hematology and Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel Aviv University, Tel Hashomer, Israel.
N KarinDepartment of Immunology, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
N IlanCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
I VlodavskyCancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Sheba 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 CA106456NCI NIH HHS R01 CA106456
6 · The paper itself

Abstract

In order to explore the mechanism(s) underlying the pro-tumorigenic capacity of heparanase, we established an inducible Tet-on system. Heparanase expression was markedly increased following addition of doxycycline (Dox) to the culture medium of CAG human myeloma cells infected with the inducible heparanase gene construct, resulting in increased colony number and size in soft agar. Moreover, tumor xenografts produced by CAG-heparanase cells were markedly increased in mice supplemented with Dox in their drinking water compared with control mice maintained without Dox. Consistently, we found that heparanase induction is associated with decreased levels of CXCL10, suggesting that this chemokine exerts tumor-suppressor properties in myeloma. Indeed, recombinant CXCL10 attenuated the proliferation of CAG, U266 and RPMI-8266 myeloma cells. Similarly, CXCL10 attenuated the proliferation of human umbilical vein endothelial cells, implying that CXCL10 exhibits anti-angiogenic capacity. Strikingly, development of tumor xenografts produced by CAG-heparanase cells overexpressing CXCL10 was markedly reduced compared with control cells. Moreover, tumor growth was significantly attenuated in mice inoculated with human or mouse myeloma cells and treated with CXCL10-Ig fusion protein, indicating that CXCL10 functions as a potent anti-myeloma cytokine.

Indexed as

AnimalsAnti-Bacterial AgentsCell ProliferationChemokine CXCL10Disease ProgressionDown-RegulationDoxycyclineGene ExpressionGene Expression Regulation, NeoplasticGlucuronidaseHeparanaseHumansMiceMultiple MyelomaTumor Cells, CulturedAnti-Bacterial AgentsChemokine CXCL10CXCL10 protein, humanCxcl10 protein, mouseDoxycyclineGlucuronidaseHeparanase

Identifiers

PMID24699306
PMCPMC4185261
OpenAlexW2033039805

What OpenQuestion holds

Textmetadata
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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.