Evidence map›Paper›PMID 21447736›Full record

ArticleCancer research2011

Role of heparanase in radiation-enhanced invasiveness of pancreatic carcinoma.

Amichay Meirovitz, Esther Hermano, Immanuel Lerner, Eyal Zcharia, Claudio Pisano, Tamar Peretz, Michael Elkin

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Targeting syndecan-1: new opportunities in cancer therapy.American journal of physiology. Cell physiology · 2022
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Significance of host heparanase in promoting tumor growth and metastasis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
  13. Article
  14. Article
  15. Non-Anticoagulant Heparins as Heparanase Inhibitors.Advances in experimental medicine and biology · 2020
    Review
  16. Article
  17. Review
  18. World journal of gastroenterology · 2018
    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

7 authors at 1 institution in 1 country.

Amichay MeirovitzSharett Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Esther Hermano
Immanuel Lerner
Eyal Zcharia
Claudio Pisano
Tamar Peretz
Michael Elkin
Sigma Tau (Italy) · 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 R01 CA106456NCI NIH HHS R01-CA106456-06
6 · The paper itself

Abstract

Pancreatic cancer is characterized by very low survival rates because of high intrinsic resistance to conventional therapies. Ionizing radiation (IR)-enhanced tumor invasiveness is emerging as one mechanism responsible for the limited benefit of radiotherapy in pancreatic cancer. In this study, we establish the role of heparanase-the only known mammalian endoglycosidase that cleaves heparan sulfate-in modulating the response of pancreatic cancer to radiotherapy. We found that clinically relevant doses of IR augment the invasive capability of pancreatic carcinoma cells in vitro and in vivo by upregulating heparanase. Changes in the levels of the transcription factor Egr-1 occurred in pancreatic cancer cells following radiation, underlying the stimulatory effect of IR on heparanase expression. Importantly, the specific heparanase inhibitor SST0001 abolished IR-enhanced invasiveness of pancreatic carcinoma cells in vitro, whereas combined treatment with SST0001 and IR, but not IR alone, attenuated the spread of orthotopic pancreatic tumors in vivo. Taken together, our results suggest that combining radiotherapy with heparanase inhibition is an effective strategy to prevent tumor resistance and dissemination, observed in many IR-treated pancreatic cancer patients. Further, the molecular mechanism underlying heparanase upregulation in pancreatic cancer that we identified in response to IR may help identify patients in which radiotherapeutic intervention may confer increased risk of metastatic spread, where antiheparanase therapy may be particularly beneficial.

Indexed as

AnimalsCell Line, TumorDose-Response Relationship, RadiationEarly Growth Response Protein 1Enzyme InhibitorsGlucuronidaseHeparanaseHumansMaleMiceMice, SCIDNeoplasm InvasivenessPancreatic NeoplasmsEarly Growth Response Protein 1EGR1 protein, humanEnzyme InhibitorsGlucuronidaseHeparanase

Identifiers

PMID21447736
PMCPMC3070855
OpenAlexW2123169639

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.