Evidence map›Paper›PMID 38334603›Full record

ArticleCells2024

A New Synthesized Dicarboxylated Oxy-Heparin Efficiently Attenuates Tumor Growth and Metastasis.

Li Li, Uri Barash, Neta Ilan, Malik Farhoud, Xiao Zhang, Israel Vlodavsky, Jin-Ping Li

Open access · goldAbstract read
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. 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 2 institutions in 2 countries.

Li LiShenzhen Hepalink Pharmaceutical Group Co., Ltd., Shenzhen 518057, China.
Uri BarashTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 3525422, Israel.ORCID 0000-0003-1049-270X
Neta IlanTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 3525422, Israel.
Malik FarhoudTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 3525422, Israel.
Xiao ZhangDepartment of Medical Cell Biology, Uppsala University, 751 23 Uppsala, Sweden.
Israel VlodavskyTechnion Integrated Cancer Center, Rappaport Faculty of Medicine, Technion, Haifa 3525422, Israel.
Jin-Ping LiDepartment of Medical Biochemistry and Microbiology, SciLifeLab, Uppsala University, 751 23 Uppsala, Sweden.
Technion – Israel Institute of Technology · ILUppsala University · SE

Funding

Israel Cancer Association ICAIsrael Science Foundation ISF-102119Shenzhen Science and Technology Program JSGG20210802154545033Swedish Cancer Society CAN211417PjSwedish Research Council 2021-01094US-Israel Binational Science Foundation BSF-2021059
6 · The paper itself

Abstract

Heparanase (Hpa1) is expressed by tumor cells and cells of the tumor microenvironment and functions to remodel the extracellular matrix (ECM) and regulate the bioavailability of ECM-bound factors that support tumor growth. Heparanase expression is upregulated in human carcinomas, sarcomas, and hematological malignancies, correlating with increased tumor metastasis, vascular density, and shorter postoperative survival of cancer patients, and encouraging the development of heparanase inhibitors as anti-cancer drugs. Among these are heparin/HS mimetics, the only heparanase-inhibiting compounds that are being evaluated in clinical trials. We have synthesized dicarboxylated oxy-heparins (DCoxHs) containing three carboxylate groups per split residue (DC-Hep). The resulting lead compound (termed XII) was upscaled, characterized, and examined for its effectiveness in tumor models. Potent anti-tumorigenic effects were obtained in models of pancreatic carcinoma, breast cancer, mesothelioma, and myeloma, yielding tumor growth inhibition (TGI) values ranging from 21 to 70% and extending the survival time of the mice. Of particular significance was the inhibition of spontaneous metastasis in an orthotopic model of breast carcinoma following resection of the primary tumor. It appears that apart from inhibition of heparanase enzymatic activity, compound XII reduces the levels of heparanase protein and inhibits its cellular uptake and activation. Heparanase-dependent and -independent effects of XII are being investigated. Collectively, our pre-clinical studies with compound XII strongly justify its examination in cancer patients.

Indexed as

Antineoplastic AgentsBreast NeoplasmsAnimalsCarcinogenesisFemaleGlucuronidaseHeparinHumansMiceTumor MicroenvironmentAntineoplastic AgentsGlucuronidaseHeparinbreast carcinomachemically modified heparinheparanasemesotheliomametastasispancreatic carcinomaprimary tumor growthtumor growth inhibition

Identifiers

PMID38334603
PMCPMC10854774
OpenAlexW4391174781

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.