Evidence map›Paper›PMID 21703423›Full record

ArticleThe American journal of pathology2011

Combination therapy of an inhibitor of group VIA phospholipase A2 with paclitaxel is highly effective in blocking ovarian cancer development.

Hui Li, Zhenwen Zhao, Caryl Antalis, Zhanzhong Zhao, Robert Emerson, Gang Wei, Sheng Zhang, Zhong-Yin Zhang, Yan Xu

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Macrophage polarization is linked to CaJournal of lipid research · 2020
    Article
  6. β-Lactones: A Novel Class of CaJournal of medicinal chemistry · 2019
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Elevated and secreted phospholipase A₂ activities as new potential therapeutic targets in human epithelial ovarian cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  13. Review
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

9 authors at 2 institutions in 2 countries.

Hui LiDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Zhenwen Zhao
Caryl Antalis
Zhanzhong Zhao
Robert Emerson
Gang Wei
Sheng Zhang
Zhong-Yin Zhang
Yan Xu
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

Novel Lipid Signaling Pathways in Ovarian Cancer CellsR01CA095042 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI XU, YAN · 2003 to 2007
$1.7M
Targeting PRL Phosphatases for Cancer TherapyR01CA126937 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI ZHANG, ZHONG-YIN · 2008 to 2012
$1.5M
NCI NIH HHS CA126937NCI NIH HHS R01 CA095042NCI NIH HHS R01 CA126937NCI NIH HHS R01CA95042
6 · The paper itself

Abstract

We and others have shown that calcium-independent phospholipase A(2) (iPLA(2)) is involved in epithelial ovarian cancer (EOC). Hence, we propose that iPLA(2) is a potential effective and novel target for EOC. We tested this concept and found that bromoenol lactone (BEL), a selective inhibitor of iPLA(2), significantly inhibited EOC metastatic tumor growth in mouse xenograft models using human SKOV3 and HEY ovarian cancer cells. Moreover, the combination of BEL with paclitaxel (PTX), one of the most commonly used therapeutic agents in EOC, almost completely blocked tumor development in the xenograft mouse model. BEL showed no detectable cytotoxic effects in mice. Another iPLA(2) inhibitor, FKGK11, also inhibited tumor development in the xenograft mouse model, supporting that the major target of action was iPLA(2). The additional effects of BEL with PTX in vivo likely stem from their distinct cellular effects. BEL and FKGK11 reduced adhesion, migration, and invasion of EOC cells in vitro; the reduced ability to adhere, migrate, and invade seems to increase the vulnerability of tumor cells to PTX. These results provide an important basis for the development of new treatment modalities for EOC.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicAntineoplastic Combined Chemotherapy ProtocolsCell AdhesionCell Line, TumorCell MovementCell ProliferationFemaleFluorocarbonsGroup IV Phospholipases A2HumansImmunoenzyme TechniquesKetonesMiceMice, Inbred NODMice, SCID1,1,1,2,2-pentafluoro-7-phenylheptan-3-one6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-oneAntineoplastic Agents, PhytogenicFluorocarbonsGroup IV Phospholipases A2KetonesNaphthalenesPaclitaxelPhosphodiesterase InhibitorsPyrones

Identifiers

PMID21703423
PMCPMC3123860
OpenAlexW2102746333

What OpenQuestion holds

Textmetadata
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.