Evidence map›Paper›PMID 23846978›Full record

ArticleMolecular carcinogenesis2014

Suppression of inflammatory cascade is implicated in methyl amooranin-mediated inhibition of experimental mammary carcinogenesis.

Animesh Mandal, Deepak Bhatia, Anupam Bishayee

Open access · bronzeAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Oleanane triterpenoids in the prevention and therapy of breast cancer: current evidence and future perspectives.Phytochemistry reviews : proceedings of the Phytochemical Society of Europe · 2014
    Article
  8. Review
  9. 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

3 authors at 2 institutions in 1 country.

Animesh MandalDepartment of Pharmaceutical Sciences College of Pharmacy, Northeast Ohio Medical University, Rootstown, Ohio.
Deepak Bhatia
Anupam Bishayee
Northeast Ohio Medical University · USAmerican University of Health Sciences · US

Funding

A synthetic triterpenoid in breast cancer chemopreventionR03CA136014 · NCI · NORTHEAST OHIO MEDICAL UNIVERSITY · PI BISHAYEE, ANUPAM · 2009 to 2010
$154k
NCI NIH HHS R03 CA136014NCI NIH HHS R03CA136014
6 · The paper itself

Abstract

Breast cancer represents the second leading cause of cancer-related deaths among women worldwide and preventive therapy could reverse or delay the devastating impact of this disease. Methyl-amooranin (methyl-25-hydroxy-3-oxoolean-12-en-28-oate, AMR-Me), a novel synthetic oleanane triterpenoid, reduced the incidence and burden of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors in rats through antiproliferative and proapoptotic effects. Since chronic inflammation plays an important role in the pathogenesis of breast cancer and several synthetic oleanane compounds are known potent anti-inflammatory agents, we aim to investigate anti-inflammatory mechanisms of AMR-Me by monitoring various proinflammatory and stress markers, such as cyclooxygenase-2 (COX-2) and heat shock protein 90 (HSP90), and nuclear factor-κB (NF-κB) signaling during DMBA mammary tumorigenesis in rats. Mammary tumors were harvested from a chemopreventive study in which AMR-Me (0.8-1.6 mg/kg) was found to inhibit mammary carcinogenesis in a dose-response manner. The expressions of COX-2, HSP90, NF-κB, and inhibitory κB-α (IκB-α) were determined by immunohistochemistry and reverse transcription-polymerase chain reaction. AMR-Me downregulated the expression of intratumor COX-2 and HSP90, suppressed the degradation of IκB-α, and reduced the translocation of NF-κB from cytosol to nucleus. Our present study provides the first in vivo evidence that NF-κB-evoked inflammatory cascade is a major target of AMR-Me in breast cancer. Our current results together with our previous findings suggest that disruption of NF-κB signaling contributes to anti-inflammatory, antiproliferative, and apoptosis-inducing mechanisms involved in AMR-Me-mediated chemoprevention of rat mammary carcinogenesis. These encouraging mechanistic results coupled with a safety profile should facilitate the clinical development of AMR-Me as breast cancer chemopreventive drug.

Indexed as

AnimalsAnticarcinogenic AgentsAnti-Inflammatory AgentsAntineoplastic AgentsApoptosisBreast NeoplasmsCarcinogenesisCell ProliferationChemopreventionCyclooxygenase 2Down-RegulationFemaleHSP90 Heat-Shock ProteinsI-kappa B ProteinsInflammationMammary Neoplasms, ExperimentalAnticarcinogenic AgentsAnti-Inflammatory AgentsAntineoplastic AgentsCyclooxygenase 2HSP90 Heat-Shock ProteinsI-kappa B Proteinsmethyl 25-hydroxy-3-oxoolean-12-en-28-oateNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratOleanolic Acidbreast tumorCOX-2DMBAHSP90inflammationNF-κBoleanane triterpenoid

Identifiers

PMID23846978
PMCPMC3888835
OpenAlexW2147554742

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.