Evidence map›Paper›PMID 22200028›Full record

ReviewNutrients2011

Induction of cancer cell death by isoflavone: the role of multiple signaling pathways.

Yiwei Li, Dejuan Kong, Bin Bao, Aamir Ahmad, Fazlul H Sarkar

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 64 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Yiwei LiDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, 740 Hudson Webber Cancer Research Center, 4100 John R, Detroit, MI 48201, USA. yiweili@med.wayne.edu
Dejuan Kong
Bin Bao
Aamir Ahmad
Fazlul H Sarkar
Cancer Research Center · USWayne State University · US

Funding

Molecular Mechanism of Genistein (Isoflavone) in Prostate CancerR01CA083695 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2001 to 2011
$2.3M
FoxM1: A molecular target in pancreatic cancerR01CA132794 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2009 to 2013
$1.5M
NCI NIH HHS 5R01CA083695NCI NIH HHS 5R01CA132794NCI NIH HHS R01 CA083695NCI NIH HHS R01 CA132794
6 · The paper itself

Abstract

Soy isoflavones have been documented as dietary nutrients broadly classified as "natural agents" which plays important roles in reducing the incidence of hormone-related cancers in Asian countries, and have shown inhibitory effects on cancer development and progression in vitro and in vivo, suggesting the cancer preventive or therapeutic activity of soy isoflavones against cancers. Emerging experimental evidence shows that isoflavones could induce cancer cell death by regulating multiple cellular signaling pathways including Akt, NF-κB, MAPK, Wnt, androgen receptor (AR), p53 and Notch signaling, all of which have been found to be deregulated in cancer cells. Therefore, homeostatic regulation of these important cellular signaling pathways by isoflavones could be useful for the activation of cell death signaling, which could result in the induction of apoptosis of both pre-cancerous and/or cancerous cells without affecting normal cells. In this article, we have attempted to summarize the current state-of-our-knowledge regarding the induction of cancer cell death pathways by isoflavones, which is believed to be mediated through the regulation of multiple cellular signaling pathways. The knowledge gained from this article will provide a comprehensive view on the molecular mechanism(s) by which soy isoflavones may exert their effects on the prevention of tumor progression and/or treatment of human malignancies, which would also aid in stimulating further in-depth mechanistic research and foster the initiation of novel clinical trials.

Indexed as

PhytotherapyAnimalsAntineoplastic Agents, PhytogenicApoptosisCell DeathGlycine maxHumansIsoflavonesNeoplasmsPlant ExtractsSignal TransductionAntineoplastic Agents, PhytogenicIsoflavonesPlant Extractsapoptosiscell signalingisoflavone

Identifiers

PMID22200028
PMCPMC3244210
OpenAlexW1999906350

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.