The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.
Peroxisome Proliferator-Activated Receptor γ Pathway Targeting in Carcinogenesis: Implications for Chemoprevention
Open accessAbstract
The peroxisome proliferator-activated receptor (PPAR) gamma is one member of the nuclear receptor superfamily that contains in excess of 80 described receptors. PPARgamma activators are a diverse group of agents that range from endogenous fatty acids or derivatives (linolenic, linoleic, and 15-deoxy-Delta(12,14)-prostaglandin J(2)) to Food and Drug Administration-approved thiazolidinedione drugs [pioglitazone (Actos) and rosiglitazone (Avandia)] for the treatment of diabetes. Once activated, PPARgamma will preferentially bind with retinoid X receptor alpha and signal antiproliferative, antiangiogenic, and prodifferentiation pathways in several tissue types, thus making it a highly useful target for down-regulation of carcinogenesis. Although PPAR-gamma activators show many anticancer effects on cell lines, their advancement into human advanced cancer clinical trials has met with limited success. This article will review translational findings in PPARgamma activation and targeting in carcinogenesis prevention as they relate to the potential use of PPARgamma activators clinically as cancer chemoprevention strategies.
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PPARγ is currently considered a potential target for both chemoprevention and cancer therapy based on preclinical studies.
“In vitro studies indicate that PPARγ agonists have several anti-cancer activities, such as inhibiting growth and inducing apoptosis and cell differentiation (97), and PPARγ is currently considered a potential target for both chemoprevention and cancer therapy based on other preclinical studies (98,99).”
From Diabetes and Cancer (2010) · cites this paper as [99]
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Metadata
- Authors
- Ondrey, F.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Ondrey, Frank
- ORCID
- Ondrey, Frank
- Venue
- Clinical Cancer Research
- Published
- 2008-12-31
- Volume
- 15
- Issue
- 1
- Pages
- 2-8
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2148016814
- Cited by
- 126
- References
- 73
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 5 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 3 · 2015: 7 · 2014: 10 · 2013: 13 · 2012: 14
- FWCI
- 1.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- PPARγ, nuclear receptors, carcinogenesis, chemoprevention, PPARγ agonists, thiazolidinediones, pioglitazone, rosiglitazone, retinoid X receptor alpha, antiproliferative signaling, clinical translation
- MeSH terms
- Animals, Clinical Trials as Topic, Humans, Neoplasms, Neoplasms, Experimental, Signal Transduction, Drug Delivery Systems, Cell Line, Tumor, Retinoid X Receptors, PPAR gamma, Intracellular Signaling Peptides and Proteins
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