Evidence map›Paper›PMID 16331265›Full record

ArticleOncogene2006

Novel high-affinity PPARgamma agonist alone and in combination with paclitaxel inhibits human anaplastic thyroid carcinoma tumor growth via p21WAF1/CIP1.

J A Copland, L A Marlow, S Kurakata, K Fujiwara, A K C Wong, P A Kreinest, S F Williams, B R Haugen, J P Klopper, R C Smallridge

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Pioglitazone enhances cisplatin's impact on triple-negative breast cancer: Role of PPARγ in cell apoptosis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. PPARs and Angiogenesis-Implications in Pathology.International journal of molecular sciences · 2020
    Review
  11. Review
  12. Article
  13. Review
  14. Obesity, Type-2 Diabetes and Cancer: Mechanistic Insights.Critical reviews in oncogenesis · 2019
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

10 authors at 7 institutions in 2 countries.

J A CoplandDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, Florida 33224, USA. copland.john@mayo.edu
L A Marlow
S Kurakata
K Fujiwara
A K C Wong
P A Kreinest
S F Williams
B R Haugen
J P Klopper
R C Smallridge
Mayo Clinic in Florida · USDaiichi-Sankyo (Japan) · JPBiomedical Research Laboratories (United States) · USJacksonville College · USSylvester Comprehensive Cancer Center · USUniversity of Colorado Cancer Center · USUniversity of Colorado Denver · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Thiazolidinediones as Thyroid Cancer TherapyR01CA100560 · NCI · UNIVERSITY OF COLORADO DENVER · PI HAUGEN, BRYAN R. · 2005 to 2009
$1.6M
NCI NIH HHS CA100560NCI NIH HHS P30CA15083
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists demonstrate antitumor activity likely through transactivating genes that regulate cell proliferation, apoptosis, and differentiation. The PAX8/PPARgamma fusion oncogene, which is common in human follicular thyroid carcinomas appears to act via dominant negative suppression of wild-type PPARgamma, suggesting that it may be a tumor suppressor gene in thyroid cells. We have identified a novel high-affinity PPARgamma agonist (RS5444) that is dependent upon PPARgamma for its biological activity. This is the first report of this molecule and its antitumor activity. In vitro, the IC50 for growth inhibition is approximately 0.8 nM while anaplastic thyroid carcinoma (ATC) tumor growth was inhibited three- to fourfold in nude mice. siRNA against PPARgamma and a pharmacological antagonist demonstrated that functional PPARgamma was required for growth inhibitory activity of RS5444. RS5444 upregulated the cell cycle kinase inhibitor, p21WAF1/CIP1. Silencing p21WAF1/CIP1 rendered cells insensitive to RS5444. RS5444 plus paclitaxel demonstrated additive antiproliferative activity in cell culture and minimal ATC tumor growth in vivo. RS5444 did not induce apoptosis but combined with paclitaxel, doubled the apoptotic index compared to that of paclitaxel. Our data indicate that functional PPARgamma is a molecular target for therapy in ATC. We demonstrated that RS5444, a thiazolidinedione (Tzd) derivative, alone or in combination with paclitaxel, may provide therapeutic benefit to patients diagnosed with ATC.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell ProliferationChromansCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor ProteinsFemaleHumansMicePaclitaxelPPAR gammaThiazolidinedionesThyroid NeoplasmsAngiogenesis InhibitorsAntineoplastic AgentsCDKN1A protein, humanChromansCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor ProteinsefatutazonePaclitaxelPPAR gammaThiazolidinedionesTroglitazone

Identifiers

PMID16331265
OpenAlexW2055561557

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.