Evidence map›Paper›PMID 17273765›Full record

ArticleInternational journal of oncology2007

The low-toxicity 9-cis UAB30 novel retinoid down-regulates the DNA methyltransferases and has anti-telomerase activity in human breast cancer cells.

Nathan J Hansen, Rebecca C Wylie, Sharla M O Phipps, William K Love, Lucy G Andrews, Trygve O Tollefsbol

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2007. 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
1.2field-weighted citation impact, top 22% 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, 28 citations in OpenAlex.

  1. Trial
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  8. Review
  9. Article
  10. A pilot, first-in-human, pharmacokinetic study of 9cUAB30 in healthy volunteers.Cancer prevention research (Philadelphia, Pa.) · 2010
    Article
  11. Retinoid pathway and cancer therapeutics.Advanced drug delivery reviews · 2010
    Review
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Nathan J HansenDepartment of Biology, University of Alabama at Birmingham, 1300 University Boulevard, Birmingham, AL 35294, USA.
Rebecca C Wylie
Sharla M O Phipps
William K Love
Lucy G Andrews
Trygve O Tollefsbol
University of Alabama at Birmingham · US

Funding

Epigenetics of Dietary EGCG in Cancer PreventionR21CA114019 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TOLLEFSBOL, TRYGVE O · 2006 to 2007
$296k
NCI NIH HHS R21 CA114019
6 · The paper itself

Abstract

Retinoic acids and their derivatives potentiate anti-cancer effects in breast cancer cells. The aberrant expression of telomerase is critical to the continued proliferation of most cancer cells. Thus, telomerase is an attractive target for chemoprevention and treatment of breast cancer. 9cUAB30 is a novel synthetic retinoid X receptor-selective retinoic acid (RA) that effectively reduces the tumorigenic phenotype in mouse breast carcinoma with lower toxic effects than natural retinoid treatments. We have assessed 9cUAB30 retinoic acid treatment of human breast cancer cells to determine the potential of this drug as an effective telomerase inhibitor and its application to cancer therapy. 9cUAB30 was found to decrease DNA methyltransferase and telomerase expression in MDA-MB-361, T-47D, and MCF-7 human breast cancer cells and to inhibit the proliferation of these cells. This low-toxicity retinoid also reduced colony formation in soft agar assays in each of these cell types. Combination treatments of 9cUAB30 and all-trans RA proved to be synergistically more effective than either RA alone, further suggesting a possible general epigenetic mechanism that contributes to the anti-telomerase activity of the retinoids. Therefore, the novel retinoid, 9cUAB30, is effective in inhibiting the growth of human breast cancer cells, its anti-cancer effects appear to be related to telomerase inhibition and the mechanism for this process could be mediated through epigenetic modifications.

Indexed as

Down-RegulationApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDose-Response Relationship, DrugFatty Acids, UnsaturatedGene Expression Regulation, NeoplasticHumansNaphthalenesRetinoidsTelomeraseTime FactorsTretinoinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesFatty Acids, UnsaturatedNaphthalenesRetinoidsTelomeraseTretinoinUAB 30

Identifiers

PMID17273765
PMCPMC2435481
OpenAlexW2055524611

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.