Evidence map›Paper›PMID 22751729›Full record

ArticleJournal of biomolecular screening2012

A high-content assay to identify small-molecule modulators of a cancer stem cell population in luminal breast cancer.

Byong Hoon Yoo, Sunshine Daddario Axlund, Peter Kabos, Brian G Reid, Jerome Schaack, Carol A Sartorius, Daniel V LaBarbera

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomolecular screening, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 15% 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, 15 citations in OpenAlex.

  1. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  2. Article
  3. Chemical Screening of Nuclear Receptor Modulators.International journal of molecular sciences · 2020
    Review
  4. Article
  5. Screening of Conditionally Reprogrammed Patient-Derived Carcinoma Cells Identifies ERCC3-MYC Interactions as a Target in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  6. Article
  7. Steroid hormones, steroid receptors, and breast cancer stem cells.Journal of mammary gland biology and neoplasia · 2015
    Review
  8. Article
  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

7 authors at 2 institutions in 1 country.

Byong Hoon YooDepartment of Pharmaceutical Sciences, The Skaggs School of Pharmacy, The University of Colorado, Aurora, CO 80045, USA.
Sunshine Daddario Axlund
Peter Kabos
Brian G Reid
Jerome Schaack
Carol A Sartorius
Daniel V LaBarbera
University of Colorado Denver · USUniversity of Montana · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Hormones and Tumor Initiating Cells in Human Breast CancersR01CA140985 · NCI · UNIVERSITY OF COLORADO DENVER · PI SARTORIUS, CAROL ANN · 2011 to 2020
$3.0M
Regulation of anti-endocrine resistance of breast cancer by a network of non-codiK08CA164048 · NCI · UNIVERSITY OF COLORADO DENVER · PI KABOS, PETER · 2012 to 2016
$859k
NCI NIH HHS K08 CA164048NCI NIH HHS P30 CA046934NCI NIH HHS R01 CA140985
6 · The paper itself

Abstract

Breast cancers expressing hormone receptors for estrogen (ER) and progesterone (PR) represent ~70% of all cases and are treated with both ER-targeted and chemotherapies, with near 40% becoming resistant. We have previously described that in some ER(+) tumors, the resistant cells express cytokeratin 5 (CK5), a putative marker of breast stem and progenitor cells. CK5(+) cells have lost expression of ER and PR, express the tumor-initiating cell surface marker CD44, and are relatively quiescent. In addition, progestins, which increase breast cancer incidence, expand the CK5(+) subpopulation in ER(+)PR(+) breast cancer cell lines. We have developed models to induce and quantitate CK5(+)ER(-)PR(-) cells, using CK5 promoter-driven luciferase (Fluc) or green fluorescent protein (GFP) reporters stably transduced into T47D breast cancer cells (CK5Pro-GFP or CK5Pro-Luc). We validated the CK5Pro-GFP-T47D model for high-content screening in 96-well microplates and performed a pilot screen using a focused library of 280 compounds from the National Institutes of Health clinical collection. Four hits were obtained that significantly abrogated the progestin-induced CK5(+) cell population, three of which were members of the retinoid family. Hence, this approach will be useful in discovering small molecules that could potentially be developed as combination therapies, preventing the acquisition of a drug-resistant subpopulation.

Indexed as

Drug Resistance, NeoplasmAcitretinAntineoplastic Agents, HormonalBreast NeoplasmsCell Line, TumorCell ProliferationDrug DiscoveryFemaleGenes, ReporterGreen Fluorescent ProteinsHumansHyaluronan ReceptorsIsotretinoinKeratin-5LuciferasesMiconazoleAcitretinAntineoplastic Agents, HormonalCD44 protein, humanGreen Fluorescent ProteinsHyaluronan ReceptorsIsotretinoinKeratin-5LuciferasesMiconazoleProgesteroneProgestinsReceptors, EstrogenReceptors, ProgesteroneRetinoidsSmall Molecule LibrariesTretinoin

Identifiers

PMID22751729
PMCPMC4158006
OpenAlexW2101642693

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.