Evidence map›Paper›PMID 23689139›Full record

ArticleCancer letters2013

Quantitative high-throughput efficacy profiling of approved oncology drugs in inflammatory breast cancer models of acquired drug resistance and re-sensitization.

Kevin P Williams, Jennifer L Allensworth, Shalonda M Ingram, Ginger R Smith, Amy J Aldrich, Jonathan Z Sexton, Gayathri R Devi

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Inflammatory Breast Cancer: a Separate Entity.Current oncology reports · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Lapatinib resistance in HER2+ cancers: latest findings and new concepts on molecular mechanisms.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  20. Review
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.

Kevin P WilliamsBiomanufacturing Research Institute and Technology Enterprise (BRITE), North Carolina Central University, Durham, NC 27707, USA. kpwilliams@nccu.edu
Jennifer L Allensworth
Shalonda M Ingram
Ginger R Smith
Amy J Aldrich
Jonathan Z Sexton
Gayathri R Devi
North Carolina Central University · USDuke Medical Center · US

Funding

Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
The Hedgehog Pathway and Inflammatory Breast CancerSC2CA137844 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI WILLIAMS, KEVIN PETER · 2008 to 2010
$291k
NCI NIH HHS CA137844NCI NIH HHS SC2 CA137844NCI NIH HHS T32 CA009111NCI NIH HHS T32CA009111
6 · The paper itself

Abstract

Although there is no standard treatment protocol for inflammatory breast cancer (IBC), multi-modality treatment has improved survival. In this study we profiled the NCI approved oncology drug set in a qHTS format to identify those that are efficacious in basal type and ErbB2 overexpressing IBC models. Further, we characterized the sensitivity of an acquired therapeutic resistance model to the oncology drugs. We observed that lapatinib-induced acquired resistance in SUM149 cells led to cross-resistance to other targeted- and chemotherapeutic drugs. Removal of the primary drug to which the model was developed led to re-sensitization to multiple drugs to a degree comparable to the parental cell line; this coincided with the cells regaining the ability to accumulate ROS and reduced expression of anti-apoptotic factors and the antioxidant SOD2. We suggest that our findings provide a unique IBC model system for gaining an understanding of acquired therapeutic resistance and the effect of redox adaptation on anti-cancer drug efficacy.

Indexed as

High-Throughput Screening AssaysAntineoplastic AgentsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmDrug Screening Assays, AntitumorFemaleHumansInflammatory Breast NeoplasmsLapatinibQuinazolinesX-Linked Inhibitor of Apoptosis ProteinAntineoplastic AgentsLapatinibQuinazolinesXIAP protein, humanX-Linked Inhibitor of Apoptosis ProteinLapatinibqHTSRedox adaptationSUM149SUM190XIAP

Identifiers

PMID23689139
PMCPMC3763836
OpenAlexW2075870524

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.