Evidence map›Paper›PMID 28281569›Full record

ArticleScientific reports2017

Treating triple negative breast cancer cells with erlotinib plus a select antioxidant overcomes drug resistance by targeting cancer cell heterogeneity.

Bin Bao, Cristina Mitrea, Priyanga Wijesinghe, Luca Marchetti, Emily Girsch, Rebecca L Farr, Julie L Boerner, Ramzi Mohammad, Greg Dyson, Stanley R Terlecky and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  4. Mechanisms of RNA alternative splicing dysregulation in triple-negative breast cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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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

11 authors at 3 institutions in 3 countries.

Bin BaoBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Cristina MitreaBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Priyanga WijesingheBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Luca MarchettiThe Microsoft Research - University of Trento Centre for Computational and Systems Biology, Rovereto, Italy.
Emily GirschBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Rebecca L FarrDepartment of Pharmacology, Wayne State University School of Medicine, Detroit MI 48201, USA.
Julie L BoernerBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Ramzi MohammadBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Greg DysonBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
Stanley R TerleckyDepartment of Pharmacology, Wayne State University School of Medicine, Detroit MI 48201, USA.
Aliccia Bollig-FischerBarbara Ann Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI 48201, USA.
The Barbara Ann Karmanos Cancer Institute · USWayne State University · USUniversity of Trento · IT

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
NCI NIH HHS P30 CA022453
6 · The paper itself

Abstract

Among breast cancer patients, those diagnosed with the triple-negative breast cancer (TNBC) subtype have the worst prog-nosis. TNBC does not express estrogen receptor-alpha, progesterone receptor, or the HER2 oncogene; therefore, TNBC lacks targets for molecularly-guided therapies. The concept that EGFR oncogene inhibitor drugs could be used as targeted treatment against TNBC has been put forth based on estimates that 30-60% of TNBC express high levels of EGFR. However, results from clinical trials testing EGFR inhibitors, alone or in combination with cytotoxic chemotherapy, did not improve patient outcomes. Results herein offer an explanation as to why EGFR inhibitors failed TNBC patients and support how combining a select antioxidant and an EGFR-specific small molecule kinase inhibitor (SMKI) could be an effective, novel therapeutic strategy. Treatment with CAT-SKL-a re-engineered protein form of the antioxidant enzyme catalase-inhibited cancer stem-like cells (CSCs), and treatment with the EGFR-specific SMKI erlotinib inhibited non-CSCs. Thus, combining the antioxidant CAT-SKL with erlotinib targeted both CSCs and bulk cancer cells in cultures of EGFR-expressing TNBC-derived cells. We also report evidence that the mechanism for CAT-SKL inhibition of CSCs may depend on antioxidant-induced downregulation of a short alternative mRNA splicing variant of the methyl-CpG binding domain 2 gene, isoform MBD2c.

Indexed as

AntioxidantsDrug Resistance, NeoplasmErlotinib HydrochlorideFemaleHumansTriple Negative Breast NeoplasmsAntioxidantsErlotinib Hydrochloride

Identifiers

PMID28281569
PMCPMC5345072
OpenAlexW2594614544

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.