Evidence map›Paper›PMID 27648353›Full record

ReviewAmerican journal of cancer research2016

A perspective on anti-EGFR therapies targeting triple-negative breast cancer.

Katsuya Nakai, Mien-Chie Hung, Hirohito Yamaguchi

Open access · greenAbstract readReview
In one paragraph

Review in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed
13.2field-weighted citation impact, top 1% 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

215 citing papers in PubMed, 327 citations in OpenAlex.

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155 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

3 authors at 1 institution in 1 country.

Katsuya NakaiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterUSA; Department of Breast Oncology, Juntendo University School of MedicineBunkyo-ku, Tokyo, Japan.
Mien-Chie HungDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterUSA; Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University and HospitalTaichung 404, Taiwan; Department of Biotechnology, Asia UniversityTaichung 413, Taiwan.
Hirohito YamaguchiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center USA.
The University of Texas at Austin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC), which lacks estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), accounts for about 15-20% of breast cancers and is the most aggressive breast cancer subtype. There are currently no effective therapies against metastatic TNBC. Compared with other breast cancer subtypes, EGFR is frequently overexpressed in TNBC and a potential therapeutic target for this disease. There are two types of EGFR inhibitors, small molecular tyrosine kinase inhibitor (TKI) and monoclonal antibody (mAb), for the treatment of cancers, such as non-small cell lung cancer and colorectal cancer. For breast cancer, however, the clinical trials of EGFR inhibitors have failed due to low response rates. Because a small portion of patients do demonstrate response to EGFR inhibitors, it may be necessary to stratify patients to enhance the efficacy of EGFR inhibitors in TNBC and to develop the effective combination therapy for this patient population. In this review, we describe some of the molecular mechanisms underlying EGFR inhibitor sensitivity and further discuss the possible therapeutic strategies to increase the efficacy of EGFR inhibitors in TNBC.

Indexed as

drug resistanceEGFREGFR inhibitorsTNBC

Identifiers

PMID27648353
PMCPMC5004067
OpenAlexW2530480480

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.