Evidence map›Paper›PMID 28002810›Full record

ReviewOncotarget2017

Mechanisms of resistance to anti-EGFR therapy in colorectal cancer.

Ben Zhao, Lu Wang, Hong Qiu, Mingsheng Zhang, Li Sun, Ping Peng, Qianqian Yu, Xianglin Yuan

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 2 pooled it
11.0field-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

193 citing papers in PubMed, 2 syntheses or guidelines pooled it, 325 citations in OpenAlex.

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  7. Phase Ib/II Study of Cetuximab plus Pembrolizumab in Patients with Advanced RAS Wild-Type Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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133 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

8 authors at 2 institutions in 1 country.

Ben ZhaoDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Lu WangDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Hong QiuDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Mingsheng ZhangDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Li SunDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Ping PengDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Qianqian YuDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Xianglin YuanDepartment of Oncology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting the epidermal growth factor receptor (EGFR) either alone or in combination with chemotherapy is effective for patients with RAS wild type metastatic colorectal cancer (mCRC). However, only a small percentage of mCRC patients are sensitive to anti-EGFR therapy and even the best cases finally become refractory to this therapy. It has become apparent that the RAS mutations correlate with resistance to anti-EGFR therapy. However, these resistance mechanisms only account for nearly 35% to 50% of nonresponsive patients, suggesting that there might be additional mechanisms. In fact, several novel pathways leading to escape from anti-EGFR therapy have been reported in recent years. In this review, we provide an overview of known and novel mechanisms that contribute to both primary and acquired anti-EGFR therapy resistance, and enlist possible treatment strategies to overcome or reverse this resistance.

Indexed as

Drug Resistance, NeoplasmAntibodies, MonoclonalCetuximabColorectal NeoplasmsErbB ReceptorsGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMutationNeoplasm MetastasisPanitumumabProtein Kinase Inhibitorsras ProteinsSignal TransductionAntibodies, MonoclonalCetuximabEGFR protein, humanErbB ReceptorsPanitumumabProtein Kinase Inhibitorsras Proteinsacquired resistancecolorectal cancerepidermal growth factor receptorprimary resistancetargeted drug

Identifiers

PMID28002810
PMCPMC5354808
OpenAlexW2561259078

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.