Evidence map›Paper›PMID 26657506›Full record

ArticleOncotarget2016

HER2 genomic amplification in circulating tumor DNA from patients with cetuximab-resistant colorectal cancer.

Naoki Takegawa, Kimio Yonesaka, Kazuko Sakai, Hiroto Ueda, Satomi Watanabe, Yoshikane Nonagase, Tatsuya Okuno, Masayuki Takeda, Osamu Maenishi, Junji Tsurutani and 5 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Trial
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  11. HER2-Positive Metastatic Colorectal Cancer.Current treatment options in oncology · 2024
    Review
  12. Review
  13. Article
  14. Circulating Tumor DNA to Drive Treatment in Metastatic Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Review
  15. Review
  16. Article
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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

15 authors.

Naoki TakegawaDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Kimio YonesakaDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Kazuko SakaiDepartment of Genome Biology, Kinki University School of Medicine, Osaka, Japan.
Hiroto UedaDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Satomi WatanabeDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Yoshikane NonagaseDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Tatsuya OkunoDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Masayuki TakedaDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Osamu MaenishiDepartment of Pathology, Kinki University School of Medicine, Osaka, Japan.
Junji TsurutaniDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Taroh SatohDepartment of Frontier Science for Cancer and Chemotherapy, Osaka University Graduate School of Medicine, Osaka, Japan.
Isamu OkamotoCenter for Clinical and Translational Research, Kyushu University, Kyushu, Japan.
Kazuto NishioDepartment of Genome Biology, Kinki University School of Medicine, Osaka, Japan.
Takao TamuraDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.
Kazuhiko NakagawaDepartment of Medical Oncology, Kinki University School of Medicine, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with metastatic colorectal cancer (mCRC) harboring wild-type KRAS benefit from epidermal growth factor receptor (EGFR)-targeted therapy. However, patients who are treated with anti-EGFR antibodies will eventually develop the resistance to those agents. HER2 amplification is one of the mechanisms conferring resistance to anti-EGFR antibody therapy and could therefore be a potential therapeutic target. The aim of this study was to detect HER2 amplification in circulating tumor DNA (ctDNA) from patients with CRC and acquired resistance to anti-EGFR antibody therapy.

resultsOur data showed that 22% (4/18) of patients in the cohort exhibited HER2 amplification. One of these patients was found to be positive for HER2 amplification in matched tumor specimens collected after cetuximab therapy, at which point the patient had acquired cetuximab resistance, despite being negative for HER2 amplification prior to therapy.

methodsWe analyzed plasma ctDNA using digital polymerase chain reaction (PCR) from 18 patients with CRC, who had been treated with anti-EGFR antibody-based therapy (cetuximab) and subsequently acquired resistant cetuximab. HER2 gene copy number was analyzed using fluorescence in situ hybridization in tumor samples before and after acquisition of resistance to cetuximab-based therapy.

conclusionsAnalysis of plasma ctDNA by digital PCR could be useful for detecting HER2 amplification in patients with CRC who were resistant to anti-EGFR antibody therapy.

Indexed as

Gene AmplificationAgedAged, 80 and overAntineoplastic AgentsBiomarkers, TumorCetuximabCohort StudiesColorectal NeoplasmsDNA, NeoplasmDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleFollow-Up StudiesHumansImmunoenzyme TechniquesIn Situ HybridizationAntineoplastic AgentsBiomarkers, TumorCetuximabDNA, NeoplasmERBB2 protein, humanErb-b2 Receptor Tyrosine Kinasesacquired resistancecetuximabcolorectal cancerctDNAhuman epidermal growth factor receptor 2

Identifiers

PMID26657506
PMCPMC4823119

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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.