Evidence map›Paper›PMID 41505680›Full record

Observational studyJCO precision oncology2026

Genomic Profile and Resistance to Anti-Epidermal Growth Factor Receptor Antibody in RAS-Amplified Colorectal Cancer: A Study Based on a Japanese Cancer Genome Database.

Gota Fujisawa, Kenji Tamada, Takeshi Hayashi, Nobumi Suzuki, Takuma Iwata, Yu Miyakawa, Masahiro Hata, Rei Ishibashi, Yoku Hayakawa, Aya Shinozaki-Ushiku and 4 more

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in JCO precision oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Gota FujisawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-0218-200X
Kenji TamadaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Takeshi HayashiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Nobumi SuzukiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0001-9566-8828
Takuma IwataDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0001-5229-3042
Yu MiyakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0009-0007-2743-9338
Masahiro HataDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Rei IshibashiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-9649-6471
Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Aya Shinozaki-UshikuDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hidenori KageDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0003-3658-4442
Katsutoshi OdaDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Narikazu BokuDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-1438-707X
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-4074-1140

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRAS mutation is a key biomarker of anti-epidermal growth factor receptor (EGFR) antibody resistance in colorectal cancer (CRC). However, the clinical impact of RAS amplification on the efficacy of anti-EGFR therapy remains unclear. This study aimed to characterize RAS-amplified CRC and evaluate the sensitivity of these tumors to anti-EGFR antibodies.

methodsWe conducted a retrospective observational study using the Center for Cancer Genomics and Advanced Therapeutics database in Japan, which includes clinical and genomic data from patients who underwent comprehensive genomic profiling. We analyzed the data from 9,135 patients with unresectable colorectal adenocarcinoma (CRA) who underwent FoundationOne CDx testing.

resultsRAS amplification was identified in 2.1% (188/9,135) of patients with CRA. Among 1,649 patients with RAS wild-type CRA who received first-line chemotherapy with anti-EGFR antibodies, those with RAS amplification had a lower overall response rate (ORR) and a shorter time to treatment failure (TTF) compared with those without RAS amplification (ORR, 37.5% [21/56]

conclusionRAS amplification is a rare alteration that may confer resistance to anti-EGFR antibodies. Assessing RAS amplification status may help guide the appropriate use of anti-EGFR antibodies in clinical practice.

Indexed as

AdenocarcinomaColorectal NeoplasmsDrug Resistance, NeoplasmErbB ReceptorsAdultAgedAged, 80 and overDatabases, GeneticEast Asian PeopleFemaleGene AmplificationHumansJapanMaleMiddle AgedRetrospective StudiesErbB Receptors

Identifiers

PMID41505680
PMCPMC12799258

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Registered trials

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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.