Evidence map›Paper›PMID 26989027›Full record

ArticleOncotarget2016

Mutations of KRAS/NRAS/BRAF predict cetuximab resistance in metastatic colorectal cancer patients.

Hung-Chih Hsu, Tan Kien Thiam, Yen-Jung Lu, Chien Yuh Yeh, Wen-Sy Tsai, Jeng Fu You, Hsin Yuan Hung, Chi-Neu Tsai, An Hsu, Hua-Chien Chen and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 78 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 4 pooled it
9.0field-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

78 citing papers in PubMed, 4 syntheses or guidelines pooled it, 127 citations in OpenAlex.

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  13. Distinct Driver Pathway Enrichments and a High Prevalence ofInternational journal of molecular sciences · 2024
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  17. International journal of molecular sciences · 2023
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  20. A study of gene variation in All-Journal of gastrointestinal oncology · 2022
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18 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

12 authors at 3 institutions in 1 country.

Hung-Chih HsuDivision of Hematology-Oncology, Chang Gung Memorial Hospital, Kwei-Shan, Tao-Yuan 333, Taiwan.
Tan Kien ThiamACT Genomics, Neihu Dist., Taipei 114, Taiwan.
Yen-Jung LuACT Genomics, Neihu Dist., Taipei 114, Taiwan.
Chien Yuh YehCollege of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan.
Wen-Sy TsaiCollege of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan.
Jeng Fu YouCollege of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan.
Hsin Yuan HungCollege of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan.
Chi-Neu TsaiGraduate Institute of Clinical Medicine, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan.
An HsuACT Genomics, Neihu Dist., Taipei 114, Taiwan.
Hua-Chien ChenACT Genomics, Neihu Dist., Taipei 114, Taiwan.
Shu-Jen ChenACT Genomics, Neihu Dist., Taipei 114, Taiwan.
Tsai-Sheng YangDivision of Hematology-Oncology, Chang Gung Memorial Hospital, Kwei-Shan, Tao-Yuan 333, Taiwan.
Genomics Research Center, Academia Sinica · TWChang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approximately 45% of metastatic colorectal cancer (mCRC) patients with wild-type KRAS exon 2 are resistant to cetuximab treatment. We set out to identify additional genetic markers that might predict the response to cetuximab treatment. Fifty-three wild-type KRAS exon 2 mCRC patients were treated with cetuximab/irinotecan-based chemotherapy as a first- or third-line therapy. The mutational statuses of 10 EGFR pathway genes were analyzed in primary tumors using next-generation sequencing. BRAF, PIK3CA, KRAS (exons 3 and 4), NRAS, PTEN, and AKT1 mutations were detected in 6, 6, 5, 4, 1, and 1 patient, respectively. Four of the BRAF mutations were non-V600 variants. Four tumors harbored multiple co-existing (complex) mutations. All patients with BRAF mutations or complex mutation patterns were cetuximab non-responders. All patients but one harboring KRAS, NRAS, or BRAF mutations were non-responders. Mutations in any one of these three genes were associated with a poor response rate (7.1%) and reduced survival (PFS = 8.0 months) compared to wild-type patients (74.4% and 11.6 months). Our data suggest that KRAS, NRAS, and BRAF mutations predict response to cetuximab treatment in mCRC patients.

Indexed as

AdultAgedAntineoplastic AgentsBiomarkers, TumorCetuximabColorectal NeoplasmsDNA Mutational AnalysisDrug Resistance, NeoplasmFemaleGTP PhosphohydrolasesHumansKaplan-Meier EstimateMaleMembrane ProteinsMiddle AgedMutationAntineoplastic AgentsBiomarkers, TumorBRAF protein, humanCetuximabGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BRAFcetuximab resistancemetastatic colorectal cancermutationRAS

Identifiers

PMID26989027
PMCPMC5008360
OpenAlexW2344600572

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.