Evidence map›Paper›PMID 25388162›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2015

Significant association of oncogene YAP1 with poor prognosis and cetuximab resistance in colorectal cancer patients.

Keun-Wook Lee, Sung Sook Lee, Sang-Bae Kim, Bo Hwa Sohn, Hyun-Sung Lee, Hee-Jin Jang, Yun-Yong Park, Scott Kopetz, Sung Soo Kim, Sang Cheul Oh and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 161 citations in OpenAlex.

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  14. Targeting TEAD in cancer.Frontiers in oncology · 2025
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50 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

11 authors at 3 institutions in 2 countries.

Keun-Wook LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Gyeonggi-do, Korea.
Sung Sook LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Hematology-Oncology, Inje University Haeundae Paik Hospital, Busan, Korea.
Sang-Bae KimDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Bo Hwa SohnDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Hyun-Sung LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Thoracic Surgery, Center for Lung Cancer, Research Institute and Hospital, National Cancer Center, Goyang, Gyeonggi-do, Korea.
Hee-Jin JangDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Thoracic Surgery, Center for Lung Cancer, Research Institute and Hospital, National Cancer Center, Goyang, Gyeonggi-do, Korea.
Yun-Yong ParkASAN Institute for Life Sciences, ASAN Medical Center, Department of Medicine, University of Ulsan College of Medicine, Seoul, Korea.
Scott KopetzDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Sung Soo KimDepartment of Biochemistry and Molecular Biology, Medical Research Center for Bioreaction to Reactive Oxygen Species and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Korea.
Sang Cheul OhDivision of Hemato-Oncology, Department of Internal Medicine, Korea University Medical Center, Korea University College of Medicine, Seoul, Korea.
Ju-Seog LeeDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Biochemistry and Molecular Biology, Medical Research Center for Bioreaction to Reactive Oxygen Species and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Korea. jlee@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USAsan Medical Center · KRKorea University Medical Center · KR

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
DEVELOPMENT AND VALIDATION OF PROGNOSTIC MODEL FOR GASTRIC CANCERR01CA150229 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, JU-SEOG · 2010 to 2013
$1.1M
NCI NIH HHS CA016672NCI NIH HHS CA150229NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA150229
6 · The paper itself

Abstract

purposeActivation of YAP1, a novel oncogene in the Hippo pathway, has been observed in many cancers, including colorectal cancer. We investigated whether activation of YAP1 is significantly associated with prognosis or treatment outcomes in colorectal cancer. EXPERIMENTAL

designA gene expression signature reflecting YAP1 activation was identified in colorectal cancer cells, and patients with colorectal cancer were stratified into two groups according to this signature: activated YAP1 colorectal cancer (AYCC) or inactivated YAP1 colorectal cancer (IYCC). Stratified patients in five test cohorts were evaluated to determine the effect of the signature on colorectal cancer prognosis and response to cetuximab treatment.

resultsThe activated YAP1 signature was associated with poor prognosis for colorectal cancer in four independent patient cohorts with stage I-III disease (total n = 1,028). In a multivariate analysis, the impact of the YAP1 signature on disease-free survival was independent of other clinical variables [hazard ratio (HR), 1.63; 95% confidence interval (CI), 1.25-2.13; P < 0.001]. In patients with stage IV colorectal cancer and wild-type KRAS, IYCC patients had a better disease control rate and progression-free survival (PFS) after cetuximab monotherapy than did AYCC patients; however, in patients with KRAS mutations, PFS duration after cetuximab monotherapy was not different between IYCC and AYCC patients. In multivariate analysis, the effect of YAP1 activation on PFS was independent of KRAS mutation status and other clinical variables (HR, 1.82; 95% CI, 1.05-3.16; P = 0.03).

conclusionsActivation of YAP1 is highly associated with poor prognosis for colorectal cancer and may be useful in identifying patients with metastatic colorectal cancer resistant to cetuximab.

Indexed as

Adaptor Proteins, Signal TransducingAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCell Line, TumorCetuximabColorectal NeoplasmsDisease-Free SurvivalDrug Resistance, NeoplasmHumansPhosphoproteinsPrognosisTranscription FactorsTranscriptomeTreatment OutcomeYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID25388162
PMCPMC4513664
OpenAlexW2099213341

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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.