Evidence map›Paper›PMID 25032217›Full record

ReviewBioMed research international2014

Current approaches for predicting a lack of response to anti-EGFR therapy in KRAS wild-type patients.

Tze-Kiong Er, Chih-Chieh Chen, Luis Bujanda, Marta Herreros-Villanueva

Abstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. KRAS status is related to histological phenotype in gastric cancer: results from a large multicentre study.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Article
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

4 authors.

Tze-Kiong ErDivision of Molecular Diagnostics, Department of Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan ; Translational Research Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan.
Chih-Chieh ChenCenter for Lipid Biosciences, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan ; Biomedical Technology and Device Research Laboratories, Industrial Technology Research Institute, No. 195, Section 4, Chung-Hsing Road, Chutung, Hsinchu 31040, Taiwan.ORCID 0000-0003-3847-3690
Luis BujandaDepartment of Gastroenterology, Donostia Hospital, Biodonostia Institute, Center for Biomedical Research in Network for Hepatic and Digestives Diseases (CIBERehd), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), University of Basque Country, 20014 San Sebastian, Spain.
Marta Herreros-VillanuevaDepartment of Gastroenterology, Donostia Hospital, Biodonostia Institute, Center for Biomedical Research in Network for Hepatic and Digestives Diseases (CIBERehd), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), University of Basque Country, 20014 San Sebastian, Spain.ORCID 0000-0002-6905-0693

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting epidermal growth factor receptor (EGFR) has been one of the most effective colorectal cancer strategies. Anti-EGFR antibodies function by binding to the extracellular domain of EGFR, preventing its activation, and ultimately providing clinical benefit. KRAS mutations in codons 12 and 13 are recognized prognostic and predictive biomarkers that should be analyzed at the clinic prior to the administration of anti-EGFR therapy. However, still an important fraction of KRAS wild-type patients do not respond to the treatment. The identification of additional genetic determinants of primary or secondary resistance to EGFR targeted therapy for further improving the selection of patients is urgent. Herein, we review the latest published literature highlighting the most important genes that may predict resistance to anti-EGFR monoclonal antibodies in colorectal cancer patients. According to the available findings, the evaluation of BRAF, NRAS, PIK3CA, and PTEN status could be the right strategy to select patients who are likely to respond to anti-EGFR therapies. In the future, the combination of those biomarkers will help establish consensus that can be introduced into clinical practice.

Indexed as

Antibodies, NeoplasmAntineoplastic AgentsClass I Phosphatidylinositol 3-KinasesColorectal NeoplasmsDrug Resistance, NeoplasmErbB ReceptorsGTP PhosphohydrolasesHumansMembrane ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)PTEN Phosphohydrolaseras ProteinsAntibodies, NeoplasmAntineoplastic AgentsBRAF protein, humanClass I Phosphatidylinositol 3-KinasesEGFR protein, humanErbB ReceptorsGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePTEN protein, humanras Proteins

Identifiers

PMID25032217
PMCPMC4086227

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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.