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Cited by 291Colorectal Cancer Treatments and StudiesLung Cancer Treatments and MutationsPI3K/AKT/mTOR signaling in cancer

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

PIK3CA Mutations Are Not a Major Determinant of Resistance to the Epidermal Growth Factor Receptor Inhibitor Cetuximab in Metastatic Colorectal Cancer

Prenen, Hans, De Schutter, Jef, Jacobs, Bart, De Roock, Wendy, Biesmans, Bart, Claes, Bart, Lambrechts, Diether, Van Cutsem, Eric, Tejpar, Sabine·2009·Clinical Cancer Research
DOI 10.1158/1078-0432.ccr-08-2961
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Abstract

Purpose: It has been reported that activating KRAS mutations negatively affect response to anti–epidermal growth factor receptor (EGFR) monoclonal antibodies in metastatic colorectal cancer. The mutation status of signaling molecules downstream of the EGFR target is thus crucial to predict clinical benefit to EGFR-targeted therapies. Other mechanisms of resistance to EGFR inhibitors could involve activating mutations of the other main EGFR effector pathway, i.e., the PI3K/PTEN/AKT pathway. Experimental Design: We analyzed the PIK3CA and KRAS mutation status in a large group (n = 200) of chemorefractory metastatic colorectal cancers treated with cetuximab (Erbitux) in monotherapy or in combination with irinotecan, and correlated the mutation status with outcome. Results: Twenty-three (12%) of the 200 samples carried 1 of the PIK3CA mutations included in our assay. We found no correlation between the presence of a PIK3CA mutation and impaired response to cetuximab. Conclusions: Our findings do not provide any evidence for a strong role of PIK3CA mutations as a single marker in determining response to cetuximab in chemorefractory metastatic colorectal cancer.

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Metadata

Authors
Prenen, H., De Schutter, J., Jacobs, B., De Roock, W., Biesmans, B., Claes, B., Lambrechts, D., Van Cutsem, E., & Tejpar, S.
Affiliations
  • 1Department of Digestive Oncology, University Hospital Gasthuisberg,
  • 2Center for Human Genetics K.U.Leuven, and
  • KU Leuven (BE)
ORCID
Venue
Clinical Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2009-04-30
Volume
15
Issue
9
Pages
3184-3188
ISSN
  • 1078-0432 (ISSN-L)
  • 1557-3265
DOI
10.1158/1078-0432.ccr-08-2961
OpenAlex
W2028035144
Cited by
291
References
31
Citations by year
2025: 1 · 2024: 6 · 2023: 4 · 2022: 3 · 2021: 1 · 2020: 8 · 2019: 7 · 2018: 6 · 2017: 8 · 2016: 20 · 2015: 23 · 2014: 31 · 2013: 34 · 2012: 34
FWCI
22.99
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Cancer Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
PIK3CA mutation, cetuximab, EGFR inhibitors, metastatic colorectal cancer, KRAS mutation, PI3K/Akt signaling, drug resistance, irinotecan, predictive biomarkers, chemorefractory cancer
MeSH terms
Cetuximab, Irinotecan, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Antineoplastic Combined Chemotherapy Protocols, Camptothecin, Humans, Male, Middle Aged, Mutation, Neoplasm Staging, Prognosis, Proto-Oncogene Proteins, Colorectal Neoplasms, Cohort Studies, Survival Rate, Proto-Oncogene Proteins p21(ras), Treatment Outcome, ras Proteins, Drug Resistance, Neoplasm, Phosphatidylinositol 3-Kinases, Maximum Tolerated Dose, Class I Phosphatidylinositol 3-Kinases, Antibodies, Monoclonal, Humanized, ErbB Receptors

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