PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients
Open accessAbstract
Background It has been reported that KRAS mutations (and to a lesser extent KRAS mutations with the BRAF V600E mutation) negatively affect response to anti-epidermal growth factor receptor (EGFR) mAbs in metastatic colorectal cancer (mCRC) patients, while the biological impact of the EGFR pathway represented by PI3K/PTEN/AKT on anti-EGFR treatment is still not clear.Patients and methods We analysed formalin-fixed samples from a cohort of 32 mCRC patients treated with cetuximab by means of EGFR immunohistochemistry, EGFR and PTEN FISH analysis, and KRAS, BRAF, PI3KCA, and PTEN genomic sequencing.Results Ten (31%) of 32 patients showed a partial response to cetuximab and 22 (69%) did not [nonresponder (NR)]. EGFR immunophenotype and FISH-based gene status did not predict an anti-EGFR mAb response, whereas KRAS mutations (24%) and PI3K pathway activation, by means of PI3KCA mutations (13%) or PTEN mutation (10%)/loss (13%), were significantly restricted to, respectively, 41% and 37% of NRs.Conclusion These findings suggested that KRAS mutations and PI3KCA/PTEN deregulation significantly correlate with resistance to cetuximab. In line with this, patients carrying KRAS mutations or with activated PI3K profiles can benefit from targeted treatments only by switching off molecules belonging to the downstream signalling of activated EGFR, such as mammalian target of rapamycin.
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Loss of function of PTEN occurs in 30% of sporadic colorectal cancers.
“Loss of function of PTEN, which antagonizes PI3K activity, occurs in 30 % of sporadic CRCs through a variety of mechanisms [73, 74].”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [73]
Both PIK3CA exon 20 mutations and loss of PTEN expression are promising predictors of tumor suitability for anti-EGFR therapies.
“In summary, both PIK3CA exon 20 mutations and loss of PTEN expression are promising predictors of tumor suitability for anti-EGFR therapies.”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [73]
PTEN inactivation is associated with nonresponsiveness to anti-EGFR monoclonal antibodies in metastatic colorectal cancer patients.
“PTEN inactivation (usually assessed as lack of protein expression) has been associated with nonresponsiveness to anti-EGFR moAbs in mCRC patients in several studies [19, 73, 75, 76]”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [73]
Phosphor-EGFR is capable of initiating the PI3K/AKT/mTOR pathway, and PI3K mutation and aberrant AKT/mTOR activation promote resistance to anti-EGFR monoclonal antibodies.
“Phosphor-EGFR is capable of initiating the PI3K/AKT/mTOR pathway, and PI3K mutation and aberrant AKT/mTOR activation promote resistance to anti-EGFR mAbs [104].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [104]
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- Authors
- Perrone, F., Lampis, A., Orsenigo, M., Di Bartolomeo, M., Gevorgyan, A., Losa, M., Frattini, M., Riva, C., Andreola, S., Bajetta, E., Bertario, L., Leo, E., Pierotti, M. A., & Pilotti, S.
- Affiliations
- Fondazione IRCCS Istituto Nazionale dei Tumori (IT)
- Istituto Cantonale di Patologia (CH)
- Corresponding author
- Pilotti, S.
- Venue
- Annals of Oncology
- Publisher
- Elsevier BV
- Published
- 2009-01
- Volume
- 20
- Issue
- 1
- Pages
- 84-90
- ISSN
- 0923-7534 (ISSN-L)
- OpenAlex
- W2114048774
- Cited by
- 410
- References
- 28
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 16 · 2023: 4 · 2022: 13 · 2021: 6 · 2020: 11 · 2019: 12 · 2018: 9 · 2017: 21 · 2016: 25 · 2015: 31 · 2014: 37 · 2013: 38 · 2012: 38
- FWCI
- 24.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Annals of Oncology (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università Vita-Salute San Raffaele (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- 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
- cetuximab, metastatic colorectal cancer, PIK3CA mutation, PTEN loss, KRAS mutation, BRAF V600E mutation, anti-EGFR therapy, drug resistance, mTOR, predictive biomarkers, EGFR immunohistochemistry
- MeSH terms
- Cetuximab, Adult, Aged, Antibodies, Monoclonal, Antineoplastic Agents, DNA Mutational Analysis, Female, Humans, Male, Middle Aged, Mutation, Neoplasm Metastasis, Nuclear Proteins, Genes, ras, Transcription Factors, Colorectal Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Disease-Free Survival, Genes, erbB-1, Drug Resistance, Neoplasm, PTEN Phosphohydrolase, Antibodies, Monoclonal, Humanized
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