PTEN status in advanced colorectal cancer treated with cetuximab
Open accessAbstract
BACKGROUND: Loss of phosphatase and tensin homologue deleted in chromosome 10 (PTEN) function in advanced colorectal cancer (CRC) may represent one of the resistance mechanisms to cetuximab by interfering with the epidermal growth factor receptor signal transduction pathway. METHODS: PTEN expression tested by indirect immunofluorescence was evaluated both on primary (n=43) and on metastatic (n=24) sites in CRC patients treated with cetuximab. RESULTS: The loss of PTEN expression tested on metastatic sites was negatively associated with response (100% progressive disease (PD) in PTEN-negative cases vs 30% PD in PTEN-positive cases; P<0.05), PFS (0.8 vs 8.2 months; P<0.001) and OS (2.9 vs 14.2 months; P<0.001). CONCLUSION: A potential role of PTEN in the anti-tumour activity of cetuximab could be hypothesised.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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 [78]
Patients with PTEN-negative status showed a worse response rate and shorter progression-free survival than those with PTEN-positive status.
“Patients with PTEN-negative status showed a worse response rate and shorter progression-free survival (PFS) than those with PTEN-positive status [106, 108, 109].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [108]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 13 · Cited by 83
- Authors
- Negri, F. V., Bozzetti, C., Lagrasta, C. A., Crafa, P., Bonasoni, M. P., Camisa, R., Pedrazzi, G., & Ardizzoni, A.
- Affiliations
- Ospedale di Parma (IT)
- Santa Maria Nuova Hospital (IT)
- University of Parma (IT)
- Corresponding author
- Negri, F V
- Venue
- British Journal of Cancer
- Published
- 2009-12-01
- Volume
- 102
- Issue
- 1
- Pages
- 162-164
- ISSN
- 0007-0920 (ISSN-L)
- 1532-1827
- PMC
- PMC2813733
- OpenAlex
- W2002019030
- Cited by
- 83
- References
- 13
- Citations by year
- 2024: 5 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 4 · 2019: 5 · 2018: 3 · 2017: 9 · 2016: 3 · 2015: 2 · 2014: 11 · 2013: 6 · 2012: 15
- FWCI
- 5.17
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- www.springer.com/tdm (unspecified)
- Locations
- British Journal of Cancer (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- PTEN, advanced colorectal cancer, cetuximab, anti-EGFR therapy, drug resistance, metastatic colorectal cancer, PTEN expression, progression-free survival, overall survival, epidermal growth factor receptor signaling
- MeSH terms
- Cetuximab, Irinotecan, Oxaliplatin, Adenocarcinoma, Antibodies, Monoclonal, Antineoplastic Combined Chemotherapy Protocols, Camptothecin, Follow-Up Studies, Humans, Neoplasm Proteins, Organoplatinum Compounds, Colorectal Neoplasms, Signal Transduction, Salvage Therapy, Treatment Outcome, Gene Deletion, Gene Dosage, Drug Resistance, Neoplasm, Phosphatidylinositol 3-Kinases, Gene Expression Profiling, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Antibodies, Monoclonal, Humanized, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review