PTEN status in advanced colorectal cancer treated with cetuximab

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...

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Detalles Bibliográficos
Autores principales: Negri, F V, Bozzetti, C, Lagrasta, C A, Crafa, P, Bonasoni, M P, Camisa, R, Pedrazzi, G, Ardizzoni, A
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2010
Materias:
Short Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813733/
https://www.ncbi.nlm.nih.gov/pubmed/19953097
http://dx.doi.org/10.1038/sj.bjc.6605471
Descripción
Sumario: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.

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