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4 results on '"and Canestrari, E."'

3. KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer.

Author

Loupakis, F., Ruzzo, A., Cremolini, C., Vincenzi, B., Salvatore, L., Santini, D., Masi, G., Stasi, I., Canestrari, E., Rulli, E., Floriani, I., Bencardino, K., Galluccio, N., Catalano, V., Tonini, G., Magnani, M., Fontanini, G., Basolo, F., Falcone, A., and Graziano, F.

Subjects
GENETIC mutation, CETUXIMAB, COLON cancer, RAS proteins, CHEMICAL resistance, ANTINEOPLASTIC agents, ADENOCARCINOMA, CAMPTOTHECIN, COLON tumors, COMPARATIVE studies, DRUG resistance in cancer cells, EPIDERMAL growth factor, GENES, RESEARCH methodology, MEDICAL cooperation, MONOCLONAL antibodies, PROGNOSIS, PROTEINS, RECTUM tumors, RESEARCH, TRANSFERASES, EVALUATION research, KAPLAN-Meier estimator, SEQUENCE analysis
Abstract

Background: KRAS codons 12 and 13 mutations predict resistance to anti-EGFR monoclonal antibodies (moAbs) in metastatic colorectal cancer. Also, BRAF V600E mutation has been associated with resistance. Additional KRAS mutations are described in CRC.Methods: We investigated the role of KRAS codons 61 and 146 and BRAF V600E mutations in predicting resistance to cetuximab plus irinotecan in a cohort of KRAS codons 12 and 13 wild-type patients.Results: Among 87 KRAS codons 12 and 13 wild-type patients, KRAS codons 61 and 146 were mutated in 7 and 1 case, respectively. None of mutated patients responded vs 22 of 68 wild type (P=0.096). Eleven patients were not evaluable. KRAS mutations were associated with shorter progression-free survival (PFS, HR: 0.46, P=0.028). None of 13 BRAF-mutated patients responded vs 24 of 74 BRAF wild type (P=0.016). BRAF mutation was associated with a trend towards shorter PFS (HR: 0.59, P=0.073). In the subgroup of BRAF wild-type patients, KRAS codons 61/146 mutations determined a lower response rate (0 vs 37%, P=0.047) and worse PFS (HR: 0.45, P=0.023). Patients bearing KRAS or BRAF mutations had poorer response rate (0 vs 37%, P=0.0005) and PFS (HR: 0.51, P=0.006) compared with KRAS and BRAF wild-type patients.Conclusion: Assessing KRAS codons 61/146 and BRAF V600E mutations might help optimising the selection of the candidate patients to receive anti-EGFR moAbs. [ABSTRACT FROM AUTHOR]

Published
2009
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4. High concordance of BRAF status between primary colorectal tumours and related metastatic sites: implications for clinical practice

Author

Francesco Alfredo Zito, Giuseppe Tonini, Annamaria Ruzzo, Alfredo Falcone, Chiara Cremolini, Giuseppe Colucci, Michele Caraglia, Nicola Silvestris, Emanuele Canestrari, Bruno Vincenzi, Lisa Salvatore, Fotios Loupakis, Francesco Graziano, Chiara Spoto, Daniele Santini, N Galluccio, Santini, D, Spoto, C, Loupakis, F, Vincenzi, B, Silvestris, N, Cremolini, C, Canestrari, E, Graziano, F, Galluccio, N, Salvatore, L, Caraglia, Michele, Zito, Fa, Colucci, G, Falcone, A, Tonini, G, and Ruzzo, A.

Subjects
Adult, Proto-Oncogene Proteins B-raf, Concordance, Rectum, macromolecular substances, medicine.disease_cause, Metastasis, Humans, Medicine, Panitumumab, Aged, Retrospective Studies, Aged, 80 and over, business.industry, Liver Neoplasms, Cancer, Retrospective cohort study, DNA, Neoplasm, Hematology, Middle Aged, Prognosis, medicine.disease, digestive system diseases, Clinical Practice, medicine.anatomical_structure, Oncology, Mutation, Cancer research, KRAS, Colorectal Neoplasms, business, medicine.drug
Abstract

Purpose. Several studies have suggested that KRAS somatic mutations may predict resistance to cetuximaband panitumumab-based treatments in metastatic colo

Published
2010

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