Emanuela Dell'Aquila1, Daniele Rossini2, Alessandro Galletti3, Marco Stellato4, Alessandra Boccaccino2, Veronica Conca2, Marco Maria Germani2, Francesca Bergamo5, Francesca Daniel5, Andrea Spagnoletti6, Leonardo Provenzano6, Gianluca Tomasello7, Alberto Zaniboni8, Angela Buonadonna9, Laura Fanchini10, Samanta Cupini11, Chiara Carlomagno12, Salvatore Caponnetto13, Stefania Rapisardi14, Daniele Santini3. 1. Department of Medical Oncology, Campus Bio-Medico University of Rome, Rome, Italy; Medical Oncology 1, IRCCS Regina Elena National Cancer Institute, Rome, Italy. 2. Department of Translational Research and New Technologies in Medicine, University of Pisa, Pisa, Italy. 3. Department of Medical Oncology, Campus Bio-Medico University of Rome, Rome, Italy. 4. Department of Medical Oncology, Campus Bio-Medico University of Rome, Rome, Italy. Electronic address: m.stellato@unicampus.it. 5. Oncology Unit, Department of Oncology, Veneto Institute of Oncology IOV - IRCCS, Padova, Italy. 6. Medical Oncology Department, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. 7. Division of Medicine and Medical Oncology, Hospital of Cremona, Cremona, Italy. 8. Department of Oncology, Fondazione Poliambulanza Brescia, Brescia, Italy. 9. Department of Medical Oncology, Centro di Riferimento Oncologico (CRO), IRCCS, Aviano (PN), Italy. 10. ColoRectal Cancer Unit-Department of Oncology, AOU Città della Salute e della Scienza di Torino, Torino, Italy. 11. Department of Oncology, Azienda Toscana Nord Ovest, Division of Medical Oncology, Livorno Hospital, Livorno, Italy. 12. Department of Clinical Medicine and Surgery, University Federico II, Naples, Italy. 13. Department of Radiological, Oncological and Pathological Science, Sapienza University of Rome, Rome, Italy. 14. Oncology Unit, ARNAS Garibaldi Catania, Catania, Italy.
Abstract
BACKGROUND: Obesity is associated with an increased risk of development and recurrence of colorectal cancer. The role of obesity in metastatic colorectal cancer patients (pts) is still unclear, especially in those treated with triplet plus bevacizumab (bev). The aim of our study was to evaluate the prognostic and predictive role of BMI in metastatic colorectal cancer pts treated with FOLFOXIRI plus bev or FOLFIRI/FOLFOX plus bev in the TRIBE and TRIBE-2 trial. MATERIALS AND METHODS: A total of 1160 pts enrolled in TRIBE and TRIBE-2 trials were included. Baseline height and weight were used to assign pts to one of the following BMI categories: underweight (group A = BMI <18.5 kg/m2; 52 pts), normal (group B = BMI 18.5-29.9 kg/m2; 952 pts) and obese (group C > 30 kg/m2; 156 pts). RESULTS: In our population, no differences in terms of PFS (P = .43) or OS (P = .99) resulted between 3 groups. No interaction effect between treatment arm and BMI was evident in terms of PFS (Group A HR: 0.65 [95%CI: 0.36-1.16]; Group B HR: 0.77 [95%CI: 0.67-0.88]; Group C HR: 0.67 [95%CI: 0.48-0.93]; P for interaction = .75) or OS (Group A HR: 0.57 [95%CI: 0.29-1.12]; Group B HR: 0.85 [95%CI: 0.73-0.99];Group C HR: 0.69 [95%CI: 0.48-1.01] P for interaction = .36). No statistically significant difference in terms of dose reductions due to toxicities were found according to BMI in the overall population (P = .48) and in pts treated with FOLFOXIRI plus bev (P = .57). CONCLUSION: BMI was neither prognostic or predictive for PFS and OS in our population. Our analyses showed that the advantage of FOLFOXIRI plus bev versus FOLFIRI/FOLFOX plus bev was independent from BMI.
BACKGROUND: Obesity is associated with an increased risk of development and recurrence of colorectal cancer. The role of obesity in metastatic colorectal cancer patients (pts) is still unclear, especially in those treated with triplet plus bevacizumab (bev). The aim of our study was to evaluate the prognostic and predictive role of BMI in metastatic colorectal cancer pts treated with FOLFOXIRI plus bev or FOLFIRI/FOLFOX plus bev in the TRIBE and TRIBE-2 trial. MATERIALS AND METHODS: A total of 1160 pts enrolled in TRIBE and TRIBE-2 trials were included. Baseline height and weight were used to assign pts to one of the following BMI categories: underweight (group A = BMI <18.5 kg/m2; 52 pts), normal (group B = BMI 18.5-29.9 kg/m2; 952 pts) and obese (group C > 30 kg/m2; 156 pts). RESULTS: In our population, no differences in terms of PFS (P = .43) or OS (P = .99) resulted between 3 groups. No interaction effect between treatment arm and BMI was evident in terms of PFS (Group A HR: 0.65 [95%CI: 0.36-1.16]; Group B HR: 0.77 [95%CI: 0.67-0.88]; Group C HR: 0.67 [95%CI: 0.48-0.93]; P for interaction = .75) or OS (Group A HR: 0.57 [95%CI: 0.29-1.12]; Group B HR: 0.85 [95%CI: 0.73-0.99];Group C HR: 0.69 [95%CI: 0.48-1.01] P for interaction = .36). No statistically significant difference in terms of dose reductions due to toxicities were found according to BMI in the overall population (P = .48) and in pts treated with FOLFOXIRI plus bev (P = .57). CONCLUSION: BMI was neither prognostic or predictive for PFS and OS in our population. Our analyses showed that the advantage of FOLFOXIRI plus bev versus FOLFIRI/FOLFOX plus bev was independent from BMI.