David Sefrioui1, Ludivine Beaussire2, Pierre Michel3, Frédéric Di Fiore4, André Gillibert5, France Blanchard6, Emmanuel Toure6, Céline Bazille7, Anne Perdrix8, Frédéric Ziegler9, Alice Gangloff3, Mélanie Hassine10, Caroline Elie10, Anne-Laure Bignon11, Aurélie Parzy12, Philippe Gomez13, Caroline Thill5, Florian Clatot14, Jean-Christophe Sabourin6, Thierry Frebourg15, Jacques Benichou5, Karine Bouhier-Leporrier11, Marie-Pierre Gallais12, Nasrin Sarafan-Vasseur2. 1. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine and Department of Hepatogastroenterology, Rouen, France. david.sefrioui@chu-rouen.fr. 2. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, Rouen, France. 3. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine and Department of Hepatogastroenterology, Rouen, France. 4. Department of Hepatogastroenterology and Department of Medical Oncology, Henri Becquerel Centre, Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, Rouen, France. 5. Department of Biostatistics, Normandie Univ, UNIROUEN, Rouen University Hospital, Rouen, France. 6. Department of Pathology, Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, Rouen, France. 7. Department of Pathology, Caen University Hospital, Caen, France. 8. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine and Department of Biopathology, Henri Becquerel Centre, Rouen, France. 9. Normandie Univ, UNIROUEN, INSERM U1073, Rouen University Hospital and General Biochemistry Laboratory, Institute of Clinical Biology, Rouen, France. 10. Department of Hepatogastroenterology, Elbeuf Hospital, Elbeuf, France. 11. Department of Hepatogastroenterology, Caen University Hospital, Caen, France. 12. Department of Hepatogastroenterology, Francois Baclesse Centre, Caen, France. 13. Department of Medical Oncology, Frédéric Joliot Centre, Rouen, France. 14. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine and Department of Medical Oncology, Henri Becquerel Centre, Rouen, France. 15. Normandie Univ, UNIROUEN, Inserm U1245, IRON Group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine and Department of Genetics, Rouen, France.
Abstract
BACKGROUND: We previously reported that CEA kinetics are a marker of progressive disease (PD) in metastatic colorectal cancer (mCRC). This study was specifically designed to confirm CEA kinetics for predicting PD and to evaluate CA19-9, cell-free DNA (cfDNA), circulating tumour DNA (ctDNA) and circulating tumour cell (CTC) kinetics. METHODS: Patients starting a chemotherapy (CT) with pre-treatment CEA > 5 ng/mL and/or CA19.9 > 30 UI/mL were prospectively included. Samples were collected from baseline to cycle 4 for CEA and CA19-9 and at baseline and the sixth week for other markers. CEA kinetics were calculated from the first to the third or fourth CT cycle. RESULTS: A total of 192 mCRC patients were included. CEA kinetics based on the previously identified >0.05 threshold was significantly associated with PD (p < 0.0001). By dichotomising by the median value, cfDNA, ctDNA and CA19-9 were associated with PD, PFS and OS in multivariate analysis. A circulating scoring system (CSS) combining CEA kinetics and baseline CA19-9 and cfDNA values classified patients based on high (n = 58) and low risk (n = 113) of PD and was independently associated with PD (ORa = 4.6, p < 0.0001), PFS (HRa = 2.07, p < 0.0001) and OS (HRa = 2.55, p < 0.0001). CONCLUSIONS: CEA kinetics alone or combined with baseline CA19-9 and cfDNA are clinically relevant for predicting outcomes in mCRC. TRIAL REGISTRATION NUMBER: NCT01212510.
BACKGROUND: We previously reported that CEA kinetics are a marker of progressive disease (PD) in metastatic colorectal cancer (mCRC). This study was specifically designed to confirm CEA kinetics for predicting PD and to evaluate CA19-9, cell-free DNA (cfDNA), circulating tumour DNA (ctDNA) and circulating tumour cell (CTC) kinetics. METHODS: Patients starting a chemotherapy (CT) with pre-treatment CEA > 5 ng/mL and/or CA19.9 > 30 UI/mL were prospectively included. Samples were collected from baseline to cycle 4 for CEA and CA19-9 and at baseline and the sixth week for other markers. CEA kinetics were calculated from the first to the third or fourth CT cycle. RESULTS: A total of 192 mCRC patients were included. CEA kinetics based on the previously identified >0.05 threshold was significantly associated with PD (p < 0.0001). By dichotomising by the median value, cfDNA, ctDNA and CA19-9 were associated with PD, PFS and OS in multivariate analysis. A circulating scoring system (CSS) combining CEA kinetics and baseline CA19-9 and cfDNA values classified patients based on high (n = 58) and low risk (n = 113) of PD and was independently associated with PD (ORa = 4.6, p < 0.0001), PFS (HRa = 2.07, p < 0.0001) and OS (HRa = 2.55, p < 0.0001). CONCLUSIONS: CEA kinetics alone or combined with baseline CA19-9 and cfDNA are clinically relevant for predicting outcomes in mCRC. TRIAL REGISTRATION NUMBER: NCT01212510.
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