Simon Pernot1, Cecile Badoual2, Magali Terme3, Florence Castan4, Aurelie Cazes5, Olivier Bouche6, Jaafar Bennouna7, Eric Francois8, Francois Ghiringhelli9, Christelle De La Fouchardiere10, Emmanuelle Samalin11, Jean Baptiste Bachet12, Christophe Borg13, Michel Ducreux14, Elie Marcheteau3, Trevor Stanbury15, Sophie Gourgou4, David Malka14, Julien Taieb16. 1. INSERM U970 - PARCC (Paris Cardiovascular Research Center), Paris Descartes University, Sorbonne Paris Cité, Paris, France; Hôpital Européen Georges-Pompidou, APHP, Department of GI Oncology, Paris Descartes University, Sorbonne Paris Cité, Paris, France. 2. INSERM U970 - PARCC (Paris Cardiovascular Research Center), Paris Descartes University, Sorbonne Paris Cité, Paris, France; Hôpital Européen Georges-Pompidou, APHP, Department of Pathology, Paris Descartes University, Sorbonne Paris Cité, Paris, France. 3. INSERM U970 - PARCC (Paris Cardiovascular Research Center), Paris Descartes University, Sorbonne Paris Cité, Paris, France. 4. Biostatistics Unit, CTD INCa, ICM-Montpellier Cancer Institute, Montpellier, France. 5. Hôpital Européen Georges-Pompidou, APHP, Department of Pathology, Paris Descartes University, Sorbonne Paris Cité, Paris, France. 6. CHU Robert Debré, Reims, France. 7. Institut de Cancérologie de l'Ouest - Site René Gauducheau, Saint Herblain, France. 8. Centre Antoine-Lacassagne, Nice, France. 9. Centre Georges-François Leclerc, Dijon, France. 10. Centre Léon Bérard, Lyon, France. 11. CRLC Val d'Aurelle, Montpellier, France. 12. Hôpital de la Pitié Salpétrière Hospital, Paris, France. 13. Medical Oncology Unit, CHU Minjoz, Besancon, France. 14. Gustave Roussy, Université Paris-Saclay, Département de Médecine Oncologique, Villejuif, F-94805, France. 15. UNICANCER, Paris, France. 16. INSERM U970 - PARCC (Paris Cardiovascular Research Center), Paris Descartes University, Sorbonne Paris Cité, Paris, France; Hôpital Européen Georges-Pompidou, APHP, Department of GI Oncology, Paris Descartes University, Sorbonne Paris Cité, Paris, France. Electronic address: jtaieb75@gmail.com.
Abstract
BACKGROUND: The identification of dynamic biomarkers in advanced gastric and oesogastric junction adenocarcinoma (GOA) could help to tailor strategies for each patient. Enumeration of circulating tumour cells (CTCs) is approved by the US Food and Drug Administration in breast, colon and prostate cancer but is not in advanced GOA. Our study aims to establish the optimal threshold and the clinical significance of CTC count in advanced GOA before and during treatment. METHODS:One hundred six patients with untreated advanced GOA were included in the ancillary study of the PRODIGE 17-ACCORD 20 trial. CTCs were detected in the peripheral blood using the CellSearch system on day 0 (D0) and day 28 (D28). The prognostic value of CTCs at D0 and D28 was analysed by testing several thresholds. RESULTS: At baseline, median CTC count was 1 (range, 0-415). While CTCs ≥1, 2 or 3 at D0 were all significantly associated with worse overall survival (OS) and progression-free survival (PFS), CTCs ≥2 were the optimal threshold, on D0 or D28. CTCs ≥2 at D28 were also predictive of disease control. Taking into account both D0 and D28 CTC count defined 3 groups (low/low, high/low and low-high/high) with significantly different PFS (p = 0.0002) and OS (p = 0.003). CONCLUSION: Quantification of CTCs at baseline and during treatment may be a useful prognostic tool in advanced GOA, as it is associated with worse PFS and OS. A threshold ≥2 CTCs seems to have the best discriminant value. Change in CTC count between baseline and D28 could help to tailor treatment to each individual patient.
RCT Entities:
BACKGROUND: The identification of dynamic biomarkers in advanced gastric and oesogastric junction adenocarcinoma (GOA) could help to tailor strategies for each patient. Enumeration of circulating tumour cells (CTCs) is approved by the US Food and Drug Administration in breast, colon and prostate cancer but is not in advanced GOA. Our study aims to establish the optimal threshold and the clinical significance of CTC count in advanced GOA before and during treatment. METHODS: One hundred six patients with untreated advanced GOA were included in the ancillary study of the PRODIGE 17-ACCORD 20 trial. CTCs were detected in the peripheral blood using the CellSearch system on day 0 (D0) and day 28 (D28). The prognostic value of CTCs at D0 and D28 was analysed by testing several thresholds. RESULTS: At baseline, median CTC count was 1 (range, 0-415). While CTCs ≥1, 2 or 3 at D0 were all significantly associated with worse overall survival (OS) and progression-free survival (PFS), CTCs ≥2 were the optimal threshold, on D0 or D28. CTCs ≥2 at D28 were also predictive of disease control. Taking into account both D0 and D28 CTC count defined 3 groups (low/low, high/low and low-high/high) with significantly different PFS (p = 0.0002) and OS (p = 0.003). CONCLUSION: Quantification of CTCs at baseline and during treatment may be a useful prognostic tool in advanced GOA, as it is associated with worse PFS and OS. A threshold ≥2 CTCs seems to have the best discriminant value. Change in CTC count between baseline and D28 could help to tailor treatment to each individual patient.
Authors: Yoshiaki Shoji; Satoru Furuhashi; Daniel F Kelly; Anton J Bilchik; Dave S B Hoon; Matias A Bustos Journal: Clin Exp Metastasis Date: 2021-05-05 Impact factor: 5.150