M Samimi1,2,3, L Molet4,5, M Fleury1,2,6, H Laude4,5, A Carlotti4, C Gardair1,7, M Baudin1,2, L Gouguet1,2, E Maubec8,9, M Avenel-Audran10, E Esteve11, E Wierzbicka-Hainaut12, N Beneton13, F Aubin14, F Rozenberg4,5, N Dupin4,5, M F Avril4,5, G Lorette1,2,3, S Guyetant1,7, P Coursaget1,2, A Touzé1,2. 1. Université François Rabelais, Tours, France. 2. INRA, UMR 1282 ISP, 31 Avenue Monge, 37200, Tours, France. 3. Dermatology Department, CHU Tours, Avenue de la République, 37170, Tours, France. 4. Assistance Publique des Hôpitaux de Paris, Virology, Pathology and Dermatology Departments, Hôpital Cochin, 27 Rue du Fbg Saint-Jacques, 75679, Paris CEDEX 14, France. 5. Institut Cochin, Inserm U1016, Université Paris Descartes, 22 Rue Méchain, 75014, Paris, France. 6. LUNAM Université, Groupe d'Etude des Interactions Hôte-Pathogéne, UPRES EA 3142, Angers, France. 7. Pathology Department, CHU Tours, Avenue de la République, 37170, Tours, France. 8. Assistance Publique des Hôpitaux de Paris, Dermatology Department, Hôpital Bichat, 46 Rue Henri Huchard, 75877, Paris CEDEX 18, France. 9. Assistance Publique des Hôpitaux de Paris, Dermatology Department, Hôpital Avicenne, 125, rue de Stalingrad, 93009, Bobigny, France. 10. LUNAM Université, CHU Angers, Dermatology Department, 4 Rue Larrey, 49933, Angers, France. 11. CHR Orléans, Dermatology Department, 14 Avenue de l'Hôpital, 45067, Orléans CEDEX 2, France. 12. CHU Poitiers, Dermatology Department, 2 Rue de la Milétrie, 86021, Poitiers CEDEX, France. 13. CHR Le Mans, Dermatology Department, 194 Avenue Rubillard, 72037, Le Mans CEDEX 09, France. 14. Université de Franche Comté, EA3181, SFR 4234, CHU Besançon, Dermatology Department, 2 Boulevard Fleming, 25030, Besançon, France.
Abstract
BACKGROUND: Merkel cell polyomavirus (MCPyV) is the main aetiological agent of Merkel cell carcinoma (MCC). Serum antibodies against the major MCPyV capsid protein (VP1) are detected in the general population, whereas antibodies against MCPyV oncoproteins (T antigens) have been reported specifically in patients with MCC. OBJECTIVES: The primary aim was to assess whether detection of serum antibodies against MCPyV proteins at baseline was associated with disease outcome in patients with MCC. The secondary aim was to establish whether evolution of these antibodies during follow-up was associated with the course of the disease. METHODS: Serum T-antigen and VP1 antibodies were assessed by enzyme-linked immunosorbent assay using recombinant proteins in a cohort of 143 patients with MCC, including 84 patients with serum samples available at baseline. RESULTS: Low titres of VP1 antibodies at baseline (< 10 000) were significantly and independently associated with increased risk of recurrence [hazard ratio (HR) 2·71, 95% confidence interval (CI) 1·13-6·53, P = 0·026] and death (HR 3·74, 95% CI 1·53-9·18, P = 0·004), whereas T-antigen antibodies were not found to be associated with outcome. VP1 antibodies did not differ between patients in remission and those with recurrence or progression during follow-up. However, T-antigen antibodies were more frequently detected in patients with recurrence or progression at 12 months (P = 0·020) and 24 months (P = 0·016) after diagnosis. CONCLUSIONS: VP1 antibodies constitute a prognostic marker at baseline, whereas T-antigen antibodies constitute a marker of disease recurrence or progression if detected > 12 months after diagnosis.
BACKGROUND:Merkel cell polyomavirus (MCPyV) is the main aetiological agent of Merkel cell carcinoma (MCC). Serum antibodies against the major MCPyV capsid protein (VP1) are detected in the general population, whereas antibodies against MCPyV oncoproteins (T antigens) have been reported specifically in patients with MCC. OBJECTIVES: The primary aim was to assess whether detection of serum antibodies against MCPyV proteins at baseline was associated with disease outcome in patients with MCC. The secondary aim was to establish whether evolution of these antibodies during follow-up was associated with the course of the disease. METHODS: Serum T-antigen and VP1 antibodies were assessed by enzyme-linked immunosorbent assay using recombinant proteins in a cohort of 143 patients with MCC, including 84 patients with serum samples available at baseline. RESULTS: Low titres of VP1 antibodies at baseline (< 10 000) were significantly and independently associated with increased risk of recurrence [hazard ratio (HR) 2·71, 95% confidence interval (CI) 1·13-6·53, P = 0·026] and death (HR 3·74, 95% CI 1·53-9·18, P = 0·004), whereas T-antigen antibodies were not found to be associated with outcome. VP1 antibodies did not differ between patients in remission and those with recurrence or progression during follow-up. However, T-antigen antibodies were more frequently detected in patients with recurrence or progression at 12 months (P = 0·020) and 24 months (P = 0·016) after diagnosis. CONCLUSIONS: VP1 antibodies constitute a prognostic marker at baseline, whereas T-antigen antibodies constitute a marker of disease recurrence or progression if detected > 12 months after diagnosis.
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