LAUSR

(50%) of available biopsy and ctDNA samples respectively. Concordance between genetic profiles of biopsy and ctDNA was accurate for 22/30 patients (73.3%). Mutations of NFKBIE, TNFAIP3, STAT6, PTPN1, B2M, XPO1, ITPKB, GNA13 and SOCS1were found in 11.7% (mean number of variants by sample [range]: 1 [0-1]), 25% (1.1 [0-2]), 21.7% (1.4 [0-2]), 1.7% (1 [0-1]), 25% (1.3 [0-3]), 6.7% (1 [0-1]), 15% (1.4 [0-3]), 5% (1.3 [0-2]) and 31.7% (1.8 [0-7]) of all patients, respectively. Unsupervised hierarchical clustering was performed among the 9 genes to represent the association of alterations (See Figure 1). Higher level of [ctDNA] at diagnosis was associated with adverse characteristics: age ≥45 years, presence of anemia (hemoglobin <10.5g/dl), albuminemia <40g/l, sedimentation rate ≥50mm, stage III-IV, lymphocytes count <0.6 G/L, presence of B symptoms, International prognostic Index ≥3, elevated LDH. The ITPKB and B2M mutated patients displayed more disseminated disease (≥ 4 median nodal areas versus [vs] 3 for non-mutated patients, p = 0.005) and XPO1 mutations were associated with female sex (p = 0.042). Median VAF were higher in ctDNA than in biopsy (3.23% vs 2.15%, p = 0.023) and there was a moderate correlation between higher metabolic tumor volume (MTV) and higher [ctDNA] (r = 0.36, p = 0.005). Regarding early therapeutic response, 45 patients (83%, NA = 6) had a negative positron emission tomography (PET) after C2 (Deauville Score 1-3). Mean of DeltaSUVmax after C2 was -78.8%. We analyzed ctDNA after C2 for 45 patients (70%). A rapid clearance of ctDNA in all cases was observed after C2. Conclusions: Variants detection in ctDNA is suitable to depict the genetic features of cHL at diagnosis and may help to assess early treatment response, in complement to PET. [ctDNA] level and genotype are correlated with clinical characteristics and presentation.