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Introduction: The mechanism of relapsed CD19(−) B‐ALL after anti‐CD19 immunotherapy (Kymriah [CART‐19] and blinatumomab) is under active investigation. Our study aims to assess LILRB1 as a novel B‐cell marker for detecting CD19(−) B‐lymphoblasts and to analyze the clinicopathologic/genetic features of such disease to provide biological insight into relapse. Methods: Six patients (3 males/3 females, median age of 14 years) with relapsed CD19(−) B‐ALL were analyzed for cytogenetic/genetic profile and immunophenotype. Results: CD19(−) B‐ALL emerged after an interval of 5.8 months following anti‐CD19 therapy. Five of six patients had B‐cell aplasia, indicative of a persistent effect of CART or blinatumomab at relapse. Importantly, LILRB1 was variably expressed on CD19(−) and CD19(+) B lymphoblasts, strong on CD34(+) lymphoblasts and dim/partial on CD34(−) lymphoblasts. Three of six patients with paired B‐ALL samples (pre‐ and post‐anti‐CD19 therapy) carried complex and different cytogenetic abnormalities, either as completely different or sharing a subset of cytogenetic abnormalities. Conclusion: LILRB1 can be used as a novel B‐cell marker to identify CD19(−) B lymphoblasts. The emergence of CD19(−) B‐ALL appears to be associated with complex cytogenetic evolutions. The mechanism of CD19(−) B‐ALL relapse under anti‐CD19 immune pressure remains to be explored by comprehensive molecular studies. [ABSTRACT FROM AUTHOR]

• First case of a cHL with t(11;14) identified by chromosome and FISH analysis with sustained CCND1 expression. • Mantle cell lymphoma and cHL are closely related sharing a common post germinal precursor with t(11;14)+. • Early acquisition of genetic lesions, such as loss of 9q, suggests the potential to develop a cHL phenotype with deregulated cell cycle and signaling pathways. Classic Hodgkin lymphoma (cHL) is characterized by the presence of Hodgkin Reed-Sternberg (HRS) cells. Although HRS cells express PAX5 , cHL frequently lacks other B-cell markers. There is now evidence that HRS cells are monoclonal and are derived from germinal center B-cells. In terms of genetic aberrations, cHL frequently exhibit activated NF-kB signaling pathway. In this study, we present a case of cHL harboring a t(11;14) (q13;q32)/ CCND1 :: IGH , identified by chromosome and fluorescence in situ hybridization analysis and with CCND1 expression in HRS cells. We also analyzed recurrent cytogenetic aberrations in t(11;14) positive mantle cell lymphoma (MCL) and those found in cHL from the literature to assess genetic overlap, clonal evolution, and to identify potential signaling pathways in cHL with CCND1 :: IGH. This analysis suggests the development of t(11;14)+ cHL and MCL from a transformed precursor cell with t(11;14) through genetic evolution and consequent deregulated pathways, including the NF-κB and NOTCH1 signaling. [ABSTRACT FROM AUTHOR]