Podgornik, H. (Helena)

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    Cytogenetic complexity in chronic lymphocytic leukemia: definitions, associations, and clinical impact
    (ASH Publications, 2019) Baliakas, P. (Panagiotis); Jeromin, S. (Sabine); Iskas, M. (Michalis); Puiggros, A. (Anna); Plevova, k. (Karla); Nguyen-Khac, F. (Florence); Davis, Z. (Zadie); Rigolin, G.M. (Gian Matteo); Visentin, A. (Andrea); Xochelli, A. (Aliki); Delgado, J. (Julio); Baran-Marszak, F. (Fanny); Stalika, E. (Evangelia); Abrisqueta, P. (Pau); Durechova, K. (Kristina); Papaioannou, G. (George); Eclache, V. (Virginie); Dimou, M. (Maria); Iliakis, T. (Theodoros); Collado, R. (Rosa); Doubek, M. (Michael); Calasanz-Abinzano, M.J. (Maria Jose); Ruiz-Xiville, N. (Neus); Moreno, C. (Carolina); Jarosova, M. (Marie); Leeksma, A.C. (Alexander C.); Panayiotidis, P. (Panayiotis); Podgornik, H. (Helena); Cymbalista, F. (Florence); Anagnostopoulos, A. (Achilles)
    Recent evidence suggests that complex karyotype (CK) defined by the presence of ≥3 chromosomal aberrations (structural and/or numerical) identified by using chromosome-banding analysis (CBA) may be relevant for treatment decision-making in chronic lymphocytic leukemia (CLL). However, many challenges toward the routine clinical application of CBA remain. In a retrospective study of 5290 patients with available CBA data, we explored both clinicobiological associations and the clinical impact of CK in CLL. We found that patients with ≥5 abnormalities, defined as high-CK, exhibit uniformly dismal clinical outcomes, independently of clinical stage, TP53 aberrations (deletion of chromosome 17p and/or TP53 mutations [TP53abs]), and the expression of somatically hypermutated (M-CLL) or unmutated immunoglobulin heavy variable genes. Thus, they contrasted with CK cases with 3 or 4 aberrations (low-CK and intermediate-CK, respectively) who followed aggressive disease courses only in the presence of TP53abs. At the other end of the spectrum, patients with CK and +12,+19 displayed an exceptionally indolent profile. Building upon CK, TP53abs, and immunoglobulin heavy variable gene somatic hypermutation status, we propose a novel hierarchical model in which patients with high-CK exhibit the worst prognosis, whereas those with mutated CLL lacking CK or TP53abs, as well as CK with +12,+19, show the longest overall survival. Thus, CK should not be axiomatically considered unfavorable in CLL, representing a heterogeneous group with variable clinical behavior. High-CK with ≥5 chromosomal aberrations emerges as prognostically adverse, independent of other biomarkers. Prospective clinical validation is warranted before ultimately incorporating high-CK in risk stratification of CLL.