The primary genetic event in MCL is the t(11;14)(q13;q32) CCND1/IGH translocation (in green). The cell carrying the cyclin D1 translocation can either follow a path similar to that of naïve B cells with unmutated immunoglobulin genes (conventional MCL, in blue). These MCL tumors mostly express SOX11. Approximately half of the tumors have ATM aberrations and, as shown in the article by Nadeu et al, they are genetically unstable with a high number of copy number alterations and structural variants. Alternatively, the cells with cyclin D1 translocations show evidence of a germinal center experience with mutated immunoglobulin genes and low expression of SOX11 (nonnodal MCL, in red). Nadeu et al show that the nonnodal MCL tumors are characterized by fewer copy number alterations and structural variants with the exception of del17p/TP53 which is enriched. Nonnodal MCL cells also carry a higher frequency of CCND1 somatic mutations.

The primary genetic event in MCL is the t(11;14)(q13;q32) CCND1/IGH translocation (in green). The cell carrying the cyclin D1 translocation can either follow a path similar to that of naïve B cells with unmutated immunoglobulin genes (conventional MCL, in blue). These MCL tumors mostly express SOX11. Approximately half of the tumors have ATM aberrations and, as shown in the article by Nadeu et al, they are genetically unstable with a high number of copy number alterations and structural variants. Alternatively, the cells with cyclin D1 translocations show evidence of a germinal center experience with mutated immunoglobulin genes and low expression of SOX11 (nonnodal MCL, in red). Nadeu et al show that the nonnodal MCL tumors are characterized by fewer copy number alterations and structural variants with the exception of del17p/TP53 which is enriched. Nonnodal MCL cells also carry a higher frequency of CCND1 somatic mutations.

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