Figure 2.
Comparative analysis of genomic features in prMZL compared with other primary manifestations. (A) Genome-wide frequency plot showing chromosomal amplifications, deletions, and CN-LOH across sMZL, nMZL, MALT/eMZL, and prMZL subtypes. The x-axis represents chromosomes, and the y-axis denotes the frequency of alterations. Key genes within significant regions are annotated. A more detailed representation of aberrations affecting chromosome 3 as a most prominent target of somatic copy number variants is provided in supplemental Figure 3. (B) Comparison of gene-specific copy number alterations (amplifications or deletions) among sMZL, nMZL, MALT/eMZL, and prMZL subtypes. Percentages indicate the proportion of tumors with alterations in each gene, with statistical significance noted for specific comparisons; P values are shown for comparisons against prMZL. (C) Frequencies of significant chromosomal amplifications in sMZL, nMZL, MALT/eMZL, and prMZL. The y-axis highlights key chromosomal regions, whereas the x-axis shows the percentage of tumors harboring these alterations. Statistical significance is annotated (P values). (D) Frequencies of significant chromosomal deletions in sMZL, nMZL, MALT/eMZL, and prMZL. The y-axis highlights key chromosomal regions, and the x-axis represents the percentage of tumors with these alterations. Pairwise comparison of mutation frequencies across MZL subtypes using logistic regression models with post hoc analysis via estimated marginal means, yielding adjusted P values (Tukey method) and odds ratios for differential mutational enrichment. The respective data sets were not reanalyzed, but rather, the published results were extracted for comparative analyses. Reported P values reflect comparisons between prMZL and each individual MZL subtype. CN-LOH, copy-neutral loss of heterozygosity; nMZL, nodal MZL; sMZL, splenic MZL.

Comparative analysis of genomic features in prMZL compared with other primary manifestations. (A) Genome-wide frequency plot showing chromosomal amplifications, deletions, and CN-LOH across sMZL, nMZL, MALT/eMZL, and prMZL subtypes. The x-axis represents chromosomes, and the y-axis denotes the frequency of alterations. Key genes within significant regions are annotated. A more detailed representation of aberrations affecting chromosome 3 as a most prominent target of somatic copy number variants is provided in supplemental Figure 3. (B) Comparison of gene-specific copy number alterations (amplifications or deletions) among sMZL, nMZL, MALT/eMZL, and prMZL subtypes. Percentages indicate the proportion of tumors with alterations in each gene, with statistical significance noted for specific comparisons; P values are shown for comparisons against prMZL. (C) Frequencies of significant chromosomal amplifications in sMZL, nMZL, MALT/eMZL, and prMZL. The y-axis highlights key chromosomal regions, whereas the x-axis shows the percentage of tumors harboring these alterations. Statistical significance is annotated (P values). (D) Frequencies of significant chromosomal deletions in sMZL, nMZL, MALT/eMZL, and prMZL. The y-axis highlights key chromosomal regions, and the x-axis represents the percentage of tumors with these alterations. Pairwise comparison of mutation frequencies across MZL subtypes using logistic regression models with post hoc analysis via estimated marginal means, yielding adjusted P values (Tukey method) and odds ratios for differential mutational enrichment. The respective data sets were not reanalyzed, but rather, the published results were extracted for comparative analyses. Reported P values reflect comparisons between prMZL and each individual MZL subtype. CN-LOH, copy-neutral loss of heterozygosity; nMZL, nodal MZL; sMZL, splenic MZL.

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