Figure 1.
Figure 1. The global methylation pattern of HCL differs from other indolent B-cell tumors and normal B-cell subpopulations. (A) Unsupervised hierarchical clustering (Euclidean distance, complete linkage). (B) Multidimensional scaling plot showing a 2-dimensional projection of distances across the different histotypes within the series. Methylation profiling (histotype_Meth) included HCL, naive B cells (preGC_Bcell), GC founder B cells (B cells upon antigen encountering, GCfounder_Bcell), low-, intermediate-, and high-maturity memory B cells (loMat_postGC_Bcell, inMat_postGC_Bcell, and hiMat_postGC_Bcell, respectively), splenic MGZ B cells (MGZ_Bcell), CLL samples (U-CLL IGHV, M-CLL IGHV, IGHV3-21+ [CLL–VH3-21]), and SMZL.

The global methylation pattern of HCL differs from other indolent B-cell tumors and normal B-cell subpopulations. (A) Unsupervised hierarchical clustering (Euclidean distance, complete linkage). (B) Multidimensional scaling plot showing a 2-dimensional projection of distances across the different histotypes within the series. Methylation profiling (histotype_Meth) included HCL, naive B cells (preGC_Bcell), GC founder B cells (B cells upon antigen encountering, GCfounder_Bcell), low-, intermediate-, and high-maturity memory B cells (loMat_postGC_Bcell, inMat_postGC_Bcell, and hiMat_postGC_Bcell, respectively), splenic MGZ B cells (MGZ_Bcell), CLL samples (U-CLL IGHV, M-CLL IGHV, IGHV3-21+ [CLL–VH3-21]), and SMZL.

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