Figure 1.
TBX21 expression is higher in CLL cells than in B cells of healthy donors. (A) Gene expression of TBX21 in CLL cells (n = 41) and B cells from age-matched healthy controls (HC B cells; n = 11). P values were obtained by the unpaired t test. (B) Flow cytometric analysis of T-bet levels in CLL cells (n = 20) and B cells from age-matched healthy controls (n = 5). P values were obtained by the unpaired t test. (C) Gene expression of TBX21 in untransformed B-cell subsets (n = 5-7) and CLL cells (n = 10). Bar limits indicate mean expression and error bars indicate standard error of the mean. P values were obtained by the 1-way analysis of variance (ANOVA), controlling the false discovery rate (FDR) using the Benjamini-Hochberg (BH) method. (D) Expression of ABC marker genes in CLL cells (n = 10) and untransformed B-cell subsets (n = 5-7). High (green) and low (blue) expressions in the ABCs are depicted on the right. (E) Analysis of the association between TBX21 gene expression and the presence of specific driver genetic alterations. Point estimates with 95% confidence intervals were calculated for the whole CLL cohort and IGHV subtypes using 2-sided t tests and controlling the FDR using the BH method. The point estimates represent the difference between the mean TBX21 expression in individuals with CLL with and without each corresponding alteration. The point estimates were color-coded based on FDR. The OncoPrint shows the association of genetic driver alterations with higher or lower expression of TBX21, along with additional clinical information such as IGHV status, time to first treatment, and patient status (treated/untreated). Samples are ordered from lower to higher TBX21 gene expression. Monoclonal B lymphocytosis cases are excluded from this analysis. Genetic driver alterations are depicted using distinct colors corresponding to the alteration type. The number of samples with mutations, as well as the percentage of mutated samples over the whole cohort, is shown on the right. The analyzed data set consisted of gene expression microarray data from 364 CLL samples.33 (F) Chromatin landscape of TBX21 showing the median ATAC-seq, H3K27ac chromatin immunoprecipitation sequencing and positive-strand RNA-seq levels from 7 patients with CLL and 15 samples from 4 different B-cell subpopulations of healthy controls (naïve, germinal center, memory B cells, and plasma cells). ∗P ≤ .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

TBX21 expression is higher in CLL cells than in B cells of healthy donors. (A) Gene expression of TBX21 in CLL cells (n = 41) and B cells from age-matched healthy controls (HC B cells; n = 11). P values were obtained by the unpaired t test. (B) Flow cytometric analysis of T-bet levels in CLL cells (n = 20) and B cells from age-matched healthy controls (n = 5). P values were obtained by the unpaired t test. (C) Gene expression of TBX21 in untransformed B-cell subsets (n = 5-7) and CLL cells (n = 10). Bar limits indicate mean expression and error bars indicate standard error of the mean. P values were obtained by the 1-way analysis of variance (ANOVA), controlling the false discovery rate (FDR) using the Benjamini-Hochberg (BH) method. (D) Expression of ABC marker genes in CLL cells (n = 10) and untransformed B-cell subsets (n = 5-7). High (green) and low (blue) expressions in the ABCs are depicted on the right. (E) Analysis of the association between TBX21 gene expression and the presence of specific driver genetic alterations. Point estimates with 95% confidence intervals were calculated for the whole CLL cohort and IGHV subtypes using 2-sided t tests and controlling the FDR using the BH method. The point estimates represent the difference between the mean TBX21 expression in individuals with CLL with and without each corresponding alteration. The point estimates were color-coded based on FDR. The OncoPrint shows the association of genetic driver alterations with higher or lower expression of TBX21, along with additional clinical information such as IGHV status, time to first treatment, and patient status (treated/untreated). Samples are ordered from lower to higher TBX21 gene expression. Monoclonal B lymphocytosis cases are excluded from this analysis. Genetic driver alterations are depicted using distinct colors corresponding to the alteration type. The number of samples with mutations, as well as the percentage of mutated samples over the whole cohort, is shown on the right. The analyzed data set consisted of gene expression microarray data from 364 CLL samples.33 (F) Chromatin landscape of TBX21 showing the median ATAC-seq, H3K27ac chromatin immunoprecipitation sequencing and positive-strand RNA-seq levels from 7 patients with CLL and 15 samples from 4 different B-cell subpopulations of healthy controls (naïve, germinal center, memory B cells, and plasma cells). ∗P ≤ .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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