Figure 6.
Toward development of antibody-based panels for predicting TKI responses. (A) A custom 38-antibody panel was designed for mass cytometry to detect the cell abundance gradients and GE profiles uncovered by our single-cell map. (B) The mean expression of indicated markers was assessed within the Lin−CD34+CD38− population of control and CML samples. (C) CD34+ HSPCs from the CyTOF data set was subjected to standard gating schemes to identify 6 HSPC populations: HSC, MPP, LMPP, CMP, megakaryocyte-erythroid progenitor (MEP), and GMP. MEP proportions were compared across CML groups A through C. (D) A flow cytometry panel was optimized to measure the frequency of ERPs across control and CML Groups A through C. An independent cohort of 6 patients of group A was used for this analysis, as well as the same set of group B and group C samples. (E) CD34− cells from the CyTOF data set were subjected to standard biaxial gating to identify NK cells (far right). The total abundance of NK cells with the CD34− population of samples and the mean expression of HLA-DR and CD7 within the NK cell population are shown. (F) A flow cytometry panel was optimized (supplemental Figure 13A) to measure the frequency of adaptive-like NK cells identified as CD57+NKG2C(KLRC2)+ cells within CD56dim CD16bright NK cell population. (G) A flow cytometry panel was optimized (supplemental Figure 13B) to measure the frequency of the NKG2A(KLRC1)+ NK subset within the CD56dim CD16bright NK cell population. Statistical tests for all data are shown in Figure 6; 2-tailed t test. Supplemental Figures 11-13 and supplemental Tables 25 and 26 are linked with the data in Figure 6.

Toward development of antibody-based panels for predicting TKI responses. (A) A custom 38-antibody panel was designed for mass cytometry to detect the cell abundance gradients and GE profiles uncovered by our single-cell map. (B) The mean expression of indicated markers was assessed within the LinCD34+CD38 population of control and CML samples. (C) CD34+ HSPCs from the CyTOF data set was subjected to standard gating schemes to identify 6 HSPC populations: HSC, MPP, LMPP, CMP, megakaryocyte-erythroid progenitor (MEP), and GMP. MEP proportions were compared across CML groups A through C. (D) A flow cytometry panel was optimized to measure the frequency of ERPs across control and CML Groups A through C. An independent cohort of 6 patients of group A was used for this analysis, as well as the same set of group B and group C samples. (E) CD34 cells from the CyTOF data set were subjected to standard biaxial gating to identify NK cells (far right). The total abundance of NK cells with the CD34 population of samples and the mean expression of HLA-DR and CD7 within the NK cell population are shown. (F) A flow cytometry panel was optimized (supplemental Figure 13A) to measure the frequency of adaptive-like NK cells identified as CD57+NKG2C(KLRC2)+ cells within CD56dim CD16bright NK cell population. (G) A flow cytometry panel was optimized (supplemental Figure 13B) to measure the frequency of the NKG2A(KLRC1)+ NK subset within the CD56dim CD16bright NK cell population. Statistical tests for all data are shown in Figure 6; 2-tailed t test. Supplemental Figures 11-13 and supplemental Tables 25 and 26 are linked with the data in Figure 6.

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