Figure 3.
Expression of the CTRA gene set, cellular origin, and HSC lineage. (A) Linear model–based estimates of fold-difference from the mean in expression in a 51-gene CTRA contrast score in PBMCs from propranolol-treated patients relative to controls from baseline to T2 and T3 (P = .017) (adjusting for age, sex, race, BMI, smoking history, cytogenetics, and stage) (P = .017). (B) Bioinformatic measures of CD16− classical monocyte activation within PBMC population as indicated by TOA cell-type diagnosticity z scores (P = .005).38 (C) Propranolol-treated patients showed relative upregulation of HSC-containing CD34+ cells (P = .011) and relative downregulation of myeloid progenitor–containing CD33+ cells (P = .001). Error bars indicate SE.

Expression of the CTRA gene set, cellular origin, and HSC lineage. (A) Linear model–based estimates of fold-difference from the mean in expression in a 51-gene CTRA contrast score in PBMCs from propranolol-treated patients relative to controls from baseline to T2 and T3 (P = .017) (adjusting for age, sex, race, BMI, smoking history, cytogenetics, and stage) (P = .017). (B) Bioinformatic measures of CD16 classical monocyte activation within PBMC population as indicated by TOA cell-type diagnosticity z scores (P = .005).38  (C) Propranolol-treated patients showed relative upregulation of HSC-containing CD34+ cells (P = .011) and relative downregulation of myeloid progenitor–containing CD33+ cells (P = .001). Error bars indicate SE.

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