Figure 1.
AHR Ligands are produced by AML cells lines and primary AML blasts. Conditioned media were harvested from AML cell lines (A), primary human AML blasts (B), or from murine leukemic cells (C) and used to treat HepG2 liver cells. RNA was isolated from HepG2 cells following 24-hour treatment, and CYP1A1 gene expression was evaluated by qPCR in each cohort as an indicator of AHR pathway activation. Data presented as expression relative to CYP1A1 expression in HepG2 cells treated with media only. A minimum of 2 independent experiments were conducted, representative figure depicted. (D) Kaplan-Meier overall survival curve comparing patients with higher mRNA expression of AHR-regulated genes (CYP1A1, CYP1A2, CYP1B1, UGT1A1, CYP2S1, and AHRR) relative to the mean expression in adult de novo AML. These data were generated through cBioPortal interface, based on data generated by The Cancer Genome Atlas Research Network. Student t test, *P < .05; **P < .01; ***P < .001. Error bars indicate standard deviation (SD).

AHR Ligands are produced by AML cells lines and primary AML blasts. Conditioned media were harvested from AML cell lines (A), primary human AML blasts (B), or from murine leukemic cells (C) and used to treat HepG2 liver cells. RNA was isolated from HepG2 cells following 24-hour treatment, and CYP1A1 gene expression was evaluated by qPCR in each cohort as an indicator of AHR pathway activation. Data presented as expression relative to CYP1A1 expression in HepG2 cells treated with media only. A minimum of 2 independent experiments were conducted, representative figure depicted. (D) Kaplan-Meier overall survival curve comparing patients with higher mRNA expression of AHR-regulated genes (CYP1A1, CYP1A2, CYP1B1, UGT1A1, CYP2S1, and AHRR) relative to the mean expression in adult de novo AML. These data were generated through cBioPortal interface, based on data generated by The Cancer Genome Atlas Research Network. Student t test, *P < .05; **P < .01; ***P < .001. Error bars indicate standard deviation (SD).

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