Figure 1
Figure 1. Aur-A is highly expressed in de novo primary AML bone marrow cells. (A) Endogenous expression of Aur-A in the representative AML samples and normal BMMCs (top). Primary leukemic blasts obtained from patients with AML were lysed and proteins were analyzed by Western blot analysis. GAPDH served as a loading control. The ratio of the intensity of the bands corresponded to Aur-A and GAPDH (bottom). AML samples were arbitrary divided into Aur-A-low and Aur-A-high cases, as described in “Statistical analysis.” UPN indicates unique patient number. (B) Bone marrow (BM) samples were collected from AML patients or normal donors and subjected to immunocytochemical staining with antibody against Aur-A. The Aur-A-high group exhibited strong staining of Aur-A (right), whereas the normal (left) and Aur-A-low group (middle) of AML samples showed weak staining (original magnification, ×400).

Aur-A is highly expressed in de novo primary AML bone marrow cells. (A) Endogenous expression of Aur-A in the representative AML samples and normal BMMCs (top). Primary leukemic blasts obtained from patients with AML were lysed and proteins were analyzed by Western blot analysis. GAPDH served as a loading control. The ratio of the intensity of the bands corresponded to Aur-A and GAPDH (bottom). AML samples were arbitrary divided into Aur-A-low and Aur-A-high cases, as described in “Statistical analysis.” UPN indicates unique patient number. (B) Bone marrow (BM) samples were collected from AML patients or normal donors and subjected to immunocytochemical staining with antibody against Aur-A. The Aur-A-high group exhibited strong staining of Aur-A (right), whereas the normal (left) and Aur-A-low group (middle) of AML samples showed weak staining (original magnification, ×400).

Close Modal

or Create an Account

Close Modal
Close Modal