Figure 3.

Inverse Relation between CDK6 and p16^INK4a Expression in Human Lymphomas

(A) [³H]thymidine incorporation of Cdk6^+/+, INK4a/ARF^−/−, INK4a/ARF^−/−+Cdk6, and INK4a/ARF^−/−+Cdk6R31C p185^BCR-ABL-transformed cells (n = 3; Cdk6^+/+ versus INK4a/ARF^−/−, ^∗∗p = 0.002; INK4a/ARF^−/−+Cdk6, ^∗∗p = 0.001; INK4a/ARF^−/−+Cdk6R31C,^∗∗p = 0.005).

(B) Kaplan-Meier plot of Rag2^−/− mice intravenously transplanted with Cdk6^+/+, INK4a/ARF^−/−, INK4a/ARF^−/−+Cdk6, and INK4a/ARF^−/−+Cdk6R31C cells (n = 3 cell lines/genotype; mean survival: 18 [Cdk6^+/+], 15 [INK4a/ARF^−/−], 15 [INK4a/ARF^−/−+Cdk6], and 15.5 [INK4a/ARF^−/−+Cdk6R31C] days; ^∗p = 0.02).

(C) Immunohistochemical stainings of a B cell lymphoma tissue array including 16 lymphoma samples and two control lymph nodes for CDK6 and p16^INK4a. Representative examples including different types of B cell lymphoma, a diffuse large B cell lymphoma (patient A), two follicular lymphomas (patients B and C), and one control lymph node (left) are depicted. Original magnification 20×.

(D and E) The expression of CD30, CDK6, and p16^INK4a was analyzed for 17 NPM-ALK-positive (E) and 11 NPM-ALK-negative (D) lymphoma cases with immunohistochemistry. Representative cases for NPM-ALK-positive (patients D and E) and NPM-ALK-negative (patients F and G) cases are depicted. Original magnification 20×.

Error bars indicate the mean ± SEM. See also Figure S3.