Expression data from pre-B ALL tumors isolated from ingeneered mice from the indicated genotypes. Mus musculus

The Ink4a/Arf tumor supressors play crucial roles in inhibiting cell cycle progression at the G1/S checkpoint. Activating mutations in the KrasG12D oncogene is one of the most frequent changes in human cancer, with resultant constitutive mitogenic signaling within the cell. We generated cohorts of CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice to evaluate the combined contributions of Ink/Arf loss and KrasG12D activation in pre-B ALL lymphomas. In this data set we include the expression data obtained from pre-B ALL lymphomas isolated from mice with simultaneous deletion of the Ink/Arf locus and activation of KrasG12D oncogene (and CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice). Overall design: A total 10 mRNA samples were isolated from pre-B ALL arising in CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice.

Ink4a/Arf肿瘤抑制因子（Ink4a/Arf tumor suppressors，原文存在笔误为supressors）在G1/S检验点（G1/S checkpoint）抑制细胞周期进程的过程中发挥关键作用。KrasG12D致癌基因（KrasG12D oncogene）的激活性突变是人类癌症中最为常见的分子改变之一，可引发细胞内组成性有丝分裂原信号通路持续激活。我们构建了CD19Cre; KrasG12D/+; Ink4a/ArfL/+小鼠队列，以评估Ink/Arf缺失与KrasG12D激活在pre-B急性淋巴细胞白血病（pre-B ALL）淋巴瘤发生中的联合调控作用。本数据集收录了从同时缺失Ink/Arf位点且激活KrasG12D致癌基因的小鼠（即CD19Cre; KrasG12D/+; Ink4a/ArfL/+小鼠）中分离得到的pre-B ALL淋巴瘤的表达谱数据。整体实验设计：共从CD19Cre; KrasG12D/+; Ink4a/ArfL/+小鼠体内发生的pre-B急性淋巴细胞白血病中分离获得10份mRNA样本。