Expression data from mouse MLL/AF10(OM-LZ) myeloid leukemia cells harboring wild-type KRAS, KRAS-G12C, wild-type PTPN11, PTPN11-G503A, without or with Hoxa11

Cooperation of MLL/AF10 with RAS pathway mutations accelerated myeloid leukemia development. The detail molecular mechanism is analyzed by identification of the differentially expressed genes between MLL/AF10 cells harboring wild-type and mutant RAS pathway genes and by with or without Hoxa11. We used cDNA microarray to compare transcriptomes between mouse MLL/AF10 myeloid leukemia cells harboring wild-type KRAS and harboring KRAS-G12C (AKw1G and AK3G), or between MLL/AF10 cells harboring wild-type PTPN11 and harboring PTPN11-G503A (APw-1 and APm-1), or between MLL/AF10 cells without and with Hoxa11 (12G-V and 12G-H11). RNAs were prepared from the in vitro cultured cells, RNA was amplified and hybridized to the Affymetrix Mouse Transcriptome Array 1.0 (MTA-1_0) chips.

MLL/AF10与RAS通路突变的协同作用可加速髓系白血病的发生发展。本研究通过鉴定携带野生型与突变型RAS通路基因的MLL/AF10细胞，以及携带或不携带Hoxa11的MLL/AF10细胞之间的差异表达基因，解析其具体分子机制。本研究采用cDNA微阵列（cDNA microarray）技术，对以下各组小鼠MLL/AF10髓系白血病细胞的转录组进行比较：携带野生型KRAS与KRAS-G12C突变的细胞（AKw1G与AK3G）、携带野生型PTPN11与PTPN11-G503A突变的细胞（APw-1与APm-1），以及不携带与携带Hoxa11的细胞（12G-V与12G-H11）。实验以体外培养的细胞为材料，提取RNA并进行扩增后，与Affymetrix小鼠转录组芯片1.0（MTA-1_0）进行杂交。