ChIP-sequencing of murine T-cell acute lymphoblastic leukemia (T-ALL) cell lines to investigate histone methylation profiling of lymphocyte deficient for Tet2 and mutated for DNMT3A

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive proliferation of T-lymphocytes usually associated with oncogenic activation of NOTCH1 signaling. Using a bone marrow transplantation approach, we have modeled murine CD4+ CD8+ T-ALL by overexpressing DNMT3A R882H in Tet2-/- multipotent progenitors. T-ALL derived from NOTCH1 L1601PdelP Tet2-/-, NOTCH1 L1601PdelP Tet2+/+ or TCL1A progenitors were used for comparison, as well as normal Tet2+/+ and Tet2-/- CD4+ CD8+ double positive (DP) thymocytes.

T细胞急性淋巴细胞白血病（T-cell acute lymphoblastic leukemia, T-ALL）是一类侵袭性T淋巴细胞增殖性疾病，通常与NOTCH1信号通路的致癌性激活相关。本研究采用骨髓移植策略，通过在Tet2基因敲除（Tet2-/-）的多能祖细胞中过表达DNMT3A R882H，构建了小鼠CD4+CD8+ T-ALL模型。为开展对照分析，本研究还使用了源自NOTCH1 L1601PdelP Tet2-/-、NOTCH1 L1601PdelP Tet2野生型（Tet2+/+）或TCL1A祖细胞的T-ALL样本，以及正常的Tet2+/+和Tet2-/- CD4+CD8+双阳性（DP）胸腺细胞。