Project description:We established a mouse model to study the development of therapy-related myeloid neoplasms (t-MN) arising from TP53-mutant clonal hematopoiesis. Mice carrying conditional Trp53-fl-R245W-GFP alleles, in combination with the inducible hematopoietic-specific Cre driver (SCL-CreERT), allow induction of either monoallelic or biallelic Trp53 missense mutations. To mimic cytotoxic therapies implicated in t-MN pathogenesis, mice were exposed to sublethal γ-irradiation, which promoted the development of hematologic malignancies, including acute erythroid leukemia. We then subjected these leukemias to bulk RNA sequencing to characterize their transcriptomic landscape.
Project description:We investigated DNA methylomes of 227 pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles. The current study identified a link between DNA methylome of B-cell acute lymphoblastic leukemias (B-ALLs) and embryonic stem cell (ESC) bivalency, through which tumor cells can mimic the pluripotency of ESCs.
Project description:We investigated DNA methylomes of 227 pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles. The current study identified a link between DNA methylome of B-cell acute lymphoblastic leukemias (B-ALLs) and embryonic stem cell (ESC) bivalency, through which tumor cells can mimic the pluripotency of ESCs.
Project description:We investigated DNA methylomes of 227 pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles. The current study identified a link between DNA methylome of B-cell acute lymphoblastic leukemias (B-ALLs) and embryonic stem cell (ESC) bivalency, through which tumor cells can mimic the pluripotency of ESCs.
Project description:CEBPA/PU.1/TCF7 ChIP-seq of 6 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Low-coverage whole genome sequencing (ChIP input) of the same samples is also included as a control to be used in peak calling.
Project description:CTCF ChIP-seq of 39 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011059 (dataset).
Project description:Hi-C of 17 primary samples obtained from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). As healthy controls, Hi-C of CD34+ HSPCs from 3 healthy donors were used. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011051 (dataset).
Project description:H3K27ac ChIP-seq of 79 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). In addition, 4 samples derived from CD34+ cord blood cells of healthy donors were included. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011060 (dataset).