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Omics score: 0

Mus musculus

ABSTRACT: Effect of Bach2 overexpression in BCL6+/+ and -/- BCR-ABL1 transformed pre-B cells

OTHER RELATED OMICS DATASETS IN: E-GEOD-30883E-GEOD-20987E-GEOD-41042

PROVIDER: PRJNA175640 | ENA |

REPOSITORIES: ENA

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Effect of Bach2 overexpression in BCL6+/+ and -/- BCR-ABL1 transformed pre-B cells

Project description:The aim was to investigate how BCL6 genotype affects Bach2 dependent gene expression changes. We compared gene expression profiles of BCL6+/+ and BCL6-/- BCR-ABL1 transformed pre-B cells after inducible overexpression of Bach2.

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Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

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Project description:To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib). BCR-ABL1 transformed B cell precursors of BCL6 wildtype and BCL6 knockout mice were either treated with 10ÂµM STI571 (Imatinib) for 16 hours or cultured in absence of STI571. Three samples for each condition were processed.

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Project description:In order to investigate the function of Bach2 in pre-B ALL, we isolated bone marrow cells from wildtype and Bach2 knockout mice of C57Bl6 background and transformed them with BCR-ABL1. We compared the gene expression profiles of Bach2 wildtype and knockout pre-B ALL cells, both with and without imatinib treatment (2uM for 16h).

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Genomic analysis of relapsed Acute Lymphoblastic Leukaemia in children

Project description:Identification of de novo copy number abnormalities arising in relapsed paediatric ALL in matched presentation and relapse samples. We identified deletions of BACH2, (BTB and CNC homology 1, basic leucine zipper transcription factor 2) at relapse. To study the role of Bach2 in pre-B ALL in a genetic experiment, we transformed pre-B cells from Bach2–/– mice with BCR-ABL1. Our findings identify Bach2 as a novel tumor suppressor upstream of p53 in pre-B ALL.

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