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 10µM STI571 (Imatinib) for 16 hours or cultured in absence of STI571. Three samples for each condition were processed.
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).
Project description:To elucidate the mechanism of ETV5-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed ETV5+/+ and ETV5-/- B cell precursors. BCR-ABL1 transformed B cell precursors of ETV5wild-type and ETV5 knockout mice were subjected to RNA isolation
Project description:To elucidate the mechanism of Dusp6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed Dusp6+/+ and Dusp6-/- B cell precursors. BCR-ABL1 transformed B cell precursors of Dusp6 wildtype and Dusp6 knockout mice were subjected to RNA isolation
Project description:This comparative genomic hybridization (CGH) study investigated the effect of BCL6 on clonal evolution in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). The frequencies of copy number alterations in BCR-ABL1-transformed BCL6+/+ and BCL6-/- leukemias were determined. Three BCR-ABL1-transformed BCL6+/+ and BCL6-/- ALL samples derived from mice were maintained for 4 month in cell culture and were subjected to CGH analysis. As control samples, normal untransformed splenoytes were used.
Project description:This comparative genomic hybridization (CGH) study investigated the effect of BCL6 on clonal evolution in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). The frequencies of copy number alterations in BCR-ABL1-transformed BCL6+/+ and BCL6-/- leukemias were determined.