36 research outputs found
t(8;14)(q24;q32) - t(2;8)(p12;q24) - t(8;22)(q24;q11)
Review on t(8;14)(q24;q32) - t(2;8)(p12;q24) - t(8;22)(q24;q11), with data on clinics, and the genes involved
CDKN1B (cyclin-dependent kinase inhibitor 1 B )
Review on CDKN1B (cyclin-dependent kinase inhibitor 1 B ), with data on DNA, on the protein encoded, and where the gene is implicated
i(17q) in myeloid malignancies
Review on i(17q) in myeloid malignancies, with data on clinics, and the genes involved
t(11;14)(p13;q11) - t(7;11)(q35;p13)
Review on t(11;14)(p13;q11) - t(7;11)(q35;p13), with data on clinics, and the genes involved
12p abnormalities in myeloid malignancies
Review on 12p abnormalities in myeloid malignancies, with data on clinics, and the genes involved
del(6q) abnormalities in lymphoid malignancies
Review on del(6q) abnormalities in lymphoid malignancies, with data on clinics, and the genes involved
Ontogenic changes in hematopoietic hierarchy determine pediatric specificity and disease phenotype in fusion oncogene-driven myeloid leukemia
Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as ETO2–GLIS2, are associated with acute megakaryoblastic or other myeloid leukemia subtypes in an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed that ETO2–GLIS2 expression in fetal hematopoietic stem cells induced rapid megakaryoblastic leukemia whereas expression in adult bone marrow hematopoietic stem cells resulted in a shift toward myeloid transformation with a strikingly delayed in vivo leukemogenic potential. Chromatin accessibility and single-cell transcriptome analyses indicate ontogeny-dependent intrinsic and ETO2–GLIS2-induced differences in the activities of key transcription factors, including ERG, SPI1, GATA1, and CEBPA. Importantly, switching off the fusion oncogene restored terminal differentiation of the leukemic blasts. Together, these data show that aggressiveness and phenotypes in pediatric acute myeloid leukemia result from an ontogeny-related differential susceptibility to transformation by fusion oncogenes. SIGNIFICANCE: This work demonstrates that the clinical phenotype of pediatric acute myeloid leukemia is determined by ontogeny-dependent susceptibility for transformation by oncogenic fusion genes. The phenotype is maintained by potentially reversible alteration of key transcription factors, indicating that targeting of the fusions may overcome the differentiation blockage and revert the leukemic state
del(20q) in myeloid malignancies
Review on del(20q) in myeloid malignancies, with data on clinics, and the genes involved