Project description:Mixed-lineage leukemias represent about 3-5% of acute leukemias occurring in patients of all ages and comprise several different subtypes (biphenotypic, bilineal, and lineage switch). The optimal therapeutic approach to these cases, especially in pediatric patients, has not been defined. We used microarrays to detail the gene expression of pediatric patients with biophenotypic leukemia. Keywords: Patient sample accumulation
Project description:St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project(PCGP): Whole Genome Sequencing of Childhood Retinoblastoma
Project description:St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project(PCGP): Whole Genome Sequencing of Childhood Medulloblastoma
Project description:Mixed-lineage leukemias represent about 3-5% of acute leukemias occurring in patients of all ages and comprise several different subtypes (biphenotypic, bilineal, and lineage switch). The optimal therapeutic approach to these cases, especially in pediatric patients, has not been defined. We used microarrays to detail the gene expression of pediatric patients with biophenotypic leukemia. Experiment Overall Design: The patient samples were selected from database review, and gene expressions were accumulated for the corresponding study period.
Project description:St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project: Whole Genome Sequencing of Childhood Hypodiploid Acute Lymphoblastic Leukemia
Project description:St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project (PCGP): Whole Genome Sequencing of Core Binding Factor Acute Myeloid Leukemia
Project description:St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project (PCGP): Somatic Mutations in Pediatric AML FAB-M7 Subtype by Whole Transcriptome Sequencing
Project description:To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia. The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12). Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL). Patients who failed to achieve complete remission with AML-directed therapy could often be induced with a regimen of prednisone, vincristine, and L-asparaginase. Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML. We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly. We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.