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389 results for “Acute myeloid leukemia (AML)”
acute myeloid leukemia (AML)
GEO Series GSE1065. Homo sapiens. 14 samples. Type: Genome variation profiling by genome tiling array.
Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]
GEO Series GSE264719. Mus musculus. 12 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Germline Genetics of Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML)
Myelodysplastic syndromes (MDS) are part of a heterogeneous and overlapping group of clonal diseases that arise in the hematopoietic stem or progenitor cells and also include acute myeloid leukemia (AML), myeloproliferative neoplasms (MPN), and the hybrid MDS/MPN entities. Individuals with MDS have a high risk of progressing to leukemia, with approximately 30% expected to develop AML. This study evaluates genetic susceptibility to myeloid malignancy using data from population-based case control studies of myelodysplastic syndromes and acute myeloid leukemia in adults (ages 18-85 years) and pediatric MDS cases with banked samples at the Center for International Blood and Marrow Transplant Research (CIBMTR). Adult cases were identified through the Minnesota Cancer Reporting System and controls were recruited from the State Driver's License/Identification Card list. DNA samples were collected via mouthwash collection kits (AML cases and controls) or Oragene saliva collection kits (adult MDS cases and controls). Pediatric MDS samples were banked at CIBMTR prior to receipt of a transplant and DNA was extracted from isolated T cells or whole blood samples. Genotyping data were generated using the Illumina Global Diversity array and quality control and genotype calling was conducted using established best practices. Our primary analyses investigated the contribution of genetic variation to MDS risk and evaluated the role of the killer cell immunoglobulin receptors (KIR) on incidence and survival.
TARGET: Acute Myeloid Leukemia (AML)
There are 200+ fully characterized patient cases with AML (all tumor/normal pairs, 100 with relapse sample as well) that make up the TARGET AML dataset, each with gene expression, tumor and paired normal copy number analyses, methylation and comprehensive next-generation sequencing to include whole genome sequencing, mRNA-seq and miRNA-seq. A subset of these cases will also have whole exome sequencing data available as well. There are additionally a large number of cases with partial molecular characterization making this a large and informative genomic dataset. Additionally, the TARGET AML cohort includes some highly aggressive subtypes including AML "induction failures." Upon diagnosis, AML patients without high-risk genetic markers undergo standard chemotherapy, called the primary induction phase. This phase lasts about 30 days and is designed to eliminate cancer cells. Success of treatment is measured by the percentage of myeloblasts, i.e. immature white blood cells, detected in the patient following primary induction. Patients with greater than 15% myeloblasts did not sufficiently respond to standard therapy and are "induction failures." Currently, these patients have very poor prognoses and few clinical options. There are 30 patient cases that make up the TARGET AML Induction failure dataset, each with a primary tumor sample, a "normal" fibroblast sample grown from the patient's bone marrow, and a sample obtained at the end of induction. The trios for each case are characterized with next generation sequencing platforms to include whole genome, miRNA-Seq and mRNA-Seq. Gene expression and copy number analyses were also determined from mRNA-seq and whole genome sequencing respectively.
CRISPR Phenotypic enrichment screen for epigenetic regulators of MEIS1 expression in acute myeloid leukemia (AML) [CRISPRScreens]
GEO Series GSE217778. Homo sapiens. 6 samples. Type: Other.
RNA-seq in murine acute myeloid leukemia (AML) cells with and without knockdown of Tet1
GEO Series GSE116548. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)
GEO Series GSE266623. Mus musculus. 2 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
acute myeloid leukemia (AML)
GEO Series GSE1066. Homo sapiens. 4 samples. Type: Genome variation profiling by genome tiling array.
TARGET: Acute Myeloid Leukemia (AML)
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