Molecular assessment of participants from pediatric AML trials showed that recurrent structural alterations and age-specific mutational profiles can be used to stratify subjects in terms of overall and progression-free survival, and it highlighted the need for age-tailored targeted therapies.
Researchers identified abundant expression of miR-106a, a marker for treatment resistance, in relapsed and refractory pediatric AML through a comprehensive miRNA profile to identify potential biomarkers as predictors for improved outcomes.
Authors performed comprehensive analysis of WT and identified convergence of numerous genetic changes on limited developmental pathways resulting in oncogenesis. Findings suggested that targeting common pathways was better for intervention than targeting individual gene mutations.
In this first comprehensive genomic study of T-lineage acute lymphoblastic leukemia (T-ALL),researchers identified a large number of unrecognized driver mutations and associated altered pathways. These results have significant therapeutic weight in children with T-ALL.
Investigators examined whether circulating miRNAs can be used as prognostic biomarkers in osteosarcoma patients. miR-21, miR-221, and miR-106a were found to be expressed significantly higher in cancer samples and were correlated with outcome.
Researchers from Children's Oncology Group reported on the key role that loss of TP53 plays in the development of anaplasia in Wilms tumors which might reflect the risk of relapse and death in children with this disease.
TARGET researchers performed comprehensive genomic analysis on 186 cases of pediatric AML with samples from marrow or peripheral blood and identified oncogenic colony-stimulating factor 3 receptor (CSF3R) mutations as a distinct molecular subtype of pediatric AML.
This study used whole exome capture sequencing to compare biopsies from the same patient at diagnosis, remission and relapse and revealed that there was significant variability between these stages.
Investigators performed genomic characterization of extra-cranial malignant rhabdoid tumors and found dysregulation of neural crest development genes.
Scientists studied the DNA variant in the LMO1 gene which leads to neuroblastoma development.