Scientists proposed a framework to investigate the genomic alterations in neuroblastoma subtypes and identified, TEAD4, a transcription factor as a novel target for therapy.
TARGET researchers analysed DNA changes and sequenced the genomes, exomes, and transcriptomes of 1,699 pediatric leukemia and solid tumors. They identified 142 genes associated with cancer in these pediatric patients, of which only 45% matched those found in similar studies of adult cancers.
TARGET investigator’s study of nearly 1,000 pediatric acute myeloid leukemia (AML) cases reveals marked differences between the genomic landscapes of pediatric and adult AML and offers directions for future work.
TARGET’s AML researchers demonstrate that recurrent structural alterations and age-specific mutational profiles can be used stratify pediatric subjects in terms of both overall and progression-free survival, and highlight the need for age-tailored targeted therapies for pediatric AML.
TARGET 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.
TARGET’s AML 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.
TARGET researchers performed comprehensive analysis of Wilms Tumors and identified convergence of numerous genetic changes on limited developmental pathways resulting in oncogenesis. Findings suggests targeting common pathways is better for intervention instead of individual gene mutations.
TARGET researchers perform the first comprehensive genomic study of T-lineage acute lymphoblastic leukemia (T-ALL) and identify a large number of unrecognized driver mutations in targetable pathways. These results have significant therapeutic weight in children with T-ALL.
TARGET investigators report on the key role that loss of TP53 plays in the development of anaplasia in Wilms tumors and may reflect the risk of relapse and death in children with this disease.