A microRNA polycistron, the mir-17–92 cluster, is identified as a potential human oncogene. This cluster is located in a DNA region amplified in human B-cell lymphomas. The study compared B-cell lymphoma samples and cell lines with normal tissues and found that the levels of primary or mature microRNAs from the mir-17–92 locus are significantly increased in these cancers. Enforced expression of the mir-17–92 cluster with c-myc expression accelerated tumour development in a mouse B-cell lymphoma model. Tumours from haematopoietic stem cells expressing a subset of the mir-17–92 cluster and c-myc showed an absence of apoptosis, a characteristic not seen in c-myc-induced lymphomas. These findings suggest that non-coding RNAs, specifically microRNAs, can modulate tumour formation and that the mir-17–92 cluster is a potential human oncogene. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression. They are processed by Drosha and Dicer to produce mature miRNAs. These miRNAs are incorporated into the RNA interference (RNAi) complex, RISC, and target specific messenger RNAs for translational repression or cleavage. While many miRNAs have been cloned, only a few have been functionally characterized. Examples include lin-4 and let-7 in C. elegans, and miR-273 in chemosensory neurons. Bantam stimulates cell growth and prevents apoptosis in Drosophila, and miR-181 enhances B-cell differentiation in mammals. Microarray-based studies showed specific alterations in human miRNA expression profiles correlated with tumour phenotypes. The mir-17–92 cistron is located at 13q31, a genomic locus amplified in various lymphomas. The c13orf25 transcript is the functional precursor of seven microRNAs, including miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b-1, and miR-92-1. These miRNAs are related to homologous clusters on chromosome X and 7. The study confirmed increased gene dosage at the c13orf25 locus in three cell lines and found that six miRNAs correlated with increased gene dosage. Five were from the mir-17–92 cistron, and the sixth, miR-106a, was likely due to cross-hybridization. Expression levels of these miRNAs correlated with the copy number of the mir-17–92 locus. In human tumour samples, pri-mir-17–92A microRNA polycistron, the mir-17–92 cluster, is identified as a potential human oncogene. This cluster is located in a DNA region amplified in human B-cell lymphomas. The study compared B-cell lymphoma samples and cell lines with normal tissues and found that the levels of primary or mature microRNAs from the mir-17–92 locus are significantly increased in these cancers. Enforced expression of the mir-17–92 cluster with c-myc expression accelerated tumour development in a mouse B-cell lymphoma model. Tumours from haematopoietic stem cells expressing a subset of the mir-17–92 cluster and c-myc showed an absence of apoptosis, a characteristic not seen in c-myc-induced lymphomas. These findings suggest that non-coding RNAs, specifically microRNAs, can modulate tumour formation and that the mir-17–92 cluster is a potential human oncogene. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression. They are processed by Drosha and Dicer to produce mature miRNAs. These miRNAs are incorporated into the RNA interference (RNAi) complex, RISC, and target specific messenger RNAs for translational repression or cleavage. While many miRNAs have been cloned, only a few have been functionally characterized. Examples include lin-4 and let-7 in C. elegans, and miR-273 in chemosensory neurons. Bantam stimulates cell growth and prevents apoptosis in Drosophila, and miR-181 enhances B-cell differentiation in mammals. Microarray-based studies showed specific alterations in human miRNA expression profiles correlated with tumour phenotypes. The mir-17–92 cistron is located at 13q31, a genomic locus amplified in various lymphomas. The c13orf25 transcript is the functional precursor of seven microRNAs, including miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b-1, and miR-92-1. These miRNAs are related to homologous clusters on chromosome X and 7. The study confirmed increased gene dosage at the c13orf25 locus in three cell lines and found that six miRNAs correlated with increased gene dosage. Five were from the mir-17–92 cistron, and the sixth, miR-106a, was likely due to cross-hybridization. Expression levels of these miRNAs correlated with the copy number of the mir-17–92 locus. In human tumour samples, pri-mir-17–92