1. Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA
2. Department of Cell and Developmental Biology and
3. Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599, USA
4. Memorial Sloan-Kettering Cancer Center, Division of Molecular Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, New York 10021, USA
5. *These authors contributed equally to this work

Correspondence to: Gregory J. Hannon¹Scott M. Hammond^2,3 Correspondence and requests for materials should be addressed to G.J.H. (Email: hannon@cshl.edu) or S.M.H. (Email: hammond@med.unc.edu).
Microarray data have been deposited in NCBI-GEO under accession numbers GSM45026-GSM45065 and GSE-2399.

To date, more than 200 microRNAs have been described in humans; however, the precise functions of these regulatory, non-coding RNAs remains largely obscure. One cluster of microRNAs, the mir-17–92 polycistron, is located in a region of DNA that is amplified in human B-cell lymphomas¹. Here we compared B-cell lymphoma samples and cell lines to normal tissues, and found that the levels of the primary or mature microRNAs derived from the mir-17–92 locus are often substantially increased in these cancers. Enforced expression of the mir-17–92 cluster acted with c-myc expression to accelerate tumour development in a mouse B-cell lymphoma model. Tumours derived from haematopoietic stem cells expressing a subset of the mir-17–92 cluster and c-myc could be distinguished by an absence of apoptosis that was otherwise prevalent in c-myc-induced lymphomas. Together, these studies indicate that non-coding RNAs, specifically microRNAs, can modulate tumour formation, and implicate the mir-17–92 cluster as a potential human oncogene.

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