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The relatively recent discovery of micro RNAs (mi RNAs) has exposed an extra layer of gene expression regulation that affects many physiological and pathological processes of biology. Dysregulation of mi RNAs is a ubiquitous feature of cancer in general, including lymphomas. The identity of these aberrantly-expressed mi RNAs has been thoroughly investigated in all but a few types of lymphomas, however their functional role in lymphomagenesis much less so. This review focuses on those mi RNAs that have an experimentally confirmed functional role in the pathogenesis of the most frequent forms of lymphoma. In particular, the MIR15A/16-1 cluster, MIR21, MIR155, MIR17 HG ( MIR17-92 cluster) , MIR34A and MIR125B, which have in vivo animal model evidence for their involvement in lymphomagenesis, are highlighted. [ABSTRACT FROM AUTHOR]

The transcriptome of the CD34+ cells was determined in a group of 10 patients with the 5q− syndrome using a comprehensive array platform, and was compared with the transcriptome of CD34+ cells from 16 healthy control subjects and 14 patients with refractory anaemia and a normal karyotype. The majority of the genes assigned to the commonly deleted region (CDR) of the 5q− syndrome at 5q31–q32 showed a reduction in expression levels in patients with the 5q− syndrome, consistent with the loss of one allele. Candidate genes showing haploinsufficiency in the 5q− syndrome included the tumour suppressor gene SPARC and RPS14, a component of the 40S ribosomal subunit. Two genes mapping to the CDR, RBM22 and CSNK1A1, showed a >50% reduction in gene expression, consistent with the downregulation of the remaining allele. This study identified several significantly deregulated gene pathways in patients with the 5q− syndrome and gene pathway analysis data supports the proposal that SPARC may play a role in the pathogenesis of the 5q− syndrome. This study suggests that several of the genes mapping to the CDR of the 5q− syndrome play a role in the pathogenesis of this disorder. [ABSTRACT FROM AUTHOR]