Though independently related to the same histologic tumor entity, the target genes rearranged by these aberrations encode proteins with different functions. HMGA2 is located within the region 12q14,15 which is frequently affected by chromosomal alterations and encodes a DNA-binding non-histone protein mainly expressed during embryogenesis and in embryonic as well as in adult stem cells. PLAG1 mapping to 8q12 encodes a genuine transcription factor encompassing seven zinc finger domains and a carboxyterminal transactivation domain. PLAG1 is developmentally regulated and highly expressed in certain fetal tissues. Oncogenic activation of PLAG1 plays a key role in the development of lipoblastomas, hepatoblastomas, chronic lymphocytic leukemia as well as in pediatric gastro-intestinal stromal tumors. PLAG1 has been found to bind the insulin-like growth factor gene promoter and to stimulate its activity. Similar but not identical to what is seen in pleomorphic adenomas both genes participate in the genesis of benign adipose INCB28060 tissue tumors. Chromosomal translocations affecting 12q14,15 and targeting HMGA2 are a common finding in lipomas often as a t. In contrast, translocations of 8q12 are a recurrent cytogenetic deviation in lipoblastomas, i. e. rare benign adipose tissue tumors of early childhood. Interestingly, pleomorphic adenomas and lipoblastomas share the most frequent type of this rearrangement, i.e. a simple reciprocal translocation t. Recently, an infantile lipoblastoma with rearrangements of the HMGA2 locus has been described as well. These findings raise the question why transcriptional activation of either of these two genes leads to the formation of tumors as similar as lipomas and lipoblastomas. One likely explanation is that they both act as part of a common pathway. Besides pleomorphic adenomas and adipose tissue tumors, another link between these two genes has recently emerged: in thyroid tumors, the expression level of HMGA2 has been found to allow a good discrimination between benign and malignant thyroid lesions. Likewise, Prasad et al. have recently studied the genomewide mRNA expression patterns of benign and malignant thyroid tumors in a systematic approach aimed at the identification of those genes best suited to distinguish between both types of thyroid lesions. The expression of HMGA2 ranked at the first position followed by Kallikrein 7, Mannose receptor, C type 2, Leucine-rich repeat kinase 2, and PLAG1. Because of the apparent relationship of HMGA2 and PLAG1 in the molecular pathogenesis of salivary gland adenomas and adipose tissue tumors, we also quantified and compared the expression of HMGA2 and PLAG1 mRNA in thyroid adenomas as well as in papillary and follicular thyroid carcinomas. To further analyze the relationship between these two genes, we also quantified the PLAG1 expression in 32 uterine leiomyomas with as well as without 12q14 rearrangements. In addition, the PLAG1 expression was quantified in adipose tissue-derived stem cells upon a stimulation of HMGA2 by FGF1.