| First Author | Gracanin A | Year | 2009 |
| Journal | Cancer Res | Volume | 69 |
| Issue | 16 | Pages | 6371-4 |
| PubMed ID | 19654304 | Mgi Jnum | J:151763 |
| Mgi Id | MGI:4355250 | Doi | 10.1158/0008-5472.CAN-09-0678 |
| Citation | Gracanin A, et al. (2009) Tissue selectivity in multiple endocrine neoplasia type 1-associated tumorigenesis. Cancer Res 69(16):6371-4 |
| abstractText | The phenotype of the multiple endocrine neoplasia type 1 (MEN1) syndrome cannot be explained solely by the expression pattern of the predisposing gene MEN1 and its encoded protein, menin. This review addresses putative factors determining MEN1-associated tissue-selective tumorigenesis. Menin's interaction with mixed-lineage leukemia protein-containing histone methyl transferase (MLL-HMT) complex mediates tissue-selective tumor-suppressing and tumor-promoting effects of menin, and as such could be decisive for the predisposition of individual tissues to MEN1-associated tumorigenesis. In tissues in which menin acts as a tumor suppressor, tumorigenesis could depend on the inability of such tissues to adequately compensate for MEN1 gene loss, whereas the variable clinical presentation of MEN1 in individual patients could be a reflection of additional epigenetic factors and/or modifier genes. Further research on this topic may facilitate development of novel therapeutic strategies that could prevent or delay the onset of MEN1-associated tumorigenesis. |
