Somatic MED12 mutations in uterine leiomyosarcoma and colorectal cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-11

AUTHORS

K Kämpjärvi, N Mäkinen, O Kilpivaara, J Arola, H-R Heinonen, J Böhm, O Abdel-Wahab, H J Lehtonen, L M Pelttari, M Mehine, H Schrewe, H Nevanlinna, R L Levine, P Hokland, T Böhling, J-P Mecklin, R Bützow, L A Aaltonen, P Vahteristo

ABSTRACT

BACKGROUND: Mediator complex participates in transcriptional regulation by connecting regulatory DNA sequences to the RNA polymerase II initiation complex. Recently, we discovered through exome sequencing that as many as 70% of uterine leiomyomas harbour specific mutations in exon 2 of mediator complex subunit 12 (MED12). In this work, we examined the role of MED12 exon 2 mutations in other tumour types. METHODS: The frequency of MED12 exon 2 mutations was analysed in altogether 1158 tumours by direct sequencing. The tumour spectrum included mesenchymal tumours (extrauterine leiomyomas, endometrial polyps, lipomas, uterine leiomyosarcomas, other sarcomas, gastro-intestinal stromal tumours), hormone-dependent tumours (breast and ovarian cancers), haematological malignancies (acute myeloid leukaemias, acute lymphoid leukaemias, myeloproliferative neoplasms), and tumours associated with abnormal Wnt-signalling (colorectal cancers (CRC)). RESULTS: Five somatic alterations were observed: three in uterine leiomyosarcomas (3/41, 7%; Gly44Ser, Ala38_Leu39ins7, Glu35_Leu36delinsVal), and two in CRC (2/392, 0.5%; Gly44Cys, Ala67Val). CONCLUSION: Somatic MED12 exon 2 mutations were observed in uterine leiomyosarcomas, suggesting that a subgroup of these malignant tumours may develop from a leiomyoma precursor. Mutations in CRC samples indicate that MED12 may, albeit rarely, contribute to CRC tumorigenesis. More... »

PAGES

1761

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/bjc.2012.428

DOI

http://dx.doi.org/10.1038/bjc.2012.428

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1016247299

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23132392


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