Mxi1 tumor suppressor gene is not mutated in primary pancreatic adenocarcinoma
Amplification of the c- myc oncogene occurs in a variety of solid tumors, including pancreatic adenocarcinomas. The MXI1 gene, located at 10q24–q25, may serve to negatively regulate c- myc oncogene activity, and potentially has tumor suppressor function. As such, altered MXI1 function might contribu...
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Veröffentlicht in: | Cancer letters 1996-04, Vol.102 (1), p.73-76 |
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Sprache: | eng |
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Zusammenfassung: | Amplification of the c-
myc oncogene occurs in a variety of solid tumors, including pancreatic adenocarcinomas. The MXI1 gene, located at 10q24–q25, may serve to negatively regulate c-
myc oncogene activity, and potentially has tumor suppressor function. As such, altered MXI1 function might contribute to tumorigenesis. We examined 40 primary human pancreatic adenocarcinomas for MXI1 mutations. Single-strand conformation variant analysis and direct sequencing of the variants revealed a MXI1 polymorphism in 1 of 40 tumors. No MXI1 mutations were identified. Southern blot analyses did not reveal any gross rearrangements of MXIL These results suggest that MXI1 is unlikely to play a role in human pancreatic adenocarcinoma tumorigenesis. |
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ISSN: | 0304-3835 1872-7980 |
DOI: | 10.1016/0304-3835(96)04167-5 |