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Mitotic checkpoint gene MAD1 in hepatocellular carcinoma is associated with tumor recurrence after surgical resection
Author(s) -
Nam Chang Woo,
Park Neung Hwa,
Park Bo Ryung,
Shin Jung Woo,
Jung Seok Won,
Na Yang Won,
Seo Jae Hee
Publication year - 2008
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20999
Subject(s) - medicine , hepatocellular carcinoma , mitosis , genotype , cancer research , gene , mitotic index , gene expression , oncology , pathology , biology , genetics
Objective Underlying mechanism of mitotic checkpoint gene mitosis arrest deficiency 1 (MAD1) in human hepatocellular carcinoma (HCC) is rarely known. Materials and Methods We studied genetic change of the MAD1 gene as well as protein expression in 44 HCC and their associated non‐cancerous surrounding liver tissues. Results Genotype AG of MAD1 G‐1849 A promoter was highly significant in microscopic vascular invasion than other genotypes ( P = 0.006). Moreover, the mean tumor size of HCC with genotype AG (7.71 cm) was significantly larger than those of other genotypes (AA, 4.41 cm; GG, 4.59 cm; P = 0.033). After a median follow‐up of 22 months, 18 (41%) of the 44 patients relapsed. Eleven (32.4%) of 34 with MAD1 protein expression and 7 (70%) of 10 with no expression of MAD1 protein showed tumor recurrence. The incidence of tumor recurrence in patients with the lost MAD1 expression was significantly higher than in those with the expressed MAD1 protein ( P = 0.011). Conclusion These results suggest that MAD1 promoter genotype may be involved in tumor progression. Moreover, the loss of MAD1 protein expression may be related to the tumor recurrence after surgical resection of HCC. J. Surg. Oncol. 2008;97:567–571. © 2008 Wiley‐Liss, Inc.