Genetic mutation in hepatic adenoma: seeing is believing.
نویسنده
چکیده
Hepatic adenoma is one of the most common benign tumors in the liver, usually occurring in young females with continuous use of oral contraceptives [1]. Hepatic adenoma is sometimes accidentally detected during a physical examination or through medical imaging of the abdomen for other purposes. Some (about 10%) emergency cases presented with sudden and severe abdominal pain due to bleeding and the rupture of a large, superficial hepatic adenoma. Treatment for symptomatic cases requires complete surgical resection. For asymptomatic hepatic adenoma, regular follow-up and observation is sufficient, as tumors usually do not grow or even regress in rare cases. However, one major and unsettled problem regarding this wait-and-see policy has been the low, but true, risk of malignant transformation from hepatic adenoma to hepatocellular carcinoma (HCC). In addition, the histology characteristics of certain well-differentiated HCC cannot be confidently differentiated from that of hepatic adenoma. Careful pathological examination plus advanced imaging by contrast MRI may help in some cases, but physicians still look for more reliable diagnosis criteria for highrisk adenoma. Fortunately, new and promising genetic criteria are emerging from recent molecular genetic studies of hepatic adenoma. Genetic mutations leading to hepatic adenoma formation can be approached from two directions. The first one is the candidate gene approach, which is drawn by the known genes involved in two other common liver cancers, HCC and hepatoblastoma [2,3]. One wellknown example is the b-catenin gene (CTNNB1), which is a key molecule in the Wnt signaling pathway. When migrating into the nucleus, b-catenin can activate the transcription of a variety genes and lead to aberrant cell proliferation. In normal hepatocytes, b-catenin is usual-
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عنوان ژورنال:
- Journal of hepatology
دوره 45 6 شماره
صفحات -
تاریخ انتشار 2006