Search

Balloon-occluded retrograde transvenous obliteration (BRTO) is a highly effective therapy for gastric varices with liver cirrhosis. We have investigated the incidence of hepatocellular carcinoma (HCC) after BRTO. We enrolled 71 patients with viral hepatitis in which HCC had not appeared with liver imaging findings at the time of BRTO. The overall survival rate after BRTO was 86.8%, 76.1%, and 50.5% at 1, 3, and 5 years. The occurrence rate of HCC after BRTO was 20.9%, 41.1%, and 60.7% at 1, 3, and 5 years, especially showing a higher occurrence of HCC at one year. Meanwhile, the occurrence rate of HCC after treatment which excluded BRTO for esophagogastric varices in patients was 6.3%, 19.2%, and 42.5% at 1, 3, and 5 years. The log-rank test revealed that the occurrence rate of HCC after treatment was significantly higher in the BRTO group compared with that in the non-BRTO group (P=0.0447). The recurrence rate of HCC after BRTO was 35.8% and 80.0% at 1 and 3 years. The present study demonstrated a high incidence of HCC after BRTO in liver cirrhosis patients with viral hepatitis infection. We have suggested the potential for BRTO to accelerate hepatocarcinogenesis.

M6P/IGF2R encodes a multifunctional protein involved in lysosomal enzyme trafficking, fetal organogenesis, tumor suppression, and cytotoxic T cell-induced apoptosis. M6P/IGF2R is imprinted and expressed only from the maternally inherited allele in marsupials and rodents. In contrast, humans were initially reported to differ from the imprinted mammalian orders by not having an imprinted M6P/IGF2R; however, some studies now suggest M6P/IGF2R imprinting may be a human polymorphic trait. Mutational and functional evidence are consistent with M6P/IGF2R also being a tumor suppressor in human colon, liver, lung, breast, and ovarian cancers. M6P/IGF2R expression is also pathologically downregulated following mammalian in vitro embryo culture, resulting in fetal overgrowth and “large offspring syndrome.” Therefore, the M6P/IGF2R imprint status in humans is an unresolved question that critically impacts upon biological issues ranging from human cancer predisposition to evolution. Attempts to further characterize the imprint status of human M6P/IGF2R and loss of heterozygosity at this locus in cancer have been hindered by a lack of readily usable polymorphisms. To facilitate these genetic analyses, we have screened American and Japanese populations for M6P/IGF2R single nucleotide polymorphisms (SNPs). We have identified nine novel SNPs intragenic to human M6P/IGF2R, and have described experimental conditions for their optimal use. Three identified amino-acid variants in the M6P/IGF2R ligand-binding domains may be under selection in humans. Hum Mutat 18:25–31, 2001. © 2001 Wiley-Liss, Inc.