A study reported by Yasuhito Tanaka of the Nagoya City University Medical Department in Japan showed that the single nucleotide polymorphism (SNP) in the TLL1 gene is related to the occurrence and development of hepatocellular carcinoma after radical cure of hepatitis C virus infection. (Gastroenterology. 2017, 152: 1383-1394.) The researchers established different models by combining TLL1 gene mutation with other significant risk factors to predict the risk of liver cancer in patients with different degrees of liver fibrosis. TLL1 gene variants can be used to predict the risk of ciwon daji in patients who have achieved a sustained virological response (SVR) in clinical practice. The study included Japanese patients who still suffered from liver cancer after interferon eradication of hepatitis C virus, and used genome-wide association analysis to identify which genes were mutated. The results showed that the TNP1 gene SNP rs17047200 on chromosome 4 is closely related to the occurrence of liver cancer after eradication of hepatitis C virus. There is no obvious linkage disequilibrium between other SNPs and rs17047200, and no more promising SNPs have been found in the exons and promoter regions of TLL1. Tanaka commented: “The mutant genes of liver cancer caused by hepatitis C virus include MICA and DEPDC5, which is very different from our test results.” In a multivariate analysis, the AT / TT base pairing of rs17047200 may lead to a 78% increased risk of liver cancer (P = 0.008). In the group of patients with mild fibrosis, older age is an independent risk factor for liver cancer; in the group of severe fibrosis, postoperative alpha-fetoprotein level and low albumin level are also risk factors. In two groups of liver fibrosis rat models, the mRNA level of TLL1 has increased, but only one group of models of TLL1 mRNA level is consistent with the progress of liver fibrosis. The level of TLL1 mRNA in patients with chronic hepatitis C also increases as liver fibrosis worsens.
Tananka ya yi nuni da cewa: “Wadannan bayanai da farko suna nuna alaƙar da ke tsakanin magana ta TLL1/Tll1 da kunna hanta stellate cell ko ci gaban fibrosis na hanta a cikin dabbobi ko in vitro da kuma a cikin mutane (samfurin shine cutar kansar hanta maras barasa steatohepatitis). Yana iya yiwuwa ya fayyace sabon tsarin hanta fibrosis ko ciwon daji. Bayan mai haƙuri ya sami magani mai tsauri don cutar hanta ta C kuma ya sami SVR, ana iya amfani da gwaje-gwaje masu alaƙa da TLL1 SNP don gano mutanen da ke cikin haɗarin cutar kansar hanta. Idan an kwatanta TLL1 SNP tare da haɗuwa da shekaru, digiri na fibrosis, babban matakin alpha-fetoprotein da sauran abubuwan haɗari masu mahimmanci na iya taimakawa wajen hango hasashen haɗarin ciwon hanta bayan SVR. Babu tsarin maganin baka na interferon wanda aka haɗe tare da aikin maganin ƙwayar cuta kai tsaye, Yana zama daidaitaccen maganin cutar ciwon hanta C a cikin ƙasashe masu tasowa. Duk da haka, ana buƙatar ƙarin bincike don tantance ko maye gurbin TLL1 yana da alaƙa da abin da ya faru na ciwon hanta bayan jiyya tare da SVR-free interferon.
