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 ມະເຮັງຕັບ 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 ຊີ້ໃຫ້ເຫັນວ່າ: "ຂໍ້ມູນເຫຼົ່ານີ້ໃນເບື້ອງຕົ້ນສະແດງໃຫ້ເຫັນຄວາມສໍາພັນລະຫວ່າງການສະແດງອອກຂອງ TLL1 / Tll1 ແລະການກະຕຸ້ນຈຸລັງ hepatic stellate ຫຼືຄວາມຄືບຫນ້າຂອງ fibrosis ຕັບໃນສັດຫຼືໃນ vitro ແລະໃນມະນຸດ (ແບບຈໍາລອງແມ່ນເປັນມະເຮັງຕັບທີ່ບໍ່ແມ່ນເຫຼົ້າ steatohepatitis). ມັນອາດຈະມີຄວາມກະຈ່າງແຈ້ງກ່ຽວກັບກົນໄກໃຫມ່ຂອງ fibrosis ຕັບຫຼືມະເຮັງ. ຫຼັງຈາກຄົນເຈັບໄດ້ຮັບການປິ່ນປົວຮາກສໍາລັບເຊື້ອໄວຣັສຕັບອັກເສບ C ແລະໄດ້ຮັບ SVR, ການທົດລອງທີ່ກ່ຽວຂ້ອງກັບ TLL1 SNP ອາດຈະຖືກນໍາໃຊ້ເພື່ອກໍານົດຜູ້ທີ່ມີຄວາມສ່ຽງຕໍ່ການເປັນມະເຮັງຕັບ. ຖ້າ TLL1 SNP ຖືກປຽບທຽບກັບການປະສົມປະສານຂອງອາຍຸ, ລະດັບຂອງ fibrosis, ລະດັບ alpha-fetoprotein ສູງແລະປັດໃຈຄວາມສ່ຽງທີ່ສໍາຄັນອື່ນໆສາມາດຊ່ວຍຄາດຄະເນຄວາມສ່ຽງຂອງມະເຮັງຕັບຫຼັງຈາກ SVR. ບໍ່ມີແຜນການປິ່ນປົວທາງປາກ interferon ລວມກັບການປິ່ນປົວດ້ວຍຢາຕ້ານເຊື້ອໄວຣັສໂດຍກົງ, ໄດ້ກາຍເປັນມາດຕະຖານການປິ່ນປົວດ້ວຍເຊື້ອໄວຣັສຕັບອັກເສບ C ໃນປະເທດພັດທະນາ. ຢ່າງໃດກໍ່ຕາມ, ການຄົ້ນຄວ້າຕື່ມອີກແມ່ນຍັງຕ້ອງການເພື່ອປະເມີນວ່າການກາຍພັນຂອງ TLL1 ກ່ຽວຂ້ອງກັບການເກີດຂື້ນຂອງມະເຮັງຕັບຫຼັງຈາກການປິ່ນປົວດ້ວຍ SVR ທີ່ບໍ່ມີ interferon.
