Factors predicting occurrence and prognosis of hepatitis-B-virus-related hepatocellular carcinoma

Primary liver cancer is an important cause of cancer death, and hepatocellular carcinoma （HCC） accounts for 70%-85% of total liver cancer worldwide. Chronic hepatitis B virus （HBV） infection contributes to 〉 75% of HCC cases. High serum viral load is the most reliable indicator of viral replication in predicting development of HCC. HBV genotype C is closely associated with HCC in cirrhotic patients aged 〉 50 years, whereas genotype B is associated with development of HCC in non-cirrhotic young patients and postoperative relapse of HCC. Different HBV subgenotypes have distinct patterns of mutations, which are clearly associated with increased risk of HCC. Mutations accumulate during chronic HBV infection and predict occurrence of HCC. Chronic inflammation leads to increased frequency of viral mutation via cellular cytidine deaminase induction. Mutations are negatively selected by host immunity, whereas some immuno-escaped HBV mutants are active in hepatocarcinogenesis. Inflammatory pathways contribute to the inflammation-necrosis-regeneration process, ultimately HCC. Their hallmark molecules can predict malignancy in HBV-infected subjects. Continuing inflammation is involved in hepatocarcinogenesis and closely related to recurrence and metastasis. HBV load, genotype C, viral mutations and expression of inflammatory molecules in HBV-related HCC tissues are significantly associated with poor prognosis. Imbalance between intratumoral CD8^＋T cells and regulatory T cells or Thl and Th2 cytokines in peritumoral tissues can predict prognosis of HBV-related HCC. These factors are important for developing active prevention and surveillance of HBV-infected subjects who are more likely to develop HCC, or for tailoring suitable treatment to improve survival or postpone postoperative recurrence of HCC.

A novel TIR-NBS-LRR gene regulates immune response to Phytophthora root rot in soybean

Phytophthora root rot(PRR),caused by Phytophthora sojae,is a devastating disease of soybean.The NBSLRR gene family is a class of plant genes involved in disease resistance.miRNA mediates plant response to biotic stresses by regulating the expression of target genes at the transcriptional or post-translational level.Glyma.16G135500,encoding an NBS-LRR-type protein,is a target of gma-miR1510 that responds to pathogen infections.We cloned and overexpressed Glyma.16G135500(naming it GmTNL16)and knocked down mi R1510 using short tandem target mimic technology to identify the roles of the GmTNL16/gma-mi R1510 pair in the interaction of soybean and the oomycete.By overexpressing GmTNL16 in transgenic hairy roots of soybean,we showed that biomass of P.sojae was lower in overexpressing hairy roots than in control roots.Thus,miR1510 expression was reduced upon P.sojae infection,reflecting the induced expression of GmTNL16 conferring resistance to P.sojae in soybean.Differentially expressed genes were enriched in plant-pathogen interaction,plant hormone signal transduction,and secondary metabolism by RNA sequencing analyze.In particular,jasmonate and salicylic acid pathway-associated genes,including JAZ,COI1,TGA,and PR,responded to P.sojae infection.All of these results indicate that the GmTNL16/gma-miR1510 pair participates in soybean defense response via the JA and SA pathways.