Hepatocellular carcinoma (HCC) is one of the most common causes of cancer death. It is mainly caused by hepatitis virus B/C (HBV/HCV) infection, alcoholic consumption, and non-alcoholic steatohepatitis (NASH). Considering the increased availability of vaccine to prevent HBV, and the effective antiviral treatment for HCV, NASH is rising to become the main risk of HCC. However, the molecular mechanism underlying NASH-HCC is still not very clear. A lot of progress has been made recently, including genomic change, transcriptional difference, and specific immune population involved in the development of NASH-HCC. Based on current knowledge, it is likely that NASH-HCC has a special mechanism, which needs more investigation.
This specific Research Topic will focus on the recent discovery related to the novel mechanism in NASH, and further explore the potential risk and mechanism that drives NASH to HCC, which include specific gene or metabolic signaling pathway related to the tumor initiation in NASH-HCC, the contribution of liver inflammatory cell/ immune cell/hepatic stellate cell in NASH-HCC progression, and if there is specific NASH related gut microbiome promoting the transition from NASH to HCC.
We welcome the submission of Original Research articles, Reviews and Methods on the recent achievement to understand the molecular mechanism underlying NASH-HCC, including but not limited to the following topics:
● How tumor initiate in NASH-HCC, and what cell-type (parenchymal or non-parenchymal cell) is the cell of origin in NASH-HCC;
● Specific NASH-related macrophage, immune cell, and hepatic stellate cell population that contributes to NASH-HCC;
● Developing new NASH-HCC mouse model or organoid model;
● The role of gut-liver axis in NASH-HCC;
● Effective treatment for NASH-HCC.
Keywords:
NASH, HCC, metabolism, tumorigenesis, tumor immunity
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Hepatocellular carcinoma (HCC) is one of the most common causes of cancer death. It is mainly caused by hepatitis virus B/C (HBV/HCV) infection, alcoholic consumption, and non-alcoholic steatohepatitis (NASH). Considering the increased availability of vaccine to prevent HBV, and the effective antiviral treatment for HCV, NASH is rising to become the main risk of HCC. However, the molecular mechanism underlying NASH-HCC is still not very clear. A lot of progress has been made recently, including genomic change, transcriptional difference, and specific immune population involved in the development of NASH-HCC. Based on current knowledge, it is likely that NASH-HCC has a special mechanism, which needs more investigation.
This specific Research Topic will focus on the recent discovery related to the novel mechanism in NASH, and further explore the potential risk and mechanism that drives NASH to HCC, which include specific gene or metabolic signaling pathway related to the tumor initiation in NASH-HCC, the contribution of liver inflammatory cell/ immune cell/hepatic stellate cell in NASH-HCC progression, and if there is specific NASH related gut microbiome promoting the transition from NASH to HCC.
We welcome the submission of Original Research articles, Reviews and Methods on the recent achievement to understand the molecular mechanism underlying NASH-HCC, including but not limited to the following topics:
● How tumor initiate in NASH-HCC, and what cell-type (parenchymal or non-parenchymal cell) is the cell of origin in NASH-HCC;
● Specific NASH-related macrophage, immune cell, and hepatic stellate cell population that contributes to NASH-HCC;
● Developing new NASH-HCC mouse model or organoid model;
● The role of gut-liver axis in NASH-HCC;
● Effective treatment for NASH-HCC.
Keywords:
NASH, HCC, metabolism, tumorigenesis, tumor immunity
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.