Primary liver cancer, the majority of which are hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), is a common malignancy and the leading cause of cancer-related mortality worldwide. This heterogeneous tumor is usually resistant to immunotherapy and molecular target therapy. HCCs usually develop in tissues affected by underlying liver damage (fibrosis), while ICC's defining feature is the abundant extracellular matrix (ECM). Tumor microenvironment (TME) reprogramming usually leads to abnormal angiogenesis and immunosuppression. In addition to the diversity of gene mutation, the heterogeneity of liver cancer is partially explained by this special TME which consists of a mixture of cancer cells, immune cells, fibroblasts, endothelial cells, and ECM. As emerging components of the tumor-host interaction, TME plays an essential role in response or resistance to cancer therapy, and is increasingly recognized as the main battlefield of cancer therapy, especially for immunotherapy and anti-angiogenic therapy. However, much remains unknown about the role of TME in the development and progression of primary liver cancer drug resistance.
This Research Topic aims to deeply understand the potential role of molecules, cells, and ECM in TME reprogramming and to disclose novel anti-tumor targets involved in remodeling ECM, antagonism of stromal cells (e.g. cancer-associated fibroblasts, CAFs) and immune cells (Regulatory T cells, Treg and tumor-associated macrophages, TAMs), and vascular normalization, to retard cancer progression and reverse drug resistance. Further studies based on these novel targets of TME reprogramming are crucial for the discovery and development of potentially promising new treatment approaches in primary liver cancer.
We welcome submissions of Original Research and Review articles on the following aspects:
• State-of-art animal models, 3-D cell cultures, or novel techniques with the latest advances in molecular biology that aim to elucidate roles of the TME in drug resistance
• Remodeling of molecular, cellular, ECM, and vascular signaling pathways that influence TME in primary liver cancer
• Mechanisms by which cancerous cells circumvent chemotherapy and/or immunotherapy resistance induced by TME reprogramming in primary liver cancer
• Potential therapeutic targets and strategies for primary liver cancer via modulating TME.
Topic editor Jian Chen is employed by Sandhill Therapeutics, Inc., and declares no competing interests with regards to the Research Topic The Role of Tumor Microenvironment in Primary Liver Cancer Therapeutic Resistance.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Primary liver cancer, the majority of which are hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), is a common malignancy and the leading cause of cancer-related mortality worldwide. This heterogeneous tumor is usually resistant to immunotherapy and molecular target therapy. HCCs usually develop in tissues affected by underlying liver damage (fibrosis), while ICC's defining feature is the abundant extracellular matrix (ECM). Tumor microenvironment (TME) reprogramming usually leads to abnormal angiogenesis and immunosuppression. In addition to the diversity of gene mutation, the heterogeneity of liver cancer is partially explained by this special TME which consists of a mixture of cancer cells, immune cells, fibroblasts, endothelial cells, and ECM. As emerging components of the tumor-host interaction, TME plays an essential role in response or resistance to cancer therapy, and is increasingly recognized as the main battlefield of cancer therapy, especially for immunotherapy and anti-angiogenic therapy. However, much remains unknown about the role of TME in the development and progression of primary liver cancer drug resistance.
This Research Topic aims to deeply understand the potential role of molecules, cells, and ECM in TME reprogramming and to disclose novel anti-tumor targets involved in remodeling ECM, antagonism of stromal cells (e.g. cancer-associated fibroblasts, CAFs) and immune cells (Regulatory T cells, Treg and tumor-associated macrophages, TAMs), and vascular normalization, to retard cancer progression and reverse drug resistance. Further studies based on these novel targets of TME reprogramming are crucial for the discovery and development of potentially promising new treatment approaches in primary liver cancer.
We welcome submissions of Original Research and Review articles on the following aspects:
• State-of-art animal models, 3-D cell cultures, or novel techniques with the latest advances in molecular biology that aim to elucidate roles of the TME in drug resistance
• Remodeling of molecular, cellular, ECM, and vascular signaling pathways that influence TME in primary liver cancer
• Mechanisms by which cancerous cells circumvent chemotherapy and/or immunotherapy resistance induced by TME reprogramming in primary liver cancer
• Potential therapeutic targets and strategies for primary liver cancer via modulating TME.
Topic editor Jian Chen is employed by Sandhill Therapeutics, Inc., and declares no competing interests with regards to the Research Topic The Role of Tumor Microenvironment in Primary Liver Cancer Therapeutic Resistance.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.