Metabolic reprogramming is the hallmark of malignant tumors. Both metabolic phenotype and metabolic dependence are changed during the development of cancer from precancerous tissue to local invasion to metastasis. Cancer cells autonomously alter their flux through various metabolic pathways in order to meet the increased bioenergetic and biosynthetic demand as well as mitigate oxidative stress required for cancer cell proliferation and survival. The change of the tumor microenvironment (TME) is a key factor driving tumor metabolic reprogramming. The tumor microenvironment denotes the non-cancerous cells and components presented in the tumor, including molecules produced and released by them. The constant interactions between tumor cells and the tumor microenvironment play decisive roles in tumor initiation, progression, metastasis, and response to therapies.
More and more evidence has pointed out that the change in the tumor microenvironment is a key factor driving tumor metabolic reprogramming. However, the specific relationship between tumor metabolic reprogramming and tumor microenvironment remains unclear. Indeed, emerging evidence indicates that cancer cells are able to suppress the anti-tumor immune response by competing for and depleting essential nutrients or otherwise reducing the metabolic fitness of tumor-infiltrating immune cells. The actual process of how metabolic reprogramming and cancer immune response affect each other has not been understood.
This Research Topic will cover all malignant tumors, including gastric cancer, lung cancer, colorectal cancer, melanoma, pancreatic cancer, liver cancer, etc. This Research Topic is also interested in the development of gastrointestinal tumors and the key molecules and regulatory networks in the tumor microenvironment based on multi-omics characteristics. We welcome, original research, reviews, and mini-reviews.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Metabolic reprogramming is the hallmark of malignant tumors. Both metabolic phenotype and metabolic dependence are changed during the development of cancer from precancerous tissue to local invasion to metastasis. Cancer cells autonomously alter their flux through various metabolic pathways in order to meet the increased bioenergetic and biosynthetic demand as well as mitigate oxidative stress required for cancer cell proliferation and survival. The change of the tumor microenvironment (TME) is a key factor driving tumor metabolic reprogramming. The tumor microenvironment denotes the non-cancerous cells and components presented in the tumor, including molecules produced and released by them. The constant interactions between tumor cells and the tumor microenvironment play decisive roles in tumor initiation, progression, metastasis, and response to therapies.
More and more evidence has pointed out that the change in the tumor microenvironment is a key factor driving tumor metabolic reprogramming. However, the specific relationship between tumor metabolic reprogramming and tumor microenvironment remains unclear. Indeed, emerging evidence indicates that cancer cells are able to suppress the anti-tumor immune response by competing for and depleting essential nutrients or otherwise reducing the metabolic fitness of tumor-infiltrating immune cells. The actual process of how metabolic reprogramming and cancer immune response affect each other has not been understood.
This Research Topic will cover all malignant tumors, including gastric cancer, lung cancer, colorectal cancer, melanoma, pancreatic cancer, liver cancer, etc. This Research Topic is also interested in the development of gastrointestinal tumors and the key molecules and regulatory networks in the tumor microenvironment based on multi-omics characteristics. We welcome, original research, reviews, and mini-reviews.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
