Gastrointestinal (GI) cancer is the most common form of cancer in both men and women. It includes tumors that affect the digestive system, such as oesophageal cancer, liver cancer, stomach cancer, gallbladder & biliary tract cancer, pancreatic cancer, gastrointestinal stromal tumor (GIST), and neuroendocrine tumors (NETs), colorectal cancer, small bowel cancer, and anal cancer. The impact of diets on GI cancer has been well documented. These diets contain a special composition of diets and dietary patterns, including but not limited to the ketogenic diet, low-carbohydrate diet, vegetarian diet, Mediterranean diet, Western diet, and intermittent fasting. However, the relationship between GI cancer and diets is just as mysterious as the disease itself. Much research has pointed toward certain compositions in diets or special dietary patterns that may help suppress, or conversely, promote GI cancer. Therefore, it’s important to explore the effects of diet on GI cancer as well as the molecular mechanisms for patients with GI cancer.
This Research Topic aims to collate the latest research examining the role of certain special diets as complementary and alternative anticancer therapies for GI cancer, as well as the negative effect of some special diets on GI cancer initiation, promotion, and progression. Moreover, it aims to explore the cellular and molecular mechanisms behind the positive or negative role of certain diets in GI cancer.
To address how diet affects GI cancer initiation and progression. This could include studies that focus on:
· The effect of diets on GI cancer, including either positive or negative ones,
· Bioinformatics analysis of the effect of certain diets on GI cancer,
· Epidemiological studies connecting certain diet and GI cancer incidence,
· Sub-clinical studies and clinical trials that provide a further understanding of diet-cancer relationships,
· New mechanistic insights into certain diet-mediated cancer inhibition/promotion on gene expression level,
· Gut microbiome modulation,
· Immune function and response,
· Metabolic regulation,
· Tumor microenvironment.
Gastrointestinal (GI) cancer is the most common form of cancer in both men and women. It includes tumors that affect the digestive system, such as oesophageal cancer, liver cancer, stomach cancer, gallbladder & biliary tract cancer, pancreatic cancer, gastrointestinal stromal tumor (GIST), and neuroendocrine tumors (NETs), colorectal cancer, small bowel cancer, and anal cancer. The impact of diets on GI cancer has been well documented. These diets contain a special composition of diets and dietary patterns, including but not limited to the ketogenic diet, low-carbohydrate diet, vegetarian diet, Mediterranean diet, Western diet, and intermittent fasting. However, the relationship between GI cancer and diets is just as mysterious as the disease itself. Much research has pointed toward certain compositions in diets or special dietary patterns that may help suppress, or conversely, promote GI cancer. Therefore, it’s important to explore the effects of diet on GI cancer as well as the molecular mechanisms for patients with GI cancer.
This Research Topic aims to collate the latest research examining the role of certain special diets as complementary and alternative anticancer therapies for GI cancer, as well as the negative effect of some special diets on GI cancer initiation, promotion, and progression. Moreover, it aims to explore the cellular and molecular mechanisms behind the positive or negative role of certain diets in GI cancer.
To address how diet affects GI cancer initiation and progression. This could include studies that focus on:
· The effect of diets on GI cancer, including either positive or negative ones,
· Bioinformatics analysis of the effect of certain diets on GI cancer,
· Epidemiological studies connecting certain diet and GI cancer incidence,
· Sub-clinical studies and clinical trials that provide a further understanding of diet-cancer relationships,
· New mechanistic insights into certain diet-mediated cancer inhibition/promotion on gene expression level,
· Gut microbiome modulation,
· Immune function and response,
· Metabolic regulation,
· Tumor microenvironment.
