Dietary ω-3 Fatty Acids Mitigate Intestinal Barrier Integrity Alterations in Mice Fed a High-Fat Diet: Implications for Pancreatic Carcinogenesis.

Background: Although body fatness is a recognized risk factor for pancreatic ductal adenocarcinoma (PDAC), the underlying mechanisms of how fat composition affects pancreatic carcinogenesis are poorly understood. High-fat diets (HFDs) can disrupt intestinal barrier function, potentially accelerating carcinogenesis. Omega-3 (ω-3) polyunsaturated fatty acids (FAs) have anti-inflammatory properties and help preserve intestinal integrity.

A high-fat diet induces changes in mesenteric adipose tissue accelerating early-stage pancreatic carcinogenesis in mice.

Increased adiposity is a significant risk factor for pancreatic cancer development. Multiple preclinical studies have documented that high-fat, high calorie diets, rich in omega-6 fatty acids (FA) accelerate pancreatic cancer development. However, the effect of a high-fat, low sucrose diet (HFD), on pancreatic carcinogenesis remains unclear.

Impact of dietary fat composition and quantity in pancreatic carcinogenesis: Recent advances and controversies.

A significant number of pancreatic cancer cases are due to modifiable risk factors, with many being attributed to increased body fatness. This has sparked investigators to examine the role played by high dietary fat intake in pancreatic cancer development and the mechanisms driving this connection. However, there is currently no consensus on how dietary fat quantity and composition specifically affect pancreatic carcinogenesis.

EGCG sensitizes chemotherapeutic-induced cytotoxicity by targeting the ERK pathway in multiple cancer cell lines.

Epigallocatechin-3-gallate (EGCG), a major polyphenol component of green tea, presents anticancer efficacy. However, its exact mechanism of action is not known. In this study, we evaluated the effect of EGCG alone or in combination with current chemotherapeutics [gemcitabine, 5-flourouracil (5-FU), and doxorubicin] on pancreatic, colon, and lung cancer cell growth, as well as the mechanisms involved in the combined action.