Vitamin A Could Help Combat Aggressive Pancreatic Cancer


New insights pave the way for future treatment developments of pancreatic ductal adenocarcinoma.

Vitamin A may provide benefits in pancreatic ductal adenocarcinoma (PDAC), an aggressive and hard-to-treat cancer.

Although scientists are investigating genetic mutations and biochemical signaling pathways that enable cancer cells to spread to other areas of the body, a new study published in Nature Communications took a different approach by using cells in the laboratory.

Researchers in the study examined how mechanical changes in stellate cells affect PDAC progression. Stellate cells are a group of cells that live in the immediate environment of the tumor.

“The survival rate of pancreatic cancer has remained relatively unchanged during the last 40 years, despite advances in conventional therapies targeting cancer cells,” said researcher Armando del Rio Hernandez. “We’ve changed the focus from cancer cells to the cells that surround the tumor. We’ve combined traditional approaches to cancer biology with understanding the mechanics behind the progression of tumors. This could meet a pressing unmet clinical need in the UK and worldwide.”

Normally, in a healthy pancreas, the stellate cells are in a dormant state, storing abundant supplies of vitamin A. But with PDAC, as the disease progresses, the stellate cells become activated in response to signals from the tumor resulting in the loss of their vitamin A content.

These activated stellate cells form a dense connective tissue that surrounds the tumor, which is used by cancer cells to spread to different parts of the body. Furthermore, the tissue limits the ability of cancer-fighting drugs to reach the tumor.

In the new study, researchers found that the pancreatic stellate cells could be switched off, which could potentially prevent the tissue from forming around the tumor, through a process involving vitamin A.

Vitamin A is converted into All-Trans-Retinoic Acid (ATRA) in a healthy body, and helps regulate multiple functions including normal development and growth. In the lab cells, researchers induced this process, causing ATRA to switch off the forces that the stellate cells used to remodel their environment.

Not only did this reduce fibrosis, but it also produced an environment that would make it more difficult for a pancreatic tumor to spread.

“Other research groups in the past have explored the idea of destroying the fibrotic tissue and stellate cells altogether to weaken the tumor,” said study co-author Antonios Chronopoulos. “Our approach is much more subtle. Instead of destroying them, we simply want to revert chronically activated stellate cells to a dormant state in an attempt to reduce fibrosis and reprogram the tumor microenvironment to a health state, thus suppressing the signals that spur cancer growth.”

The study authors noted that their research only focused on the behaviors of cells in the laboratory, and cautioned that they have no evidence patients would benefit from taking vitamin A supplements.

Although more research needs to be done on the subject, including clinical trials, researchers believe their findings on the mechanisms of PDAC will help scientists explore new possibilities for tackling this type of cancer.

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