Metallic trace elements in pancreatic tissue are associated with higher risk of pancreatic adenocarcinoma - METAPANDA

Mireille Simon1, Aurore Meurat2, Sophie Stanislas3

  • 1Pau Hospital Center, Department of Gastroenterology and Digestive Oncology, 64000, Pau, France.

Abstract

Insights

This study investigated metallic trace elements (MTE) in pancreatic cancer. Higher concentrations of antimony, thallium, arsenic, and lead were associated with increased pancreatic ductal adenocarcinoma (PDAC) risk.

Area of Science:

  • Oncology
  • Environmental Health
  • Toxicology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a deadly malignancy with limited treatment options.
  • Emerging evidence suggests a potential role for metallic trace elements (MTE), or heavy metals, in PDAC development.
  • Understanding environmental risk factors is crucial for early detection and prevention strategies.

Purpose of the Study:

  • To investigate the association between tissue concentrations of 23 MTE and the risk of PDAC.
  • To compare MTE levels in pancreatic tissues from PDAC patients and control subjects.

Main Methods:

  • Tissue samples were obtained from 33 PDAC cases and 29 controls undergoing pancreatic surgery.
  • Concentrations of 23 MTE were quantified using inductively coupled plasma mass spectrometry (ICP-MS).
  • Multivariate analysis was employed to assess the association between MTE levels and PDAC risk.

Main Results:

  • Elevated tissue concentrations of antimony, thallium, arsenic, and lead were significantly associated with an increased risk of PDAC.
  • Antimony showed the strongest association (OR 6.31, p=0.006), followed by thallium (OR 3.23, p=0.033), arsenic (OR 2.96, p=0.04), and lead (OR 2.27, p=0.044).
  • This study provides novel data on a wide range of MTE in pancreatic tissues.

Conclusions:

  • The findings confirm the potential involvement of arsenic and lead in PDAC onset.
  • Antimony and thallium are identified as potential novel risk factors for PDAC.
  • Further research is warranted to elucidate the mechanisms underlying MTE's role in pancreatic carcinogenesis.