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Mixtures of Acids03:27

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Aflatoxin Mixture-Driven Intrahepatic Cholangiocarcinoma in Rats Involving G1/S Checkpoint Dysregulation.

Vinícius Menezes Braga1, Paulo Henrique Fernandes Pereira1, Letícia de Araujo Apolinario2

  • 1Department of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes, 3900, Ribeirão Preto 14049-900, SP, Brazil.

Toxins
|January 27, 2026
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Summary
This summary is machine-generated.

Aflatoxins, potent liver toxins, can induce intrahepatic cholangiocarcinoma (iCCA) in rats. This study reveals iCCA in rats exposed to aflatoxins, showing high cell proliferation and disrupted cell cycle control.

Keywords:
AFB1-dominant aflatoxin mixturePCNATP53aflatoxinscyclin D1immunohistochemistryintrahepatic cholangiocarcinomaretinoblastoma proteinβ-catenin

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Area of Science:

  • Toxicology
  • Oncology
  • Hepatology

Background:

  • Aflatoxins (AFs) are mycotoxins known for hepatotoxicity.
  • The role of AFs in inducing intrahepatic cholangiocarcinoma (iCCA) is not well understood.

Purpose of the Study:

  • To investigate the potential of an AFB1-dominant AF mixture to induce iCCA in a rat model.
  • To characterize the molecular and histological features of AF-induced iCCA.

Main Methods:

  • Male Wistar rats were administered an AFB1-dominant AF mixture via gavage for 90 days.
  • Tumors were analyzed after 12 months using histology (H&E) and immunohistochemistry (IHC) for markers like Cytokeratin-19, Hep Par-1, p53, Cyclin D1, Rb, β-catenin, and PCNA.

Main Results:

  • Histological analysis confirmed iCCA with glandular/tubular architecture, positive for Cytokeratin-19 and negative for Hep Par-1.
  • High cell proliferation (PCNA ≈ 69%) was observed.
  • p53 nuclear accumulation (83%), Cyclin D1 overexpression (67%), and Rb positivity (58%) indicated disrupted G1/S cell cycle control.
  • Aberrant Wnt activation was rare (nuclear β-catenin in 8%).

Conclusions:

  • Subchronic exposure to an AFB1-dominant AF mixture induces iCCA in rats.
  • AF-induced iCCA is characterized by high proliferative activity, p53 accumulation, and disrupted G1/S checkpoint.
  • These findings expand the known oncogenic effects of AFs and suggest the need for genomic studies.