Hepatocellular carcinoma and possible chemical and biological causes: A review

ERKEKOGLU P., ORAL D., CHAO M., Kocer-Gumusel B.

Journal of Environmental Pathology, Toxicology and Oncology, cilt.36, sa.2, ss.171-190, 2017 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 36 Sayı: 2
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1615/jenvironpatholtoxicoloncol.2017020927
  • Dergi Adı: Journal of Environmental Pathology, Toxicology and Oncology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.171-190
  • Anahtar Kelimeler: hepatocellular carcinoma, DNA-damaging chemicals, dietary contaminants, alcohol, hepatitis, STRAND BREAK REPAIR, RODENT PEROXISOME PROLIFERATOR, OXIDATIVE DNA-DAMAGE, HEPATOMA HEPG2 CELLS, VINYL-CHLORIDE, LIVER-CANCER, RISK-FACTORS, POLYCHLORINATED-BIPHENYLS, MOLECULAR-MECHANISMS, HIGH EXPRESSION
  • Hacettepe Üniversitesi Adresli: Evet

Özet

© 2017 Begell House, Inc.The development of hepatocellular carcinoma (HCC) is a multistep process. In HCC, progressive and morphologically distinct preneoplastic lesions/alterations associated with chronic liver injury, inflammation, hepatocellular degeneration/regeneration, necrosis, and small-cell dysplasia can be observed. The incidence of HCC exhibits regional and ethnic differences. Several cytotoxic and DNA-damaging chemicals are suggested to be the underlying causes of HCC—for example, acrylamide, perfluorooctanoic acid (PFOA), polychlorinated biphenyls (PCBs), benzo(a)pyrene (BaP), perfluorinated chemicals (PFCs), vinyl chloride monomer (VCM), and dietary contaminants (aflatoxins, ochratoxins). Also suggested are substances of abuse (alcohol) and biological agents, such as hepatitis B and C and human immunodeficiency virus 1 (HIV-1). These can act through genetic and/or epigenetic mechanisms. This review will shortly address the genetic and epigenetic mechanisms of HCC and focus on cytotoxic and DNA-damaging chemicals and biological agents, exposure to which are suggested to lead to HCC initiation, promotion, and/or progression.