The pathobiological impact of cigarette smoke on pancreatic cancer development (Review)

Uwe A. Wittel, Navneet Momi, Gabriel Seifert, Thorsten Wiech, Ulrich T. Hopt, Surinder K. Batra

Research output: Contribution to journalReview article

12 Scopus citations

Abstract

Despite extensive efforts, pancreatic cancer remains incurable. Most risk factors, such as genetic disposition, metabolic diseases or chronic pancreatitis cannot be influenced. By contrast, cigarette smoking, an important risk factor for pancreatic cancer, can be controlled. Despite the epidemiological evidence of the detrimental effects of cigarette smoking with regard to pancreatic cancer development and its unique property of being influenceable, our understanding of cigarette smoke-induced pancreatic carcinogenesis is limited. Current data on cigarette smoke-induced pancreatic carcinogenesis indicate multifactorial events that are triggered by nicotine, which is the major pharmacologically active constituent of tobacco smoke. In addition to nicotine, a vast number of carcinogens have the potential to reach the pancreatic gland, where they are metabolized, in some instances to even more toxic compounds. These metabolic events are not restricted to pancreatic ductal cells. Several studies show that acinar cells are also greatly affected. Furthermore, pancreatic cancer progenitor cells do not only derive from the ductal epithelial lineage, but also from acinar cells. This sheds new light on cigarette smoke-induced acinar cell damage. On this background, our objective is to outline a multifactorial model of tobacco smoke-induced pancreatic carcinogenesis.

Original languageEnglish (US)
Pages (from-to)5-14
Number of pages10
JournalInternational journal of oncology
Volume41
Issue number1
DOIs
StatePublished - Jul 2012

Keywords

  • Carcinogenesis
  • Carcinogens
  • Chronic pancreatitis
  • Cigarette smoke
  • Nicotine
  • Pancreatic cancer
  • nnk

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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