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

TY - JOUR

T1 - The pathobiological impact of cigarette smoke on pancreatic cancer development (review)

AU - Wittel, Uwe A

AU - Momi, Navneet

AU - Seifert, Gabriel

AU - Wiech, Thorsten

AU - Hopt, Ulrich T

AU - Batra, Surinder K

PY - 2012/7/1

Y1 - 2012/7/1

N2 - 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.

AB - 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.

KW - Acinar Cells

KW - Animals

KW - Carcinogens

KW - Carcinoma, Pancreatic Ductal

KW - Cell Transformation, Neoplastic

KW - Humans

KW - Nicotine

KW - Pancreas

KW - Pancreatic Neoplasms

KW - Risk Factors

KW - Smoke

KW - Tobacco

U2 - 10.3892/ijo.2012.1414

DO - 10.3892/ijo.2012.1414

M3 - SCORING: Journal article

C2 - 22446714

VL - 41

SP - 5

EP - 14

JO - INT J ONCOL

JF - INT J ONCOL

SN - 1019-6439

IS - 1

ER -