Smoking and Pancreatic Disease

Edderkaoui, Mouad; Thrower, Edwin C.

doi:10.4236/jct.2013.410a005

Cited by 49 publications

(42 citation statements)

References 62 publications

(67 reference statements)

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“…Tobacco smoking is a strong risk factor for pancreatic cancer . Tobacco smoke contains high doses of carcinogenic TSNAs, 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) and N ′‐nitrosonornicotine (NNN), which may have specificity for the pancreas . NNK metabolites can bind to DNA to form adducts and induce activating point mutations in the RAS gene, which are thought to be the most common genetic alterations in the progression of pancreatic cancer .…”

Section: Discussionmentioning

confidence: 99%

Use of moist oral snuff (snus) and pancreatic cancer: Pooled analysis of nine prospective observational studies

Araghi

Galanti

Lundberg

et al. 2017

Intl Journal of Cancer

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While smoking is a well-established risk factor for pancreatic cancer, the effect of smokeless tobacco is less well understood. We used pooled individual data from the Swedish Collaboration on Health Effects of Snus Use to assess the association between Swedish snus use and the risk of pancreatic cancer. A total of 424,152 male participants from nine cohort studies were followed up for risk of pancreatic cancer through linkage to health registers. We used shared frailty models with random effects at the study level, to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for confounding factors. During 9,276,054 person-years of observation, 1,447 men developed pancreatic cancer. Compared to never-snus use, current snus use was not associated with risk of pancreatic cancer (HR 0.96, 95% CI 0.83-1.11) after adjustment for smoking. Swedish snus use does not appear to be implicated in the development of pancreatic cancer in men. Tobacco smoke constituents other than nicotine or its metabolites may account for the relationship between smoking and pancreatic cancer.Pancreatic cancer is one of the most lethal malignancies.

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Section: Discussionmentioning

confidence: 99%

Use of moist oral snuff (snus) and pancreatic cancer: Pooled analysis of nine prospective observational studies

Araghi

Galanti

Lundberg

et al. 2017

Intl Journal of Cancer

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“…Data from Edderkaoui et al show similar upregulation of PanIN lesion formation, inflammation, fibrosis and stellate cells activation in the same animal model, but with a shorter exposure to cigarette smoke (6 weeks) (38). Their data further demonstrated a significant stimulation of EMT in the PanIN cells in mice exposed to cigarette smoke suggesting that smoking may cause early metastasis of the pre-cancer PanIN cells before even reaching the cancer stage.…”

Section: Cell Signaling Pathways Affected By Nnk and Cigarette Smoke supporting

confidence: 59%

“…Published studies indicate that exposure of mice to cigarette smoke activates pancreatic stellate cells (SC) as expressed by the level of its marker alpha-smooth muscle actin (α-SMA) and induces expression of extracellular matrix proteins (38,58).…”

Section: Smoking and Fibrosismentioning

confidence: 99%

Smoking induced pancreatitis and pancreatic cancer

Edderkaoui¹

The Pancreapedia: Exocrine Pancreas Knowledge Base

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Abstract:Acute pancreatitis, chronic pancreatitis, and pancreatic cancer are three major pancreatic diseases without any effective treatment. In this character, the latest knowledge regarding the association between these diseases and tobacco smoking is reviewed. Clinical evidence of the association is presented, followed by an overview of scientific evidence, and the potential pathways that mediate smoking-induced pancreatitis and pancreatic cancer.

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“…Studies have shown that N-nitrosamines, which are present in cigarette smoke, are directly secreted into the bile and may stimulate an inflammatory response in the pancreas 24 . As an alternative mechanism, nicotine metabolites can bind to receptors on the exocrine pancreas, thereby promoting pancreatitis and pancreatic cancer 25 . Importantly, cigarette smoking increases the risk of pancreatic cancer by 1.5 to 3 fold, depending on the duration and number of cigarette smoked 26 .…”

Section: Risk Factors For Pancreatitis and Pancreatic Cancermentioning

confidence: 99%

Phosphatidylinositol 3-Kinase

Birtolo

Ptasznik

et al. 2016

Pancreas

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Even though a strong association between inflammation and cancer has been widely accepted, the underlying precise molecular mechanisms are still largely unknown. A complex signaling network between tumor and stromal cells is responsible for the infiltration of inflammatory cells into the cancer micro-environment. Tumor stromal cells such as pancreatic stellate cells (PSCs) and immune cells create a microenvironment that protects cancer cells through a complex interaction, ultimately facilitating their local proliferation and their migration to different sites. Furthermore, PSCs have multiple functions related to local immunity, angiogenesis, inflammation and fibrosis. Recently, many studies have shown that members of the phosphoinositol-3-phosphate kinase (PI3K) family are activated in tumor cells, PSCs and tumor infiltrating inflammatory cells to promote cancer growth. Pro-inflammatory cytokines and chemokines secreted by immune cells and fibroblasts within the tumor environment can activate the PI3K pathway both in cancer and inflammatory cells. In this review, we focus on the central role of the PI3K pathway in regulating the cross-talk between immune/stromal cells and cancer cells. Understanding the role of the PI3K pathway in the development of chronic pancreatitis and cancer is crucial for the discovery of novel and efficacious treatment options.

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Smoking and Pancreatic Disease

Cited by 49 publications

References 62 publications

Use of moist oral snuff (snus) and pancreatic cancer: Pooled analysis of nine prospective observational studies

Use of moist oral snuff (snus) and pancreatic cancer: Pooled analysis of nine prospective observational studies

Smoking induced pancreatitis and pancreatic cancer

Phosphatidylinositol 3-Kinase

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