Abstract
Gallbladder cancer (GBC) is an aggressive neoplasm that in an early stage is generally asymptomatic and, in most cases, is diagnosed in advanced stages with a very low life expectancy because there is no curative treatment. Therefore, understanding the early carcinogenic mechanisms of this pathology is crucial to proposing preventive strategies for this cancer. The main risk factor is the presence of gallstones, which are associated with some environmental factors such as a sedentary lifestyle and a high-fat diet. Other risk factors such as autoimmune disorders and bacterial, parasitic and fungal infections have also been described. All these factors can generate a long-term inflammatory state characterized by the persistent activation of the immune system, the frequent release of pro-inflammatory cytokines, and the constant production of reactive oxygen species that result in a chronic damage/repair cycle, subsequently inducing the loss of the normal architecture of the gallbladder mucosa that leads to the development of GBC. This review addresses how the different risk factors could promote a chronic inflammatory state essential to the development of gallbladder carcinogenesis, which will make it possible to define some strategies such as anti-inflammatory drugs or public health proposals in the prevention of GBC.
Highlights
Gallbladder cancer (GBC) is a neoplasm that causes around 84,695 deaths per year worldwide [1], affecting more commonly women than men with an age-standardized incidence rate of 1.4 and 0.89 per 100,000 people, respectively [1]
The cumulative evidence described in this review shows that GBC is a chronic inflammatory disease promoted by different risk factors including gallstone disease (GSD), sedentary lifestyle, smoking, alcohol consumption, metabolic disorders, high-fat diet, hypercholesterolemia, and some types of infections
Gallbladder carcinogenesis has been strongly associated with specific populations (e.g., Mapuche ancestry), possibly because these populations present some genetic background (e.g., ABCG8 and TRAF3 gene variants) that predispose them to being more susceptible to gallstone formation and a greater predisposition to the development GBC, which could explain the high incidence of GBC in this population
Summary
Gallbladder cancer (GBC) is a neoplasm that causes around 84,695 deaths per year worldwide [1], affecting more commonly women than men with an age-standardized incidence rate of 1.4 and 0.89 per 100,000 people, respectively [1]. The onset of this disease is characterized by a slow and silent development, resulting in many GBC cases being frequently diagnosed at late stages when patients have a 5-year life expectancy of less than. Gallstones can lead to a chronic inflammatory state of tissue damage/regeneration characterized by an imbalance between anti- and pro-inflammatory factors that induce carcinogenic processes in the gallbladder mucosa [6]. This article reviews the relationship between environmental risk factors and the formation of chronic inflammation, and how this inflammatory process is involved in gallbladder carcinogenesis
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