Discovering the route from inflammation to pancreatic cancer

Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA - .
Minerva gastroenterologica e dietologica 12/2012; 58(4):283-97.
Source: PubMed


Pancreatic cancer (PC) remains a complex malignancy with the worst prognosis, lack of early diagnostic symptoms and resistance to conventional chemo- and radiotherapies. A better understanding of the etiology and early developmental events of PC requires profound attention. The evolution of fully blown PC from initial pancreatic injury is a multi-factorial phenomenon with a series of sequential events. The initial acute infection or tissue damage triggers inflammation that, in conjunction with innate immunity, establishes a state of homeostasis to limit harm to the body. Recurrent pancreatic injuries due to genetic susceptibility, smoking, unhealthy diet, and alcohol abuse induces a pro-inflammatory milieu, consisting of various types of immune cells, cytokines, chemokines, growth factors and restructured extracellular matrix, leading to prolonged inflammatory/chronic conditions. Cells having sustained DNA damage and/or mutagenic assault take advantage of this prolonged inflammatory response and aid in the initiation and development of neoplastic/fibrotic events. Eventually, many tumor-stromal interactions result in a chaotic environment accompanied by a loss of immune surveillance and repair response, thereby leading to PC. A better understanding of the inflammatory markers defining this "injury-inflammation-cancer" pathway would help to identify novel molecular targets for early screening and therapeutic intervention for this lethal malignancy.

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Available from: Navneet Momi,
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    • "Since prolonged inflammation is known to cause serious diseases such as cancer, diabetes, and atherosclerosis (Lyman et al., 2014; Momi et al., 2012), studies on inflammation have focused on the systemic, cellular, and molecular mechanisms of inflammatory responses. As an important barrier in the innate immune system, inflammation is a normal mechanism. "
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    Journal of Ethnopharmacology 06/2015; 2015(168):217-228. DOI:10.1016/j.jep.2015.03.0 · 3.00 Impact Factor
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