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Cancer J. 2014 May-Jun;20(3):195-202. doi: 10.1097/PPO.0000000000000045.

Pancreatic cancer, inflammation, and microbiome.

Author information

1
From the *S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, New York, NY; †Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY; and ‡Department of Cell Biology, New York University School of Medicine, New York, NY.

Abstract

Pancreatic cancer is one of the most lethal cancers worldwide. No effective screening methods exist, and available treatment modalities do not effectively treat the disease. Inflammatory conditions such as pancreatitis represent a well-known risk factor for pancreatic cancer development. Yet only in the past 2 decades has pancreatic cancer been recognized as an inflammation-driven cancer, and the precise mechanisms underlying the pathogenic role of inflammation are beginning to be explored in detail. A substantial amount of preclinical and clinical evidence suggests that bacteria are likely to influence this process by activating immune receptors and perpetuating cancer-associated inflammation. The recent explosion of investigations of the human microbiome have highlighted how perturbations of commensal bacterial populations can promote inflammation and promote disease processes, including carcinogenesis. The elucidation of the interplay between inflammation and microbiome in the context of pancreatic carcinogenesis will provide novel targets for intervention to prevent and treat pancreatic cancer more efficiently. Further studies toward this direction are urgently needed.

PMID:
24855007
PMCID:
PMC4112373
DOI:
10.1097/PPO.0000000000000045
[Indexed for MEDLINE]
Free PMC Article

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