| First Author | Poutahidis T | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 8 | Pages | e73933 |
| PubMed ID | 23991210 | Mgi Jnum | J:204916 |
| Mgi Id | MGI:5543728 | Doi | 10.1371/journal.pone.0073933 |
| Citation | Poutahidis T, et al. (2013) Pathogenic intestinal bacteria enhance prostate cancer development via systemic activation of immune cells in mice. PLoS One 8(8):e73933 |
| abstractText | A role for microbes has been suspected in prostate cancer but difficult to confirm in human patients. We show here that a gastrointestinal (GI) tract bacterial infection is sufficient to enhance prostate intraepithelial neoplasia (PIN) and microinvasive carcinoma in a mouse model. We found that animals with a genetic predilection for dysregulation of wnt signaling, Apc (Min/+) mutant mice, were significantly susceptible to prostate cancer in an inflammation-dependent manner following infection with Helicobacter hepaticus. Further, early neoplasia observed in infected Apc (Min/+) mice was transmissible to uninfected mice by intraperitoneal injection of mesenteric lymph node (MLN) cells alone from H. hepaticus-infected mutant mice. Transmissibility of neoplasia was preventable by prior neutralization of inflammation using anti-TNF-alpha antibody in infected MLN donor mice. Taken together, these data confirm that systemic inflammation triggered by GI tract bacteria plays a pivotal role in tumorigenesis of the prostate gland. |
