Intratumoral inflammation is associated with more aggressive prostate cancer.

Journal Article


Inflammation may play a role in the development and progression of many cancers, including prostate cancer. We sought to test whether histological inflammation within prostate cancer was associated with more aggressive disease.


The slides of prostatectomy specimens were reviewed by a board-certified pathologist on 287 men from a Veterans Affairs Medical Center treated with radical prostatectomy from 1992 to 2004. The area with the greatest tumor burden was scored in a blinded manner for the degree of inflammation: absent, mild, or marked. We used logistic and Cox proportional hazards regression analysis to examine whether categorically coded inflammation score was associated with adverse pathology and biochemical progression, respectively.


No inflammation was found in 49 men (17%), while 153 (53%) and 85 (30%) had mild and marked inflammation. During a median follow-up of 77 months, biochemical recurrence occurred among 126 (44%) men. On multivariate analysis, more inflammation was associated with greater risk of positive margins, capsular penetration, and seminal vesicle invasion (all p < 0.05). Marked inflammation was associated with increased PSA recurrence risk when adjusting for preoperative features only (HR 2.08, 95% CI 1.02-4.24), but not after adjusting for pathologic features.


Inflammation within prostate cancer was associated with more advanced disease, although it is unclear whether aggressive disease caused increased inflammation or inflammation caused aggressive disease.

Full Text

Duke Authors

Cited Authors

  • Klink, JC; Bañez, LL; Gerber, L; Lark, A; Vollmer, RT; Freedland, SJ

Published Date

  • December 2013

Published In

Volume / Issue

  • 31 / 6

Start / End Page

  • 1497 - 1503

PubMed ID

  • 23546767

Pubmed Central ID

  • 23546767

Electronic International Standard Serial Number (EISSN)

  • 1433-8726

International Standard Serial Number (ISSN)

  • 0724-4983

Digital Object Identifier (DOI)

  • 10.1007/s00345-013-1065-8


  • eng