TY - JOUR
T1 - Chronic inflammatory mediators enhance prostate cancer development and progression
AU - Thapa, Dinesh
AU - Ghosh, Rita
N1 - Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/3/15
Y1 - 2015/3/15
N2 - Chronic inflammation is postulated to influence prostate cancer progression. Preclinical studies have claimed that inflammatory mediators are involved in prostate cancer development and therefore suggested these as attractive targets for intervention. However, among the many pro-inflammatory mediators, there is no consensus regarding the identity of the primary one(s). In clinical studies, chronic inflammation has been found in prostate tumor specimens, and tissues resected for treatment of benign prostatic hyperplasia (BPH). Although collective evidence from molecular, experimental and clinical data suggests that inflammation can contribute or promote prostate carcinogenesis, an etiologic link has not yet been established. Moreover, the role of chronic inflammation in the onset of castration resistant and metastatic disease is unclear. Therefore it is important to open a dialog regarding recent findings on how chronic inflammatory mediators contribute to prostate cancer progression, and their usefulness to prevent disease progression. In this commentary, we assess the current literature with respect to chronic inflammation as a potential initiator and promoter of prostate carcinogenesis and discuss the prospects for its potential clinical applications.
AB - Chronic inflammation is postulated to influence prostate cancer progression. Preclinical studies have claimed that inflammatory mediators are involved in prostate cancer development and therefore suggested these as attractive targets for intervention. However, among the many pro-inflammatory mediators, there is no consensus regarding the identity of the primary one(s). In clinical studies, chronic inflammation has been found in prostate tumor specimens, and tissues resected for treatment of benign prostatic hyperplasia (BPH). Although collective evidence from molecular, experimental and clinical data suggests that inflammation can contribute or promote prostate carcinogenesis, an etiologic link has not yet been established. Moreover, the role of chronic inflammation in the onset of castration resistant and metastatic disease is unclear. Therefore it is important to open a dialog regarding recent findings on how chronic inflammatory mediators contribute to prostate cancer progression, and their usefulness to prevent disease progression. In this commentary, we assess the current literature with respect to chronic inflammation as a potential initiator and promoter of prostate carcinogenesis and discuss the prospects for its potential clinical applications.
KW - Castrate resistance
KW - Chemokines
KW - Chronic inflammation
KW - Cytokines
KW - Prostate cancer
KW - Prostate microenvironment
UR - http://www.scopus.com/inward/record.url?scp=84923922368&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84923922368&partnerID=8YFLogxK
U2 - 10.1016/j.bcp.2014.12.023
DO - 10.1016/j.bcp.2014.12.023
M3 - Comment/debate
C2 - 25593038
AN - SCOPUS:84923922368
SN - 0006-2952
VL - 94
SP - 53
EP - 62
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
IS - 2
ER -