Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior
It is currently estimated that inflammatory responses are linked to 15-20% of all deaths from cancer worldwide. Although many studies point to an important role of inflammation in prostate growth, the contribution of inflammation to castration-resistant prostate cancer is not completely understood....
Guardado en:
Autores principales: | , , |
---|---|
Formato: | JOUR |
Materias: | |
Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_13657852_v15_n3_p213_Gueron |
Aporte de: |
id |
todo:paper_13657852_v15_n3_p213_Gueron |
---|---|
record_format |
dspace |
spelling |
todo:paper_13657852_v15_n3_p213_Gueron2023-10-03T16:11:20Z Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior Gueron, G. De Siervi, A. Vazquez, E. castration-resistant prostate cancer (CRPC) chemokines inflammation metastasis reactive oxygen species (ROS) chemokine receptor CXCR4 chemokine receptor CXCR6 chemokine receptor CXCR7 heme oxygenase 1 immunoglobulin enhancer binding protein interleukin 6 interleukin 8 matrix metalloproteinase Notch receptor osteopontin parathyroid hormone related protein reactive oxygen metabolite stromal cell derived factor 1 tumor necrosis factor alpha advanced cancer cancer growth carcinogenesis castration resistant prostate cancer cell homing cell proliferation cellular stress signal chronic inflammation gene activation gene targeting human metastasis oncogene priority journal prostate cancer protein expression protein function review signal transduction tumor growth tumor microenvironment Animals Bone and Bones Chemokines Disease Progression Humans Inflammation Inflammation Mediators Male Neoplasm Metastasis Neoplasm Staging Oxidative Stress Prostatic Neoplasms Reactive Oxygen Species Receptors, Chemokine Signal Transduction Tumor Microenvironment It is currently estimated that inflammatory responses are linked to 15-20% of all deaths from cancer worldwide. Although many studies point to an important role of inflammation in prostate growth, the contribution of inflammation to castration-resistant prostate cancer is not completely understood. The presence of inflammatory mediators in tumor microenvironment raises the question whether genetic events that participate in cancer development and progression are responsible for the inflammatory milieu inside and surrounding tumors. Activated oncogenes, cytokines, chemokines and their receptors, sustained oxidative stress and antioxidant imbalance share the capacity to orchestrate these pro-inflammatory programs; however, the diversity of the inflammatory cell components will determine the final response in the prostate tissue. These observations give rise to the concept that early genetic events generate an inflammatory microenvironment promoting prostate cancer progression and creating a continuous loop that stimulates a more aggressive stage. It is imperative to dissect the molecular pathologic mechanism of inflammation involved in the generation of the castration-resistant phenotype in prostate cancer. Here, we present a hypothesis where molecular signaling triggered by inflammatory mediators may evolve in prostate cancer progression. Thus, treatment of chronic inflammation may represent an important therapeutic target in advanced prostate cancer. © 2012 Macmillan Publishers Limited All rights reserved. Fil:Gueron, G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:De Siervi, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Vazquez, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_13657852_v15_n3_p213_Gueron |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
castration-resistant prostate cancer (CRPC) chemokines inflammation metastasis reactive oxygen species (ROS) chemokine receptor CXCR4 chemokine receptor CXCR6 chemokine receptor CXCR7 heme oxygenase 1 immunoglobulin enhancer binding protein interleukin 6 interleukin 8 matrix metalloproteinase Notch receptor osteopontin parathyroid hormone related protein reactive oxygen metabolite stromal cell derived factor 1 tumor necrosis factor alpha advanced cancer cancer growth carcinogenesis castration resistant prostate cancer cell homing cell proliferation cellular stress signal chronic inflammation gene activation gene targeting human metastasis oncogene priority journal prostate cancer protein expression protein function review signal transduction tumor growth tumor microenvironment Animals Bone and Bones Chemokines Disease Progression Humans Inflammation Inflammation Mediators Male Neoplasm Metastasis Neoplasm Staging Oxidative Stress Prostatic Neoplasms Reactive Oxygen Species Receptors, Chemokine Signal Transduction Tumor Microenvironment |
spellingShingle |
castration-resistant prostate cancer (CRPC) chemokines inflammation metastasis reactive oxygen species (ROS) chemokine receptor CXCR4 chemokine receptor CXCR6 chemokine receptor CXCR7 heme oxygenase 1 immunoglobulin enhancer binding protein interleukin 6 interleukin 8 matrix metalloproteinase Notch receptor osteopontin parathyroid hormone related protein reactive oxygen metabolite stromal cell derived factor 1 tumor necrosis factor alpha advanced cancer cancer growth carcinogenesis castration resistant prostate cancer cell homing cell proliferation cellular stress signal chronic inflammation gene activation gene targeting human metastasis oncogene priority journal prostate cancer protein expression protein function review signal transduction tumor growth tumor microenvironment Animals Bone and Bones Chemokines Disease Progression Humans Inflammation Inflammation Mediators Male Neoplasm Metastasis Neoplasm Staging Oxidative Stress Prostatic Neoplasms Reactive Oxygen Species Receptors, Chemokine Signal Transduction Tumor Microenvironment Gueron, G. De Siervi, A. Vazquez, E. Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
topic_facet |
castration-resistant prostate cancer (CRPC) chemokines inflammation metastasis reactive oxygen species (ROS) chemokine receptor CXCR4 chemokine receptor CXCR6 chemokine receptor CXCR7 heme oxygenase 1 immunoglobulin enhancer binding protein interleukin 6 interleukin 8 matrix metalloproteinase Notch receptor osteopontin parathyroid hormone related protein reactive oxygen metabolite stromal cell derived factor 1 tumor necrosis factor alpha advanced cancer cancer growth carcinogenesis castration resistant prostate cancer cell homing cell proliferation cellular stress signal chronic inflammation gene activation gene targeting human metastasis oncogene priority journal prostate cancer protein expression protein function review signal transduction tumor growth tumor microenvironment Animals Bone and Bones Chemokines Disease Progression Humans Inflammation Inflammation Mediators Male Neoplasm Metastasis Neoplasm Staging Oxidative Stress Prostatic Neoplasms Reactive Oxygen Species Receptors, Chemokine Signal Transduction Tumor Microenvironment |
description |
It is currently estimated that inflammatory responses are linked to 15-20% of all deaths from cancer worldwide. Although many studies point to an important role of inflammation in prostate growth, the contribution of inflammation to castration-resistant prostate cancer is not completely understood. The presence of inflammatory mediators in tumor microenvironment raises the question whether genetic events that participate in cancer development and progression are responsible for the inflammatory milieu inside and surrounding tumors. Activated oncogenes, cytokines, chemokines and their receptors, sustained oxidative stress and antioxidant imbalance share the capacity to orchestrate these pro-inflammatory programs; however, the diversity of the inflammatory cell components will determine the final response in the prostate tissue. These observations give rise to the concept that early genetic events generate an inflammatory microenvironment promoting prostate cancer progression and creating a continuous loop that stimulates a more aggressive stage. It is imperative to dissect the molecular pathologic mechanism of inflammation involved in the generation of the castration-resistant phenotype in prostate cancer. Here, we present a hypothesis where molecular signaling triggered by inflammatory mediators may evolve in prostate cancer progression. Thus, treatment of chronic inflammation may represent an important therapeutic target in advanced prostate cancer. © 2012 Macmillan Publishers Limited All rights reserved. |
format |
JOUR |
author |
Gueron, G. De Siervi, A. Vazquez, E. |
author_facet |
Gueron, G. De Siervi, A. Vazquez, E. |
author_sort |
Gueron, G. |
title |
Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
title_short |
Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
title_full |
Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
title_fullStr |
Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
title_full_unstemmed |
Advanced prostate cancer: Reinforcing the strings between inflammation and the metastatic behavior |
title_sort |
advanced prostate cancer: reinforcing the strings between inflammation and the metastatic behavior |
url |
http://hdl.handle.net/20.500.12110/paper_13657852_v15_n3_p213_Gueron |
work_keys_str_mv |
AT guerong advancedprostatecancerreinforcingthestringsbetweeninflammationandthemetastaticbehavior AT desiervia advancedprostatecancerreinforcingthestringsbetweeninflammationandthemetastaticbehavior AT vazqueze advancedprostatecancerreinforcingthestringsbetweeninflammationandthemetastaticbehavior |
_version_ |
1807323424433897472 |