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....

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Autores principales: Gueron, G., De Siervi, A., Vazquez, E.
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_13657852_v15_n3_p213_Gueron
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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
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AT vazqueze advancedprostatecancerreinforcingthestringsbetweeninflammationandthemetastaticbehavior
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