The role of carbonic anhydrase IX in hypoxia control in OSCC

Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the invasive capacity of tumor cells, metastasis, and a worsening of the clinical evolution. Endogenous hypoxia markers are controlled by hypoxia‐re...

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Published inJournal of oral pathology & medicine Vol. 42; no. 1; pp. 1 - 8
Main Authors Pérez-Sayáns, Mario, Supuran, Claudiu T., Pastorekova, Silvia, Suárez-Peñaranda, José Manuel, Pilar, Gayoso-Diz, Barros-Angueira, Francisco, Gándara-Rey, José Manuel, García-García, Abel
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.01.2013
Wiley
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Abstract Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the invasive capacity of tumor cells, metastasis, and a worsening of the clinical evolution. Endogenous hypoxia markers are controlled by hypoxia‐related genes, formed by HIF‐1, which is related to several target genes that involve the energy metabolism, angiogenesis, and transmembrane carbonic anhydrases (CAs), mainly CA‐IX that is one of the tumor‐related carbonic anhydrases. The goal of this paper is to establish the role of CA‐IX as a hypoxia marker in OSCC, while analyzing its expression in this type of tumors and its relationship with several clinical and pathological parameters and prognosis, evaluating its relationship with angiogenesis, other hypoxia markers, and clarifying its role in chemotherapy and radiotherapy resistance.
AbstractList Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the invasive capacity of tumor cells, metastasis, and a worsening of the clinical evolution. Endogenous hypoxia markers are controlled by hypoxia‐related genes, formed by HIF‐1, which is related to several target genes that involve the energy metabolism, angiogenesis, and transmembrane carbonic anhydrases (CAs), mainly CA‐IX that is one of the tumor‐related carbonic anhydrases. The goal of this paper is to establish the role of CA‐IX as a hypoxia marker in OSCC, while analyzing its expression in this type of tumors and its relationship with several clinical and pathological parameters and prognosis, evaluating its relationship with angiogenesis, other hypoxia markers, and clarifying its role in chemotherapy and radiotherapy resistance.
Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the invasive capacity of tumor cells, metastasis, and a worsening of the clinical evolution. Endogenous hypoxia markers are controlled by hypoxia-related genes, formed by HIF-1, which is related to several target genes that involve the energy metabolism, angiogenesis, and transmembrane carbonic anhydrases (CAs), mainly CA-IX that is one of the tumor-related carbonic anhydrases. The goal of this paper is to establish the role of CA-IX as a hypoxia marker in OSCC, while analyzing its expression in this type of tumors and its relationship with several clinical and pathological parameters and prognosis, evaluating its relationship with angiogenesis, other hypoxia markers, and clarifying its role in chemotherapy and radiotherapy resistance.Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the invasive capacity of tumor cells, metastasis, and a worsening of the clinical evolution. Endogenous hypoxia markers are controlled by hypoxia-related genes, formed by HIF-1, which is related to several target genes that involve the energy metabolism, angiogenesis, and transmembrane carbonic anhydrases (CAs), mainly CA-IX that is one of the tumor-related carbonic anhydrases. The goal of this paper is to establish the role of CA-IX as a hypoxia marker in OSCC, while analyzing its expression in this type of tumors and its relationship with several clinical and pathological parameters and prognosis, evaluating its relationship with angiogenesis, other hypoxia markers, and clarifying its role in chemotherapy and radiotherapy resistance.
Author Barros-Angueira, Francisco
García-García, Abel
Pilar, Gayoso-Diz
Pastorekova, Silvia
Supuran, Claudiu T.
Gándara-Rey, José Manuel
Pérez-Sayáns, Mario
Suárez-Peñaranda, José Manuel
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Issue 1
Keywords CA-IX
Oxygen
Carbonic anhydrases
Stomatology
Hypoxia
Oral cavity disease
ENT
Malignant tumor
Oral squamous cell carcinoma
Cancer
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Snippet Tumoral microenvironments play a key role in the evolution of solid tumors. Tumor hypoxia is actively involved in the promotion of genetic instability, the...
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SubjectTerms Antigens, Neoplasm - biosynthesis
Antigens, Neoplasm - genetics
Antigens, Neoplasm - physiology
Antineoplastic Agents
Biological and medical sciences
CA-IX
Carbonic Anhydrase IX
Carbonic anhydrases
Carbonic Anhydrases - biosynthesis
Carbonic Anhydrases - genetics
Carbonic Anhydrases - physiology
Carcinoma, Squamous Cell - enzymology
Drug Resistance, Neoplasm
Erythropoietin - physiology
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Glucose Transporter Type 1 - biosynthesis
Glucose Transporter Type 1 - physiology
Head and Neck Neoplasms - enzymology
Humans
Hypoxia
Hypoxia - enzymology
Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis
Hypoxia-Inducible Factor 1, alpha Subunit - physiology
Ki-67 Antigen - biosynthesis
Ki-67 Antigen - physiology
Medical sciences
Mouth Neoplasms - enzymology
Neovascularization, Pathologic
Oral squamous cell carcinoma
Otorhinolaryngology. Stomatology
Radiation Tolerance
Receptors, Erythropoietin - physiology
Tumors
Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
Title The role of carbonic anhydrase IX in hypoxia control in OSCC
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1600-0714.2012.01144.x
https://www.ncbi.nlm.nih.gov/pubmed/22417164
https://www.proquest.com/docview/1287888436
Volume 42
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