The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Athanasios G. Papavassiliou - One of the best experts on this subject based on the ideXlab platform.
-
Molecular networks in Respiratory Epithelium carcinomas
Cancer letters, 2010Co-Authors: Athanasios G. Pallis, Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Current anti-cancer research is focused on cell surface receptors targeting, mainly epidermal growth factor receptor and vascular endothelial growth factor receptor, against which a few targeted agents are now available in clinical practice. Recent improvements of our understanding on the intracellular networks that participate in Respiratory Epithelium carcinogenesis have further elucidated the role of a variety of molecules that represent attractive targets for novel therapeutic strategies. The aim of this review is to explore the potential therapeutic opportunities of the manipulation of these pathways.
-
Epigenomics in Respiratory Epithelium carcinogenesis : Prevention and therapeutic challenges
Cancer treatment reviews, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium carcinogenesis is currently considered as the phenotypic aspect of serial genetic and epigenetic aberrations resulting in deregulation of cellular homeostasis. Recent data indicate that DNA demethylating agents and histone deacetylase inhibitors might act synergistically for the prevention of cancer development throughout the carcinogen-exposed Epithelium. Preliminary clinical trials have shown encouraging results using these new molecules in lung carcinomas therapeutics. However, the caveats that should be overtaken for efficacious antitumour activity have also emerged. Setting the context in which epigenetic modifications contribute to carcinogenesis evolution is of paramount importance in order to optimize the potency of the current and future epigenome targeting agents.
-
Roles of CREB-binding protein (CBP)/p300 in Respiratory Epithelium tumorigenesis
Cell research, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:CREB-binding protein (CBP) and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentiation and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins (e.g. p53). A major paradox in CBP/p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory Epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in Respiratory Epithelium carcinogenesis.
-
The activator protein-1 transcription factor in Respiratory Epithelium carcinogenesis.
Molecular cancer research : MCR, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium cancers are the leading cause of cancer-related death worldwide. The multistep natural history of carcinogenesis can be considered as a gradual accumulation of genetic and epigenetic aberrations, resulting in the deregulation of cellular homeostasis. Growing evidence suggests that cross-talk between membrane and nuclear receptor signaling pathways along with the activator protein-1 (AP-1) cascade and its cofactor network represent a pivotal molecular circuitry participating directly or indirectly in Respiratory Epithelium carcinogenesis. The crucial role of AP-1 transcription factor renders it an appealing target of future nuclear-directed anticancer therapeutic and chemoprevention approaches. In the present review, we will summarize the current knowledge regarding the implication of AP-1 proteins in Respiratory Epithelium carcinogenesis, highlight the ongoing research, and consider the future perspectives of their potential therapeutic interest. (Mol Cancer Res 2007;5(2):109–20)
-
Retinoid receptor cross-talk in Respiratory Epithelium cancer chemoprevention
Trends in molecular medicine, 2005Co-Authors: Michalis V. Karamouzis, Athanasios G. PapavassiliouAbstract:The rationale for using retinoids in the prevention of Respiratory Epithelium cancers is based on their ability to coordinately regulate differentiation, proliferation and apoptosis. The complex retinoid signaling pathways and their cross-reactions are modulated by multiple mechanisms that are gradually being elucidated. It is possible that significant molecular changes take place during the very early stages of Respiratory epithelial carcinogenesis, which enable cancer cells to escape apoptosis and result in unimpeded proliferation. Here, we propose that a ‘switch on/off' model dictates the cross-talk between retinoid receptors and other signal transducing pathways during Respiratory Epithelium carcinogenesis. This model might contribute to the development of novel selective retinoids and their clinical evaluation in combinatorial chemopreventive strategies.
Michalis V. Karamouzis - One of the best experts on this subject based on the ideXlab platform.
-
Molecular networks in Respiratory Epithelium carcinomas
Cancer letters, 2010Co-Authors: Athanasios G. Pallis, Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Current anti-cancer research is focused on cell surface receptors targeting, mainly epidermal growth factor receptor and vascular endothelial growth factor receptor, against which a few targeted agents are now available in clinical practice. Recent improvements of our understanding on the intracellular networks that participate in Respiratory Epithelium carcinogenesis have further elucidated the role of a variety of molecules that represent attractive targets for novel therapeutic strategies. The aim of this review is to explore the potential therapeutic opportunities of the manipulation of these pathways.
-
Epigenomics in Respiratory Epithelium carcinogenesis : Prevention and therapeutic challenges
Cancer treatment reviews, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium carcinogenesis is currently considered as the phenotypic aspect of serial genetic and epigenetic aberrations resulting in deregulation of cellular homeostasis. Recent data indicate that DNA demethylating agents and histone deacetylase inhibitors might act synergistically for the prevention of cancer development throughout the carcinogen-exposed Epithelium. Preliminary clinical trials have shown encouraging results using these new molecules in lung carcinomas therapeutics. However, the caveats that should be overtaken for efficacious antitumour activity have also emerged. Setting the context in which epigenetic modifications contribute to carcinogenesis evolution is of paramount importance in order to optimize the potency of the current and future epigenome targeting agents.
-
Roles of CREB-binding protein (CBP)/p300 in Respiratory Epithelium tumorigenesis
Cell research, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:CREB-binding protein (CBP) and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentiation and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins (e.g. p53). A major paradox in CBP/p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory Epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in Respiratory Epithelium carcinogenesis.
-
The activator protein-1 transcription factor in Respiratory Epithelium carcinogenesis.
Molecular cancer research : MCR, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium cancers are the leading cause of cancer-related death worldwide. The multistep natural history of carcinogenesis can be considered as a gradual accumulation of genetic and epigenetic aberrations, resulting in the deregulation of cellular homeostasis. Growing evidence suggests that cross-talk between membrane and nuclear receptor signaling pathways along with the activator protein-1 (AP-1) cascade and its cofactor network represent a pivotal molecular circuitry participating directly or indirectly in Respiratory Epithelium carcinogenesis. The crucial role of AP-1 transcription factor renders it an appealing target of future nuclear-directed anticancer therapeutic and chemoprevention approaches. In the present review, we will summarize the current knowledge regarding the implication of AP-1 proteins in Respiratory Epithelium carcinogenesis, highlight the ongoing research, and consider the future perspectives of their potential therapeutic interest. (Mol Cancer Res 2007;5(2):109–20)
-
Retinoid receptor cross-talk in Respiratory Epithelium cancer chemoprevention
Trends in molecular medicine, 2005Co-Authors: Michalis V. Karamouzis, Athanasios G. PapavassiliouAbstract:The rationale for using retinoids in the prevention of Respiratory Epithelium cancers is based on their ability to coordinately regulate differentiation, proliferation and apoptosis. The complex retinoid signaling pathways and their cross-reactions are modulated by multiple mechanisms that are gradually being elucidated. It is possible that significant molecular changes take place during the very early stages of Respiratory epithelial carcinogenesis, which enable cancer cells to escape apoptosis and result in unimpeded proliferation. Here, we propose that a ‘switch on/off' model dictates the cross-talk between retinoid receptors and other signal transducing pathways during Respiratory Epithelium carcinogenesis. This model might contribute to the development of novel selective retinoids and their clinical evaluation in combinatorial chemopreventive strategies.
Panagiotis A. Konstantinopoulos - One of the best experts on this subject based on the ideXlab platform.
-
Molecular networks in Respiratory Epithelium carcinomas
Cancer letters, 2010Co-Authors: Athanasios G. Pallis, Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Current anti-cancer research is focused on cell surface receptors targeting, mainly epidermal growth factor receptor and vascular endothelial growth factor receptor, against which a few targeted agents are now available in clinical practice. Recent improvements of our understanding on the intracellular networks that participate in Respiratory Epithelium carcinogenesis have further elucidated the role of a variety of molecules that represent attractive targets for novel therapeutic strategies. The aim of this review is to explore the potential therapeutic opportunities of the manipulation of these pathways.
-
Epigenomics in Respiratory Epithelium carcinogenesis : Prevention and therapeutic challenges
Cancer treatment reviews, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium carcinogenesis is currently considered as the phenotypic aspect of serial genetic and epigenetic aberrations resulting in deregulation of cellular homeostasis. Recent data indicate that DNA demethylating agents and histone deacetylase inhibitors might act synergistically for the prevention of cancer development throughout the carcinogen-exposed Epithelium. Preliminary clinical trials have shown encouraging results using these new molecules in lung carcinomas therapeutics. However, the caveats that should be overtaken for efficacious antitumour activity have also emerged. Setting the context in which epigenetic modifications contribute to carcinogenesis evolution is of paramount importance in order to optimize the potency of the current and future epigenome targeting agents.
-
Roles of CREB-binding protein (CBP)/p300 in Respiratory Epithelium tumorigenesis
Cell research, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:CREB-binding protein (CBP) and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentiation and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins (e.g. p53). A major paradox in CBP/p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory Epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in Respiratory Epithelium carcinogenesis.
-
The activator protein-1 transcription factor in Respiratory Epithelium carcinogenesis.
Molecular cancer research : MCR, 2007Co-Authors: Michalis V. Karamouzis, Panagiotis A. Konstantinopoulos, Athanasios G. PapavassiliouAbstract:Respiratory Epithelium cancers are the leading cause of cancer-related death worldwide. The multistep natural history of carcinogenesis can be considered as a gradual accumulation of genetic and epigenetic aberrations, resulting in the deregulation of cellular homeostasis. Growing evidence suggests that cross-talk between membrane and nuclear receptor signaling pathways along with the activator protein-1 (AP-1) cascade and its cofactor network represent a pivotal molecular circuitry participating directly or indirectly in Respiratory Epithelium carcinogenesis. The crucial role of AP-1 transcription factor renders it an appealing target of future nuclear-directed anticancer therapeutic and chemoprevention approaches. In the present review, we will summarize the current knowledge regarding the implication of AP-1 proteins in Respiratory Epithelium carcinogenesis, highlight the ongoing research, and consider the future perspectives of their potential therapeutic interest. (Mol Cancer Res 2007;5(2):109–20)
M.y. Mohd Heikal - One of the best experts on this subject based on the ideXlab platform.
-
Autologous Implantation of Bilayered Tissue-Engineered Respiratory Epithelium for Tracheal Mucosal Regenesis in a Sheep Model
Cells tissues organs, 2010Co-Authors: M.y. Mohd Heikal, Bin Saim Aminuddin, H.c. Chen, J. Jeevanan, S.h. Sharifah, B.h.i. RuszymahAbstract:The objective of this study was to regenerate the tracheal Epithelium using autologous nasal Respiratory epithelial cells in a sheep model. Respiratory Epithelium and fibroblast cells were harvested from nasal turbinates and cultured for 1 week. After confluence, Respiratory Epithelium and fibroblast cells were suspended in autologous fibrin polymerized separately to form a tissue-engineered Respiratory epithelial construct (TEREC). A 3 × 2 cm2 tracheal mucosal defect was created, and implanted with TEREC and titanium mesh as a temporary scaffold. The control groups were divided into 2 groups: polymerized autologous fibrin devoid of cells (group 1), and no construct implanted (group 2). All sheep were euthanized at 4 weeks of implantation. Gross observation of the trachea showed minimal luminal stenosis formation in the experimental group compared to the control groups. Macroscopic evaluation revealed significant mucosal fibrosis in control group 1 (71.8%) as compared to the experimental group (7%). Hematoxylin and eosin staining revealed the presence of minimal overgrowth of fibrous connective tissue covered by Respiratory Epithelium. A positive red fluorescence staining of PKH26 on engineered tissue 4 weeks after implantation confirmed the presence of cultured nasal Respiratory epithelial cells intercalated with native tracheal epithelial cells. Scanning electron microscopy showed the presence of short microvilli representing immature cilia on the surface of the Epithelium. Our study showed that TEREC was a good replacement for a tracheal mucosal defect and was able to promote natural regenesis of the tracheal Epithelium with minimal fibrosis. This study highlighted a new technique in the treatment of tracheal stenosis.
-
A scanning electron microscopic study of in vivo tissue engineered Respiratory Epithelium in sheep.
The Medical journal of Malaysia, 2008Co-Authors: M.y. Mohd Heikal, Bin Saim Aminuddin, Jahendran Jeevanan, H.c. Chen, S Sharifah, Bt Hj Idrus RuszymahAbstract:Abstract Normal tracheal mucociliary clearance is the key to maintaining the health and defense of Respiratory airway. Therefore the present of cilia and mucous blanket are important for tracheal Epithelium to function effectively. In the present study, we prepared a tissue engineered Respiratory Epithelium construct (TEREC) made of autologous Respiratory Epithelium cells, fibroblast and fibrin from sheep owns blood which replaced a created tracheal mucosal defect. Scanning electron microscopy (SEM) showed encouraging result where immature cilia were present on the surface of TEREC. This result indicates that engineered Respiratory Epithelium was able to function as normal tissue.
Ho L-p. - One of the best experts on this subject based on the ideXlab platform.
-
How the Respiratory Epithelium Senses and Reacts to Influenza Virus.
American journal of respiratory cell and molecular biology, 2019Co-Authors: Kambez H. Benam, Laura Denney, Ho L-p.Abstract:The human lung is constantly exposed to the environment and potential pathogens. As the interface between host and environment, the Respiratory Epithelium has evolved sophisticated sensing mechanisms as part of its defense against pathogens. In this review, we examine how the Respiratory Epithelium senses and responds to influenza A virus, the biggest cause of Respiratory viral deaths worldwide.
-
The role of Respiratory Epithelium in host defence against influenza virus infection.
Biomedical journal, 2018Co-Authors: Laura Denney, Ho L-p.Abstract:The Respiratory Epithelium is the major interface between the environment and the host. Sophisticated barrier, sensing, anti-microbial and immune regulatory mechanisms have evolved to help maintain homeostasis and to defend the lung against foreign substances and pathogens. During influenza virus infection, these specialised structural cells and populations of resident immune cells come together to mount the first response to the virus, one which would play a significant role in the immediate and long term outcome of the infection. In this review, we focus on the immune defence machinery of the Respiratory Epithelium and briefly explore how it repairs and regenerates after infection.
