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Yataro Daigo - One of the best experts on this subject based on the ideXlab platform.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strategy as follows. i)To identify up-regulated genes in non-small cell lung Cancers (NSCLCs) using the cDNA microarray, ii) To verify the candidate genes for their no or low expression in 23 normal tissues by northern-blot, iii)To validate clinicopathological significance of their protein expression by tissue microarray, iv)To verify whether they are essential for the Growth of Cancer cells by siRNA, and v)To measure their serum protein levels by ELISA. Results: We identified LASEP1 (Lung Cancer Associated Serum Protein 1) as a candidate target molecule. Immunohistochemical staining using tumor tissue microarrays consisting of 374 NSCLC confirmed positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. In addition, a high level of LASEP1 expression was associated with poor prognosis of NSCLC patients. Serum LASEP1 levels were higher in NSCLC than in healthy volunteers. The proportion of serum LASEP1-positive cases was 127 (38.6%) of 329 lung Cancers, while 4 (3.9%) of 102 healthy volunteers were falsely diagnosed. Furthermore, treatment of lung Cancer cells with siRNAs against LASEP1 suppressed its expression and resulted in Growth suppression of the lung Cancer cells; on the other hand, induction of exogenous expression of LASEP1 conferred Growth-promoting activity in vitro. We found its 50-kDa receptor (LASEPR) which interacts with LASEP1 on lung Cancer cell surface. Suppression of LASEPR expression by siRNAs inhibited the Growth of Cancer cells. The LASEP1-LASEPR interaction promoted the cell Growth in an autocrine manner. In addition, the Growth activity of the LASEP1-positive cells was neutralized by the addition of originally developed anti-LASEP1 monoclonal antibodies into their culture media. The systemic administration of the anti-LASEP1 antibody to tumor-implanted mice significantly suppressed tumor Growth without any adverse events. Conclusions: We have identified LASEP1 as potential targets for development of biomarkers and therapeutic target for lung Cancer.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strat...
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Abstract 2359: Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target.
Clinical Research, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC To identify novel biomarkers or therapeutic targets for lung Cancers, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP3 (lung Cancer-associated serum protein 3) as a candidate. Immunohistochemical analysis showed that strong positive staining of LASEP3 was observed in 198 (54.8%) of 361 NSCLCs (non-small cell lung Cancer). High level of LASEP3 expression was associated with poor prognosis of NSCLC patients. (P=0.0183 by log-rank test). Serum LASEP3 levels were higher in NSCLC patients than in healthy volunteers. The proportion of serum LASEP3-positive cases was 160 (61.8%) of 259 NSCLCs, while 6 (5.5%) of 109 healthy volunteers were falsely diagnosed. Moreover serum LASEP3 levels were significantly higher in breast and colon Cancer patients than in healthy volunteers. A combined assay using both LASEP3 and CEA increased sensitivity because 79.5% of the NSCLC patients were then diagnosed as positive, whereas only 7.3% of 109 healthy volunteers were falsely diagnosed as positive. In addition, the use of both LASEP3 and proGRP increased sensitivity because 78.3% of the lung SCLC patients were diagnosed as positive, whereas only 6.6% of 121 healthy volunteers were falsely diagnosed. LASEP3 protein was overexpressed in breast, cervical and colon Cancer tissues. Furthermore, treatment of lung Cancer cells with LASEP3-siRNAs suppressed its expression and suppressed cell Growth and invasion. To clarify the mechanism of tumor suppression by siRNAs against LASEP3, we performed flow cytometric analysis of the tumor cells transfected with these siRNAs. We found a significant increase of the cells at the G0/G1 phase. These data suggest that LASEP3 is a diagnostic and prognostic biomarker and therapeutic target for lung and various type of human Cancer. Citation Format: Atsushi Takano, Yusuke Nakamura, Yataro Daigo. Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2359. doi:10.1158/1538-7445.AM2013-2359 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
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O2–032CHARACTERIZATION OF A LUNG Cancer Growth Factor, LASEP3 AS A SEROLOGICAL AND PROGNOSTIC BIOMARKER AND THERAPEUTIC TARGET
Annals of Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:ABSTRACT Identification of early Cancer detection and prognostic biomarkers is urgently required to improve the clinical outcome. We have screened Cancer biomarkers using a strategy as follows: (a) to identify up-regulated genes in non-small-cell lung Cancers (NSCLCs) using the cDNA microarray representing 27, 648 genes and 120 lung Cancers, (b) to verify the candidate genes for their no or low expression in 23 normal tissues by northern blot analysis, (c) to validate clinicopathological significance of their protein expression by using NSCLCs tissue microarray, (d) to verify whether they are essential for the Growth of Cancer cells by siRNA assay, and (e) to measure their serum protein levels by ELISA. We identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical analysis showed LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. Strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P
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Abstract 3005: Characterization of a lung Cancer Growth Factor, LASEP1 as a serological and prognostic biomarker and a therapeutic target
Molecular and Cellular Biology, 2012Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:To identify molecules that might serve as biomarkers or targets for the development of novel molecular therapies, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical staining using tumor tissue microarrays consisting of 374 non-small cell lung Cancers (NSCLC) revealed that LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC, while that was observed in 9 (69.2%) of 13 small cell lung Cancers (SCLC). In addition, a strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3005. doi:1538-7445.AM2012-3005
Atsushi Takano - One of the best experts on this subject based on the ideXlab platform.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strategy as follows. i)To identify up-regulated genes in non-small cell lung Cancers (NSCLCs) using the cDNA microarray, ii) To verify the candidate genes for their no or low expression in 23 normal tissues by northern-blot, iii)To validate clinicopathological significance of their protein expression by tissue microarray, iv)To verify whether they are essential for the Growth of Cancer cells by siRNA, and v)To measure their serum protein levels by ELISA. Results: We identified LASEP1 (Lung Cancer Associated Serum Protein 1) as a candidate target molecule. Immunohistochemical staining using tumor tissue microarrays consisting of 374 NSCLC confirmed positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. In addition, a high level of LASEP1 expression was associated with poor prognosis of NSCLC patients. Serum LASEP1 levels were higher in NSCLC than in healthy volunteers. The proportion of serum LASEP1-positive cases was 127 (38.6%) of 329 lung Cancers, while 4 (3.9%) of 102 healthy volunteers were falsely diagnosed. Furthermore, treatment of lung Cancer cells with siRNAs against LASEP1 suppressed its expression and resulted in Growth suppression of the lung Cancer cells; on the other hand, induction of exogenous expression of LASEP1 conferred Growth-promoting activity in vitro. We found its 50-kDa receptor (LASEPR) which interacts with LASEP1 on lung Cancer cell surface. Suppression of LASEPR expression by siRNAs inhibited the Growth of Cancer cells. The LASEP1-LASEPR interaction promoted the cell Growth in an autocrine manner. In addition, the Growth activity of the LASEP1-positive cells was neutralized by the addition of originally developed anti-LASEP1 monoclonal antibodies into their culture media. The systemic administration of the anti-LASEP1 antibody to tumor-implanted mice significantly suppressed tumor Growth without any adverse events. Conclusions: We have identified LASEP1 as potential targets for development of biomarkers and therapeutic target for lung Cancer.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strat...
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Abstract 2359: Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target.
Clinical Research, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC To identify novel biomarkers or therapeutic targets for lung Cancers, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP3 (lung Cancer-associated serum protein 3) as a candidate. Immunohistochemical analysis showed that strong positive staining of LASEP3 was observed in 198 (54.8%) of 361 NSCLCs (non-small cell lung Cancer). High level of LASEP3 expression was associated with poor prognosis of NSCLC patients. (P=0.0183 by log-rank test). Serum LASEP3 levels were higher in NSCLC patients than in healthy volunteers. The proportion of serum LASEP3-positive cases was 160 (61.8%) of 259 NSCLCs, while 6 (5.5%) of 109 healthy volunteers were falsely diagnosed. Moreover serum LASEP3 levels were significantly higher in breast and colon Cancer patients than in healthy volunteers. A combined assay using both LASEP3 and CEA increased sensitivity because 79.5% of the NSCLC patients were then diagnosed as positive, whereas only 7.3% of 109 healthy volunteers were falsely diagnosed as positive. In addition, the use of both LASEP3 and proGRP increased sensitivity because 78.3% of the lung SCLC patients were diagnosed as positive, whereas only 6.6% of 121 healthy volunteers were falsely diagnosed. LASEP3 protein was overexpressed in breast, cervical and colon Cancer tissues. Furthermore, treatment of lung Cancer cells with LASEP3-siRNAs suppressed its expression and suppressed cell Growth and invasion. To clarify the mechanism of tumor suppression by siRNAs against LASEP3, we performed flow cytometric analysis of the tumor cells transfected with these siRNAs. We found a significant increase of the cells at the G0/G1 phase. These data suggest that LASEP3 is a diagnostic and prognostic biomarker and therapeutic target for lung and various type of human Cancer. Citation Format: Atsushi Takano, Yusuke Nakamura, Yataro Daigo. Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2359. doi:10.1158/1538-7445.AM2013-2359 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
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O2–032CHARACTERIZATION OF A LUNG Cancer Growth Factor, LASEP3 AS A SEROLOGICAL AND PROGNOSTIC BIOMARKER AND THERAPEUTIC TARGET
Annals of Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:ABSTRACT Identification of early Cancer detection and prognostic biomarkers is urgently required to improve the clinical outcome. We have screened Cancer biomarkers using a strategy as follows: (a) to identify up-regulated genes in non-small-cell lung Cancers (NSCLCs) using the cDNA microarray representing 27, 648 genes and 120 lung Cancers, (b) to verify the candidate genes for their no or low expression in 23 normal tissues by northern blot analysis, (c) to validate clinicopathological significance of their protein expression by using NSCLCs tissue microarray, (d) to verify whether they are essential for the Growth of Cancer cells by siRNA assay, and (e) to measure their serum protein levels by ELISA. We identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical analysis showed LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. Strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P
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Abstract 3005: Characterization of a lung Cancer Growth Factor, LASEP1 as a serological and prognostic biomarker and a therapeutic target
Molecular and Cellular Biology, 2012Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:To identify molecules that might serve as biomarkers or targets for the development of novel molecular therapies, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical staining using tumor tissue microarrays consisting of 374 non-small cell lung Cancers (NSCLC) revealed that LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC, while that was observed in 9 (69.2%) of 13 small cell lung Cancers (SCLC). In addition, a strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3005. doi:1538-7445.AM2012-3005
Yusuke Nakamura - One of the best experts on this subject based on the ideXlab platform.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strategy as follows. i)To identify up-regulated genes in non-small cell lung Cancers (NSCLCs) using the cDNA microarray, ii) To verify the candidate genes for their no or low expression in 23 normal tissues by northern-blot, iii)To validate clinicopathological significance of their protein expression by tissue microarray, iv)To verify whether they are essential for the Growth of Cancer cells by siRNA, and v)To measure their serum protein levels by ELISA. Results: We identified LASEP1 (Lung Cancer Associated Serum Protein 1) as a candidate target molecule. Immunohistochemical staining using tumor tissue microarrays consisting of 374 NSCLC confirmed positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. In addition, a high level of LASEP1 expression was associated with poor prognosis of NSCLC patients. Serum LASEP1 levels were higher in NSCLC than in healthy volunteers. The proportion of serum LASEP1-positive cases was 127 (38.6%) of 329 lung Cancers, while 4 (3.9%) of 102 healthy volunteers were falsely diagnosed. Furthermore, treatment of lung Cancer cells with siRNAs against LASEP1 suppressed its expression and resulted in Growth suppression of the lung Cancer cells; on the other hand, induction of exogenous expression of LASEP1 conferred Growth-promoting activity in vitro. We found its 50-kDa receptor (LASEPR) which interacts with LASEP1 on lung Cancer cell surface. Suppression of LASEPR expression by siRNAs inhibited the Growth of Cancer cells. The LASEP1-LASEPR interaction promoted the cell Growth in an autocrine manner. In addition, the Growth activity of the LASEP1-positive cells was neutralized by the addition of originally developed anti-LASEP1 monoclonal antibodies into their culture media. The systemic administration of the anti-LASEP1 antibody to tumor-implanted mice significantly suppressed tumor Growth without any adverse events. Conclusions: We have identified LASEP1 as potential targets for development of biomarkers and therapeutic target for lung Cancer.
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Characterization of a lung Cancer Growth Factor, LASEP1, as a serologic and prognostic biomarker and a therapeutic target.
Journal of Clinical Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:11104 Background: Identification and evaluation of oncoproteins are an effective approaches to develop novel diagnostic/prognostic biomarkers or therapeutic targets. Methods: We established a strat...
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Abstract 2359: Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target.
Clinical Research, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC To identify novel biomarkers or therapeutic targets for lung Cancers, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP3 (lung Cancer-associated serum protein 3) as a candidate. Immunohistochemical analysis showed that strong positive staining of LASEP3 was observed in 198 (54.8%) of 361 NSCLCs (non-small cell lung Cancer). High level of LASEP3 expression was associated with poor prognosis of NSCLC patients. (P=0.0183 by log-rank test). Serum LASEP3 levels were higher in NSCLC patients than in healthy volunteers. The proportion of serum LASEP3-positive cases was 160 (61.8%) of 259 NSCLCs, while 6 (5.5%) of 109 healthy volunteers were falsely diagnosed. Moreover serum LASEP3 levels were significantly higher in breast and colon Cancer patients than in healthy volunteers. A combined assay using both LASEP3 and CEA increased sensitivity because 79.5% of the NSCLC patients were then diagnosed as positive, whereas only 7.3% of 109 healthy volunteers were falsely diagnosed as positive. In addition, the use of both LASEP3 and proGRP increased sensitivity because 78.3% of the lung SCLC patients were diagnosed as positive, whereas only 6.6% of 121 healthy volunteers were falsely diagnosed. LASEP3 protein was overexpressed in breast, cervical and colon Cancer tissues. Furthermore, treatment of lung Cancer cells with LASEP3-siRNAs suppressed its expression and suppressed cell Growth and invasion. To clarify the mechanism of tumor suppression by siRNAs against LASEP3, we performed flow cytometric analysis of the tumor cells transfected with these siRNAs. We found a significant increase of the cells at the G0/G1 phase. These data suggest that LASEP3 is a diagnostic and prognostic biomarker and therapeutic target for lung and various type of human Cancer. Citation Format: Atsushi Takano, Yusuke Nakamura, Yataro Daigo. Characterization of a lung Cancer Growth Factor, LASEP3, as a serological and prognostic biomarker and a therapeutic target. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2359. doi:10.1158/1538-7445.AM2013-2359 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
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O2–032CHARACTERIZATION OF A LUNG Cancer Growth Factor, LASEP3 AS A SEROLOGICAL AND PROGNOSTIC BIOMARKER AND THERAPEUTIC TARGET
Annals of Oncology, 2013Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:ABSTRACT Identification of early Cancer detection and prognostic biomarkers is urgently required to improve the clinical outcome. We have screened Cancer biomarkers using a strategy as follows: (a) to identify up-regulated genes in non-small-cell lung Cancers (NSCLCs) using the cDNA microarray representing 27, 648 genes and 120 lung Cancers, (b) to verify the candidate genes for their no or low expression in 23 normal tissues by northern blot analysis, (c) to validate clinicopathological significance of their protein expression by using NSCLCs tissue microarray, (d) to verify whether they are essential for the Growth of Cancer cells by siRNA assay, and (e) to measure their serum protein levels by ELISA. We identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical analysis showed LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC. Strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P
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Abstract 3005: Characterization of a lung Cancer Growth Factor, LASEP1 as a serological and prognostic biomarker and a therapeutic target
Molecular and Cellular Biology, 2012Co-Authors: Atsushi Takano, Yusuke Nakamura, Yataro DaigoAbstract:To identify molecules that might serve as biomarkers or targets for the development of novel molecular therapies, we have been screening genes encoding transmembrane/secretory proteins that are up-regulated in lung Cancers, using cDNA microarrays. During this process, we identified a secreted protein, LASEP1 (lung Cancer-associated serum protein 1) as a candidate. Immunohistochemical staining using tumor tissue microarrays consisting of 374 non-small cell lung Cancers (NSCLC) revealed that LASEP1 protein was frequently over-expressed in lung Cancers; positive staining of LASEP1 was observed in 210 (56.1%) of 374 NSCLC, while that was observed in 9 (69.2%) of 13 small cell lung Cancers (SCLC). In addition, a strong LASEP1 positivity was associated with poor prognosis for patients with NSCLC (P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3005. doi:1538-7445.AM2012-3005
Brendan D Manning - One of the best experts on this subject based on the ideXlab platform.
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the pi3k akt network at the interface of oncogenic signalling and Cancer metabolism
Nature Reviews Cancer, 2020Co-Authors: Gerta Hoxhaj, Brendan D ManningAbstract:The altered metabolic programme of Cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous Growth Factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, Growth Factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription Factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human Cancer and serves to disconnect the control of cell Growth, survival and metabolism from exogenous Growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of Cancer: Growth Factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation.
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The PI3K–AKT network at the interface of oncogenic signalling and Cancer metabolism
Nature Reviews Cancer, 2020Co-Authors: Gerta Hoxhaj, Brendan D ManningAbstract:The altered metabolic programme of Cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous Growth Factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, Growth Factor-regulated phosphoinositide 3-kinase (PI3K)–AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription Factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human Cancer and serves to disconnect the control of cell Growth, survival and metabolism from exogenous Growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of Cancer: Growth Factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation. This Review discusses the PI3K–AKT signalling network and its control of Cancer cell metabolism through both direct and indirect regulation of nutrient transport and metabolic enzymes, thereby connecting oncogenic signalling and metabolic reprogramming to support Cancer cell survival and proliferation.
Gerta Hoxhaj - One of the best experts on this subject based on the ideXlab platform.
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the pi3k akt network at the interface of oncogenic signalling and Cancer metabolism
Nature Reviews Cancer, 2020Co-Authors: Gerta Hoxhaj, Brendan D ManningAbstract:The altered metabolic programme of Cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous Growth Factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, Growth Factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription Factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human Cancer and serves to disconnect the control of cell Growth, survival and metabolism from exogenous Growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of Cancer: Growth Factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation.
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The PI3K–AKT network at the interface of oncogenic signalling and Cancer metabolism
Nature Reviews Cancer, 2020Co-Authors: Gerta Hoxhaj, Brendan D ManningAbstract:The altered metabolic programme of Cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous Growth Factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, Growth Factor-regulated phosphoinositide 3-kinase (PI3K)–AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription Factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human Cancer and serves to disconnect the control of cell Growth, survival and metabolism from exogenous Growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of Cancer: Growth Factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation. This Review discusses the PI3K–AKT signalling network and its control of Cancer cell metabolism through both direct and indirect regulation of nutrient transport and metabolic enzymes, thereby connecting oncogenic signalling and metabolic reprogramming to support Cancer cell survival and proliferation.
