The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Rifat Pamukcu - One of the best experts on this subject based on the ideXlab platform.
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exisulind induction of apoptosis involves guanosine 3 5 cyclic monophosphate phosphodiesterase inhibition protein kinase g activation and attenuated β catenin
Cancer Research, 2000Co-Authors: W Thompson, Gary A Piazza, Han Li, John Fetter, Gerhard Sperl, Dennis J Ahnen, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
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Exisulind Induction of Apoptosis Involves Guanosine 3′,5′-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated β-Catenin
Cancer research, 2000Co-Authors: William J. Thompson, Gary A Piazza, John Fetter, Gerhard Sperl, Dennis J Ahnen, Li Liu, Zhu Bing, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
Dennis J Ahnen - One of the best experts on this subject based on the ideXlab platform.
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exisulind induction of apoptosis involves guanosine 3 5 cyclic monophosphate phosphodiesterase inhibition protein kinase g activation and attenuated β catenin
Cancer Research, 2000Co-Authors: W Thompson, Gary A Piazza, Han Li, John Fetter, Gerhard Sperl, Dennis J Ahnen, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
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Exisulind Induction of Apoptosis Involves Guanosine 3′,5′-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated β-Catenin
Cancer research, 2000Co-Authors: William J. Thompson, Gary A Piazza, John Fetter, Gerhard Sperl, Dennis J Ahnen, Li Liu, Zhu Bing, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
Gary A Piazza - One of the best experts on this subject based on the ideXlab platform.
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exisulind induction of apoptosis involves guanosine 3 5 cyclic monophosphate phosphodiesterase inhibition protein kinase g activation and attenuated β catenin
Cancer Research, 2000Co-Authors: W Thompson, Gary A Piazza, Han Li, John Fetter, Gerhard Sperl, Dennis J Ahnen, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
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Exisulind Induction of Apoptosis Involves Guanosine 3′,5′-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated β-Catenin
Cancer research, 2000Co-Authors: William J. Thompson, Gary A Piazza, John Fetter, Gerhard Sperl, Dennis J Ahnen, Li Liu, Zhu Bing, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
John Fetter - One of the best experts on this subject based on the ideXlab platform.
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exisulind induction of apoptosis involves guanosine 3 5 cyclic monophosphate phosphodiesterase inhibition protein kinase g activation and attenuated β catenin
Cancer Research, 2000Co-Authors: W Thompson, Gary A Piazza, Han Li, John Fetter, Gerhard Sperl, Dennis J Ahnen, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
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Exisulind Induction of Apoptosis Involves Guanosine 3′,5′-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated β-Catenin
Cancer research, 2000Co-Authors: William J. Thompson, Gary A Piazza, John Fetter, Gerhard Sperl, Dennis J Ahnen, Li Liu, Zhu Bing, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
Gerhard Sperl - One of the best experts on this subject based on the ideXlab platform.
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exisulind induction of apoptosis involves guanosine 3 5 cyclic monophosphate phosphodiesterase inhibition protein kinase g activation and attenuated β catenin
Cancer Research, 2000Co-Authors: W Thompson, Gary A Piazza, Han Li, John Fetter, Gerhard Sperl, Dennis J Ahnen, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
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Exisulind Induction of Apoptosis Involves Guanosine 3′,5′-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated β-Catenin
Cancer research, 2000Co-Authors: William J. Thompson, Gary A Piazza, John Fetter, Gerhard Sperl, Dennis J Ahnen, Li Liu, Zhu Bing, Rifat PamukcuAbstract:Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory Drug Derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3′,5′-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated β-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.
