Knudson Hypothesis

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Tamotsu Takeuchi - One of the best experts on this subject based on the ideXlab platform.

  • Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules
    Frontiers Media S.A., 2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies

  • Table_1_Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules.DOCX
    2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies.

Chiemi Saigo - One of the best experts on this subject based on the ideXlab platform.

  • Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules
    Frontiers Media S.A., 2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies

  • Table_1_Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules.DOCX
    2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies.

Yusuke Kito - One of the best experts on this subject based on the ideXlab platform.

  • Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules
    Frontiers Media S.A., 2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies

  • Table_1_Cancerous Protein Network That Inhibits the Tumor Suppressor Function of WW Domain-Containing Oxidoreductase (WWOX) by Aberrantly Expressed Molecules.DOCX
    2018
    Co-Authors: Chiemi Saigo, Yusuke Kito, Tamotsu Takeuchi
    Abstract:

    Recent findings indicate that the WW domain-containing oxidoreductase (WWOX) is a tumor suppressor protein that contains two N-terminal WW domains and a central short-chain dehydrogenase/reductase domain. WWOX protein mediates multiple signaling networks that suppress carcinogenesis through binding of its first WW domain to various cancer-associated proteins, i.e., p73, AP-2γ, and others. Although the tumor suppressor property of WWOX is inarguable, WWOX is not inactivated in the manner characteristic of the canonical Knudson Hypothesis. Impairment of both alleles of WWOX is thought to be a rare event, only occurring in a few cancer cell lines. How is the tumor suppressor function of WWOX impaired in cancer cells? Recent advances highlight that a small transmembrane protein possessing a PPxY motif, called TMEM207, and its relatives are aberrantly expressed in various cancer cells and hinder the tumor suppressor function of WWOX through inhibiting its WW domain. Here, we review the recent findings related to the pathobiological properties of TMEM207 and its relatives based on clinicopathological and experimental pathological studies.

Gunnar Westin - One of the best experts on this subject based on the ideXlab platform.

  • abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative tumor suppressor gene of small intestine neuroendocrine tumors
    Cancer Research, 2013
    Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar Westin
    Abstract:

    Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these tumors, supporting the presence of a crucial tumor suppressor gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative tumor suppressor gene in SI-NETs. This gene is currently the only known imprinted gene on chromosome 18, requiring only one gene copy inactivation event to fulfill the Knudson Hypothesis. Elongin A3 expression in SI-NETs (n=47) was heterogeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid tumor cell line and in tumor derived primary cell cultures, but not in a control cell line. Also the general histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid tumor cell line, but not in control cells suggesting further that the TCEB3C gene was epigenetically suppressed in neuroendocrine tumor cells. The TCEB3C gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative tumor suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative tumor suppressor gene of small intestine neuroendocrine tumors. [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 1982. doi:10.1158/1538-7445.AM2013-1982

Katarina Edfeldt - One of the best experts on this subject based on the ideXlab platform.

  • abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative tumor suppressor gene of small intestine neuroendocrine tumors
    Cancer Research, 2013
    Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar Westin
    Abstract:

    Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these tumors, supporting the presence of a crucial tumor suppressor gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative tumor suppressor gene in SI-NETs. This gene is currently the only known imprinted gene on chromosome 18, requiring only one gene copy inactivation event to fulfill the Knudson Hypothesis. Elongin A3 expression in SI-NETs (n=47) was heterogeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid tumor cell line and in tumor derived primary cell cultures, but not in a control cell line. Also the general histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid tumor cell line, but not in control cells suggesting further that the TCEB3C gene was epigenetically suppressed in neuroendocrine tumor cells. The TCEB3C gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative tumor suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative tumor suppressor gene of small intestine neuroendocrine tumors. [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 1982. doi:10.1158/1538-7445.AM2013-1982

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