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公开(公告)号：US20090239247A1
公开(公告)日：2009-09-24
申请号：US12396879
申请日：2009-03-03
IPC分类号： G01N33/574 , G01N33/53 , G01N33/00
CPC分类号： C12Q1/527 , G01N33/573 , G01N33/574
摘要： The MN/CA IX protein is identified herein as a hypoxia marker. The MN/CA9 gene promoter is characterized, and the location of the HIF-1 binding site within the MN/CA9 promoter is identified. Further, the hypoxia inducibility of the MN/CA9 gene and the uses of such inducibility are disclosed. In one aspect, the invention provides diagnostic/prognostic tools for determining the presence of hypoxia in a tissue in a vertebrate, preferably a human, and for measuring the relative degree of hypoxia in said vertebrate. In another aspect, the invention provides methods using tumor biopsies to predict the radioresistance of a preneoplastic/neoplastic tissue in a vertebrate subject, preferably a human patient, for diseases in which MN/CA IX levels can be used to indicate radiobiologically relevant tumor hypoxia. Such predictive methods can be used as an aid in patient therapy selection.
摘要翻译： 本文将MN / CA IX蛋白质鉴定为缺氧标记。 表征MN / CA9基因启动子，鉴定MN / CA9启动子内HIF-1结合位点的位置。 此外，公开了MN / CA9基因的缺氧诱导能力和这种诱导性的用途。 一方面，本发明提供用于确定脊椎动物，优选人类的组织中缺氧的存在并用于测量所述脊椎动物中的相对缺氧程度的诊断/预后工具。 在另一方面，本发明提供了使用肿瘤活组织检查来预测脊椎动物受试者，优选人类患者中对于其中可以使用MN / CA IX水平来表示放射生物学相关的肿瘤缺氧的疾病的肿瘤前/肿瘤组织的放射抗性的方法。 这种预测方法可用作患者治疗选择的辅助。
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公开(公告)号：US08334137B2
公开(公告)日：2012-12-18
申请号：US12972298
申请日：2010-12-17
IPC分类号： C12N5/00
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
摘要翻译： 本文所确定的是MN蛋白结合位点的位置，以及用固定的MN蛋白竞争与脊椎动物细胞附着的MN蛋白质/多肽。 这样的MN蛋白/多肽防止细胞粘附和细胞间接触的形成。 MN蛋白结合位点是可被有机或无机分子，优选有机分子，更优选特异性结合该位点的蛋白质/多肽阻断的治疗靶标。 公开了抑制异常表达MN蛋白的肿瘤前/肿瘤脊椎动物细胞生长的治疗方法。 提供编码MN-特异性抗体的可变结构域的载体和分离这些结构域的柔性接头多肽。 公开了编码与MN基因启动子或包含HIF-1共有结合序列的MN基因启动子片段有效连接的细胞毒性蛋白质/多肽的其它载体，并且哪些载体优选进一步编码细胞因子。 表征MN基因启动子，并公开MN转录抑制子的结合位点。 此外，公开了MN基因的缺氧诱导性和这种诱导性的用途。
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公开(公告)号：US20080206765A1
公开(公告)日：2008-08-28
申请号：US11932944
申请日：2007-10-31
IPC分类号： C12Q1/68
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
摘要翻译： 本文所确定的是MN蛋白结合位点的位置，以及用固定的MN蛋白竞争与脊椎动物细胞附着的MN蛋白质/多肽。 这样的MN蛋白/多肽防止细胞粘附和细胞间接触的形成。 MN蛋白结合位点是可被有机或无机分子，优选有机分子，更优选特异性结合该位点的蛋白质/多肽阻断的治疗靶标。 公开了抑制异常表达MN蛋白的肿瘤前/肿瘤脊椎动物细胞生长的治疗方法。 提供编码MN-特异性抗体的可变结构域的载体和分离这些结构域的柔性接头多肽。 公开了编码与MN基因启动子或包含HIF-1共有结合序列的MN基因启动子片段有效连接的细胞毒性蛋白质/多肽的其它载体，并且哪些载体优选进一步编码细胞因子。 表征MN基因启动子，并公开MN转录抑制子的结合位点。 此外，公开了MN基因的缺氧诱导性和这种诱导性的用途。
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公开(公告)号：US20110159583A1
公开(公告)日：2011-06-30
申请号：US12972298
申请日：2010-12-17
IPC分类号： C12N15/85
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
摘要翻译： 本文所确定的是MN蛋白结合位点的位置，以及用固定的MN蛋白竞争与脊椎动物细胞附着的MN蛋白质/多肽。 这样的MN蛋白/多肽防止细胞粘附和细胞间接触的形成。 MN蛋白结合位点是可被有机或无机分子，优选有机分子，更优选特异性结合该位点的蛋白质/多肽阻断的治疗靶标。 公开了抑制异常表达MN蛋白的肿瘤前/肿瘤脊椎动物细胞生长的治疗方法。 提供编码MN-特异性抗体的可变结构域的载体和分离这些结构域的柔性接头多肽。 公开了编码与MN基因启动子或包含HIF-1共有结合序列的MN基因启动子片段有效连接的细胞毒性蛋白质/多肽的其它载体，并且哪些载体优选进一步编码细胞因子。 表征MN基因启动子，并公开MN转录抑制子的结合位点。 此外，公开了MN基因的缺氧诱导性和这种诱导性的用途。
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公开(公告)号：US07851455B2
公开(公告)日：2010-12-14
申请号：US11932944
申请日：2007-10-31
IPC分类号： A61K38/00
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
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公开(公告)号：US07855185B2
公开(公告)日：2010-12-21
申请号：US11932997
申请日：2007-10-31
IPC分类号： A61K38/00
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
摘要翻译： 本文所确定的是MN蛋白结合位点的位置，以及用固定的MN蛋白竞争与脊椎动物细胞附着的MN蛋白质/多肽。 这样的MN蛋白/多肽防止细胞粘附和细胞间接触的形成。 MN蛋白结合位点是可被有机或无机分子，优选有机分子，更优选特异性结合该位点的蛋白质/多肽阻断的治疗靶标。 公开了抑制异常表达MN蛋白的肿瘤前/肿瘤脊椎动物细胞生长的治疗方法。 提供编码MN-特异性抗体的可变结构域的载体和分离这些结构域的柔性接头多肽。 公开了编码与MN基因启动子或包含HIF-1共有结合序列的MN基因启动子片段有效连接的细胞毒性蛋白质/多肽的其它载体，并且哪些载体优选进一步编码细胞因子。 表征MN基因启动子，并公开MN转录抑制子的结合位点。 此外，公开了MN基因的缺氧诱导性和这种诱导性的用途。
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公开(公告)号：US07910549B2
公开(公告)日：2011-03-22
申请号：US11356568
申请日：2006-02-17
IPC分类号： A61K38/00
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
摘要翻译： 本文所确定的是MN蛋白结合位点的位置，以及用固定的MN蛋白竞争与脊椎动物细胞附着的MN蛋白质/多肽。 这样的MN蛋白/多肽防止细胞粘附和细胞间接触的形成。 MN蛋白结合位点是可被有机或无机分子，优选有机分子，更优选特异性结合该位点的蛋白质/多肽阻断的治疗靶标。 公开了抑制异常表达MN蛋白的肿瘤前/肿瘤脊椎动物细胞生长的治疗方法。 提供编码MN-特异性抗体的可变结构域的载体和分离这些结构域的柔性接头多肽。 公开了编码与MN基因启动子或包含HIF-1共有结合序列的MN基因启动子片段有效连接的细胞毒性蛋白质/多肽的其它载体，并且哪些载体优选进一步编码细胞因子。 表征MN基因启动子，并公开MN转录抑制子的结合位点。 此外，公开了MN基因的缺氧诱导性和这种诱导性的用途。
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公开(公告)号：US20080220426A1
公开(公告)日：2008-09-11
申请号：US11932997
申请日：2007-10-31
IPC分类号： C12Q1/68
CPC分类号： G01N33/57492 , G01N2333/988 , G01N2800/52
摘要： Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such inducibility are disclosed.
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