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    USE OF PARP-1 INHIBITORS
    112.
    发明申请
    USE OF PARP-1 INHIBITORS 审中-公开
    PARP-1抑制剂的使用

    公开(公告)号：WO2007062413A2

    公开(公告)日：2007-05-31

    申请号：PCT/US2006/061254

    申请日：2006-11-27

    Applicant: UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY ,  SCOTTO, Kathleen, A. ,  MANDOLA, Michael

    Inventor： SCOTTO, Kathleen, A. ,  MANDOLA, Michael

    IPC: A61K31/7076 ,  A61K31/498

    CPC classification number: A61K45/06 ,  A61K31/4995 ,  A61K31/517 ,  A61K2300/00

    Abstract: A method for improving the cytotoxic effect of Ecteinascidin-743 (ET-743) or an analog thereof on a tumor cell population in a patient the method including administering to the patient, sequentially or simultaneously, a therapeutically effective combination of a composition including ET-743 and an amount of a composition including a PARP-I inhibitor effective to increase the cytotoxic effect of ET-743 on the tumor cell population. Anti-tumor compositions containing a therapeutically effective amount of ET-743 and an amount of a PARP-I inhibitor effective to increase the tumor cytotoxicity of the ET-743 are also presented.

    Abstract translation: 一种用于改善Ecteinascidin-743（ET-743）或其类似物对患者肿瘤细胞群体的细胞毒性作用的方法，所述方法包括向患者依次或同时施用包含ET- 743和包含有效增加ET-743对肿瘤细胞群体的细胞毒性作用的PARP-1抑制剂的组合物的量。 还提供含有治疗有效量的ET-743和一定量的有效增加ET-743的肿瘤细胞毒性的PARP-1抑制剂的抗肿瘤组合物。

    INHIBITION OF MRNA INTERFERASE-INDUCED APOPTOSIS IN BAK-DEFICIENT AND BAK-AND BAX-DEFICIENT MAMMALIAN CELLS
    113.
    发明申请
    INHIBITION OF MRNA INTERFERASE-INDUCED APOPTOSIS IN BAK-DEFICIENT AND BAK-AND BAX-DEFICIENT MAMMALIAN CELLS 审中-公开
    在BAK缺乏型和BAK型和BAX缺陷型MAMMALIAN细胞中MRNA干扰诱导的病毒抑制的抑制

    公开(公告)号：WO2007024991A2

    公开(公告)日：2007-03-01

    申请号：PCT/US2006/032981

    申请日：2006-08-22

    Applicant: UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY ,  SHIMAZU, Tsutomu ,  DEGENHARDT, Kurt ,  WHITE, Eileen ,  INOUYE, Masayori

    Inventor： SHIMAZU, Tsutomu ,  DEGENHARDT, Kurt ,  WHITE, Eileen ,  INOUYE, Masayori

    IPC: A61K48/00

    CPC classification number: A61K48/0066 ,  A61K48/00 ,  C07K14/4747 ,  C12N9/22 ,  C12N2800/40

    Abstract: Ribonucleases, antibiotics, bacterial toxins and viruses inhibit protein synthesis, which results in apoptosis in mammalian cells. How the BCL-2 family of proteins regulates apoptosis in response to shutoff of protein synthesis is not known. According to the present invention, an Escherichia coli toxin MazF inhibited protein synthesis by cleavage of cellular mRNA, and induced apoptosis in mammalian cells. MazF-induced apoptosis required proapoptotic BAK and its upstream regulator, the proapoptotic BH3-only protein NBK/BIK, but not BIM, PUMA or NOXA. Furthermore, NBK/BIK- or BAK-deficient cells were resistant to cell death induced by pharmacologic inhibition of translation and by virus-mediated shutoff of protein synthesis. Thus, the BH3-only protein NBK/BIK is the apical regulator of a BAK-dependent apoptotic pathway in response to shutoff of protein synthesis. Although NBK/BIK is dispensable for development, it is the BH3-only protein targeted for inactivation by viruses, suggesting that it plays a role in pathogen/toxin response through apoptosis activation.

    Abstract translation: 核糖核酸酶，抗生素，细菌毒素和病毒抑制蛋白质合成，导致哺乳动物细胞凋亡。 BCL-2家族蛋白质如何调节蛋白质合成关闭反应的细胞凋亡是未知的。 根据本发明，大肠杆菌毒素MazF通过切割细胞mRNA抑制蛋白质合成，并诱导哺乳动物细胞的细胞凋亡。 MazF诱导的细胞凋亡需要促凋亡BAK及其上游调节因子，即促凋亡BH3蛋白NBK / BIK，而不是BIM，PUMA或NOXA。 此外，NBK / BIK-或BAK缺陷细胞对由翻译的药理学抑制和蛋白质合成的病毒介导的切断引起的细胞死亡具有抗性。 因此，仅BH3蛋白NBK / BIK是响应于蛋白质合成关闭的BAK依赖性凋亡途径的顶端调节剂。 虽然NBK / BIK是不可开发的，但是仅针对通过病毒灭活的BH3蛋白，这表明它通过凋亡激活在病原体/毒素反应中起作用。

    METHODS AND KIT FOR DETECTING BREAST CANCER
    115.
    发明申请
    METHODS AND KIT FOR DETECTING BREAST CANCER 审中-公开
    检测乳腺癌的方法和工具包

    公开(公告)号：WO2006101847A2

    公开(公告)日：2006-09-28

    申请号：PCT/US2006/009168

    申请日：2006-03-15

    Applicant: UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY ,  MADURA, Kiran ,  CHEN, Li

    Inventor： MADURA, Kiran ,  CHEN, Li

    IPC: C12Q1/68

    CPC classification number: G01N33/57415

    Abstract: The present inventions relates to kits and methods for diagnosing and monitoring breast cancer. An increase in the level or activity of proteins of the ubiquitin/proteasome pathway, and ancillary proteins thereof, as compared to normal control or benign tissue is indicative of breast cancer.

    Abstract translation: 本发明涉及用于诊断和监测乳腺癌的试剂盒和方法。 与正常对照或良性组织相比，泛素/蛋白酶体途径的蛋白质和其辅助蛋白质的蛋白质的水平或活性的增加是乳腺癌的指示。

    RNA INTERFERASES AND METHODS OF USE THEREOF
    118.
    发明申请
    RNA INTERFERASES AND METHODS OF USE THEREOF 审中-公开
    RNA干扰及其使用方法

    公开(公告)号：WO2004113498A2

    公开(公告)日：2004-12-29

    申请号：PCT/US2004/018571

    申请日：2004-06-14

    Applicant: UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY ,  INOUYE, Masayori ,  ZHANG, Junjie ,  ZHANG, Yong, Long

    Inventor： INOUYE, Masayori ,  ZHANG, Junjie ,  ZHANG, Yong, Long

    IPC: C12N

    CPC classification number: C12N9/22 ,  A61K38/465 ,  C12N15/70 ,  C12P19/34 ,  C12Q1/42 ,  C12Q1/44 ,  G01N2333/922 ,  G01N2800/26

    Abstract: The present invention is directed to the discovery of a novel family of enzymes designated herein as mRNA interferases that exhibit endoribonuclease activity. The novel finding of the present inventors, therefore, presents new applications for which mRNA interferase nucleic and amino acid sequences, and compositions thereof may be used to advantage. The invention also encompasses screening methods to identify compounds/agents capable of modulating mRNA interferase activity and methods for using such compounds/agents. Also provided is a kit comprising mRNA interferase nucleic and/or amino acid sequences, mRNA interferase activity compatible buffers, and instruction materials.

    Abstract translation: 本发明涉及在本文中称为表达内切核糖核酸酶活性的mRNA干扰酶的新型家族的发现。 因此，本发明人的新发现提出了可以使用mRNA干扰酶核酸和氨基酸序列及其组合物的新用途。 本发明还包括鉴定能够调节mRNA干扰酶活性的化合物/试剂的筛选方法以及使用这些化合物/试剂的方法。 还提供了包含mRNA干扰酶核酸和/或氨基酸序列，mRNA干扰酶活性相容缓冲液和说明材料的试剂盒。

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