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    TARGETING GLUTAMINE METABOLISM IN BRAIN TUMORS
    71.
    发明申请
    TARGETING GLUTAMINE METABOLISM IN BRAIN TUMORS 审中-公开
    在脑肿瘤中靶向谷氨酰胺代谢

    公开(公告)号：US20160008380A1

    公开(公告)日：2016-01-14

    申请号：US14772837

    申请日：2014-03-06

    Applicant: THE JOHNS HOPKINS UNIVERSITY

    Inventor： Eric H. Raabe ,  Allison Hanaford ,  Sama Ahsan ,  Isabella Taylor ,  Charles Eberhart

    IPC: A61K31/655 ,  G01N33/574 ,  A61K31/42

    CPC classification number: A61K31/655 ,  A61K31/198 ,  A61K31/42 ,  G01N33/57407 ,  G01N33/57496 ,  G01N2333/4703 ,  G01N2333/98 ,  G01N2800/52

    Abstract: The present invention relates to the field of cancer. More specifically, the present invention provides methods and compositions useful for diagnosing and treating MYC-driven tumors. In one embodiment, a method for treating a cancer associated with MYC in a patient comprises the step of administering a glutamine metabolism inhibitor to the patient. In specific embodiments, the cancer associated with MYC is medulloblastoma, glioblastoma or a primitive neuroectodermal tumor.

    Abstract translation: 本发明涉及癌症领域。 更具体地，本发明提供了用于诊断和治疗MYC驱动的肿瘤的方法和组合物。 在一个实施方案中，用于治疗与患者MYC相关的癌症的方法包括向患者施用谷氨酰胺代谢抑制剂的步骤。 在具体实施方案中，与MYC相关的癌症是成神经管细胞瘤，胶质母细胞瘤或原始神经外胚层肿瘤。

    METHOD FOR INHIBITING THE SWAP-70 PROTEIN
    72.
    发明申请
    METHOD FOR INHIBITING THE SWAP-70 PROTEIN 有权
    抑制SWAP-70蛋白的方法

    公开(公告)号：US20160003846A1

    公开(公告)日：2016-01-07

    申请号：US14767210

    申请日：2014-02-07

    Applicant: THORNE LIMITED

    Inventor： Rolf JESSBERGER ,  Carlos Andres CHACON-MARTINEZ

    IPC: G01N33/68 ,  C07K14/47

    CPC classification number: G01N33/6872 ,  A61K38/16 ,  C07K14/47 ,  G01N33/566 ,  G01N2333/4703 ,  G01N2458/30 ,  G01N2500/00 ,  G01N2500/04 ,  G01N2500/10 ,  G01N2500/20

    Abstract: The invention relates to the field of biomedical and pharmacological research, in particular in the field of immunology, allergies, cancers, bone diseases and autoimmune diseases.The invention is based on the recent finding that SWAP-70 dimerises, that the dimerisation takes place via a specific, largely unique and limited region of the protein, and that this dimerisation is central to the function of the protein (and probably the stability thereof).The invention provides a screening method which makes it possible to identify new active ingredients which, by accumulating at the dimerisation domain and inhibiting SWAP-70 activity, suppress the supporting function of SWAP-70 in tumourigenesis, tumour cell migration and invasion, bone-degrading osteoclast activity, and the allergic reaction, as well as in autoimmune diseases.The object is achieved by a method for identifying a substance which inhibits the activity of SWAP-70, wherein the method comprises the following: contacting at least one test substance with SWAP-70, detecting the degree of dimerisation of SWAP-70, selecting a test substance which inhibits the dimerisation of SWAP-70.

    Abstract translation: 本发明涉及生物医学和药理研究领域，特别是在免疫学，过敏，癌症，骨病和自身免疫性疾病领域。 本发明基于最近的发现，SWAP-70二聚体，二聚化通过蛋白质的特定的，大部分独特的和有限的区域进行，并且该二聚化对蛋白质的功能是重要的（并且可能是其稳定性 ）。 本发明提供了一种筛选方法，其可以鉴定新的活性成分，其通过在二聚化域积累并抑制SWAP-70活性来抑制SWAP-70在肿瘤发生，肿瘤细胞迁移和侵袭中的支持功能，降解骨骼 破骨细胞活性和过敏反应，以及自身免疫性疾病。 该目的通过用于鉴定抑制SWAP-70的活性的物质的方法来实现，其中该方法包括以下步骤：使至少一种测试物质与SWAP-70接触，检测SWAP-70的二聚程度，选择 抑制SWAP-70二聚化的测试物质。

    COMPOSITIONS AND METHODS FOR MODULATING C-REL-DEPENDENT CYTOKINE PRODUCTION
    74.
    发明申请
    COMPOSITIONS AND METHODS FOR MODULATING C-REL-DEPENDENT CYTOKINE PRODUCTION 有权
    用于调节C依赖性细胞因子生产的组合物和方法

    公开(公告)号：US20160003804A1

    公开(公告)日：2016-01-07

    申请号：US14542453

    申请日：2014-11-14

    Applicant: Synta Pharmaceuticals Corporation

    Inventor： Rongzhen Lu ,  James Barsoum ,  Yumiko Wada

    IPC: G01N33/50 ,  G01N33/68

    CPC classification number: G01N33/5035 ,  G01N33/6872 ,  G01N2333/4703 ,  G01N2333/54 ,  G01N2500/10

    Abstract: The present invention is directed to compositions and methods for modulating c-Rel-dependent cytokine production without materially altering the level of expression of NFκB and/or the amount of IκB. The present invention is also directed to screening for modulators of c-Rel activity as determined by assaying for altered subcellular localization of c-Rel but where the level of expression of NFκB and/or the amount of IκB is materially unaltered.

    Abstract translation: 本发明涉及用于调节c依赖性依赖性细胞因子产生的组合物和方法，而不会实质性地改变NF和κB的表达水平和/或I＆Kgr B的量。 本发明还涉及通过测定c-Rel的改变的亚细胞定位确定的c-Rel活性调节剂的筛选，但其中NF和κB的表达水平和/或I＆Kgr B的量在实质上未改变。

    Methods to screen compounds for regulating USF1 activity and methods and compounds to treat cardiometabolic and lipid pathologies
    77.
    发明申请
    Methods to screen compounds for regulating USF1 activity and methods and compounds to treat cardiometabolic and lipid pathologies 有权
    筛选化合物以调节USF1活性的方法以及治疗心脏代谢和脂质病变的方法和化合物

    公开(公告)号：US20150368641A1

    公开(公告)日：2015-12-24

    申请号：US14746281

    申请日：2015-06-22

    Applicant: Terveyden ja hyvinvoinnin laitos (THL)

    Inventor： Pirkka-Pekka Laurila ,  Jarkko Soronen ,  Matti Jauhiainen ,  Anu Jalanko

    IPC: C12N15/113 ,  G01N33/50

    CPC classification number: C12N15/113 ,  C12N2310/11 ,  C12N2310/14 ,  G01N33/502 ,  G01N33/5088 ,  G01N2333/4703

    Abstract: The deficiency of Usf1 confers a remarkable number of clinically relevant beneficial metabolic effects in mice via activation of brown adipose tissue. The Usf1 deficient mice have high serum HDL-cholesterol and low triglyceride levels, a beneficial lipid profile opposite to that of human metabolic syndrome. The elevated HDL-C is associated with enhanced cholesterol efflux, and low triglycerides with decreased hepatic VLDL production and elevated triglyceride clearance. Despite their elevated food intake and lower physical activity, the Usf1 deficient mice are protected against diet-induced obesity. Their concomitant increase in energy expenditure is related to the activation of brown adipose tissue. The protective effects of Usf1 deficiency against obesity, insulin resistance, fatty liver, dyslipidemia, vascular inflammation, and atherosclerosis coupled with brown adipose tissue activation are demonstrated. Inhibition or silencing of USF1 is suggested as a therapeutic target to treat various human diseases.

    Abstract translation: Usf1的缺陷通过棕色脂肪组织的活化赋予小鼠临床上相当有益的代谢作用。 Usf1缺陷小鼠具有高血清HDL-胆固醇和低甘油三酯水平，与人类代谢综合征相反的有益脂质谱。 升高的HDL-C与胆固醇流出增加有关，低甘油三酸酯与肝脏VLDL产生减少和甘油三酯升高升高有关。 尽管食物摄取量增加，身体活动降低，但Usf1缺陷小鼠受到饮食诱导的肥胖的保护。 它们伴随的能量消耗的增加与褐色脂肪组织的活化有关。 证明Usf1缺乏对肥胖，胰岛素抵抗，脂肪肝，血脂异常，血管炎症和动脉粥样硬化以及棕色脂肪组织活化的保护作用。 建议USF1的抑制或沉默作为治疗各种人类疾病的治疗靶点。

    ANTI-DLL3 ANTIBODY
    78.
    发明申请
    ANTI-DLL3 ANTIBODY 审中-公开
    ANTI-DLL3抗体

    公开(公告)号：US20150368355A1

    公开(公告)日：2015-12-24

    申请号：US14846135

    申请日：2015-09-04

    Applicant: CHUGAI SEIYAKU KABUSHIKI KAISHA ,  THE UNIVERSITY OF TOKYO

    Inventor： Kenji YOSHIDA ,  Hiroyuki ABURATANI ,  Shumpei ISHIKAWA

    IPC: C07K16/30 ,  A61K47/48

    CPC classification number: C07K16/3023 ,  A61K2039/505 ,  C07K16/28 ,  C07K2317/24 ,  C07K2317/30 ,  C07K2317/732 ,  C07K2317/77 ,  C07K2319/30 ,  C12Q1/6886 ,  C12Q2600/118 ,  G01N33/574 ,  G01N2333/4703

    Abstract: It is intended to disclose an antibody which binds to DLL3 protein. Preferably, the antibody of the present invention recognizes a region from amino acids 216 to 492 in human DLL3 having the amino acid sequence as set forth in SEQ ID NO: 1. The present invention also provides a pharmaceutical composition, for example, an anticancer agent, comprising the antibody of the present invention as an active ingredient. The present invention further discloses a method for diagnosing cancer using the antibody of the present invention and a diagnostic drug for cancer comprising the antibody of the present invention.

    Abstract translation: 旨在公开结合DLL3蛋白的抗体。 优选地，本发明的抗体识别具有SEQ ID NO：1所示的氨基酸序列的人DLL3中的氨基酸216至492的区域。本发明还提供药物组合物，例如抗癌剂 ，其包含本发明的抗体作为活性成分。 本发明还公开了使用本发明的抗体和包含本发明的抗体的癌症诊断药物诊断癌症的方法。

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