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61. 发明申请

WO2005039491A3 CERTAIN IMPROVED COMBINATION BACTERIOLYTIC THERAPY FOR THE TREATMENT OF TUMORS 审中-公开
标题翻译：某些改进的联合用于治疗肿瘤的细菌疗法治疗
公开(公告)号：WO2005039491A3
公开(公告)日：2005-06-23
申请号：PCT/US2004034624
申请日：2004-10-21
申请人： UNIV JOHNS HOPKINS , DANG LONG , BETTEGOWDA CHETAN , KINZLER KENNETH W , VOGELSTEIN BERT
发明人： DANG LONG , BETTEGOWDA CHETAN , KINZLER KENNETH W , VOGELSTEIN BERT
IPC分类号： A01N63/00 , A61K20060101
CPC分类号： A61K35/742 , A61K31/195 , A61K31/4045 , A61K38/06 , A61K2300/00
摘要： Current approaches for treating cancer are limited, in part, by the inability of drugs to affect the poorly vascularized regions of tumors. We have found that spores of anaerobic bacteria in combination with agents which interact with microtubules can cause the destruction of both the vascular and avascular compartments of tumors. Two classes of microtubule inhibitors were found to exert markedly different effects. Some agents that inhibited microtubule synthesis such as HTI-286 and vinorelbine, caused rapid, massive hemorrhagic necrosis when used in combination with spores. In contrast, agents that stabilized microtubules, such as the taxanes docetaxel and MAC-321, resulted in slow tumor regressions that killed most neoplastic cells. Remaining cells in the poorly perfused regions of tumors could be eradicated by sporulated bacteria Mechanistic studies showed that the microtubule destabilizers, but not the microtubule stabilizers, radically reduced blood flow to tumors, thereby enlarging the hypoxic niche in which spores could germinate. A single intravenous injection of spores plus selected microtubule-interacting agents was able to cause regressions of several tumors in the absence of excessive toxicity.
摘要翻译：目前用于治疗癌症的方法部分地由于药物不能影响肿瘤血管化程度差的区域而受到限制。我们发现厌氧菌的孢子与微管相互作用的药物联合使用会导致肿瘤血管和血管腔的破坏。发现两类微管抑制剂发挥显着不同的作用。一些抑制微管合成的药物如HTI-286和长春瑞滨，当与孢子结合使用时会引起快速，大量的出血性坏死。相反，稳定微管的药物，如紫杉类多西他赛和MAC-321，导致缓慢的肿瘤消退，从而杀死大多数肿瘤细胞。机体研究表明，微管去稳定剂，但不是微管稳定剂，从根本上减少了血液流向肿瘤，从而扩大了孢子可能发芽的低氧生态位。单次静脉注射孢子加选定的微管相互作用剂能够在没有过度毒性的情况下引起几种肿瘤的消退。

62. 发明申请

WO2005039492A9 IMPROVED COMBINATION BACTERIOLYTIC THERAPY FOR THE TREATMENT OF TUMORS 审中-公开
标题翻译：改进的联合用于治疗肿瘤的细菌疗法
公开(公告)号：WO2005039492A9
公开(公告)日：2005-06-02
申请号：PCT/US2004034625
申请日：2004-10-21
申请人： UNIV JOHNS HOPKINS , DANG LONG , BETTEGOWDA CHETAN , KINZLER KENNETH W , VOGELSTEIN BERT
发明人： DANG LONG , BETTEGOWDA CHETAN , KINZLER KENNETH W , VOGELSTEIN BERT
IPC分类号： A01N63/00 , A61K20060101 , A61K
CPC分类号： A61K35/742 , A61K31/337 , A61K31/427 , A61K45/06 , Y10S435/842 , A61K2300/00
摘要： Current approaches for treating cancer are limited, in part, by the inability of drugs to affect the poorly vascularized regions of tumors. We have found that spores of anaerobic bacteria in combination with agents which interact with microtubules can cause the destruction of both the vascular and avascular compartments of tumors. Two classes of microtubule inhibitors were found to exert markedly different effects. Some agents that inhibited microtubule synthesis, such as vinorelbine, caused rapid, massive hemorrhagic necrosis when used in combination with spores. In contrast, agents that stabilized microtubules, such as the taxane docetaxel, resulted in slow tumor regressions that killed most neoplastic cells. Remaining cells in the poorly perfused regions of tumors could be eradicated by sponzlated bacteria. Mechanistic studies showed that the microtubule destabilizers, but not the microtubule stabilizers, radically reduced blood flow to tumors, thereby enlarging the hypoxic niche in which spores could germinate. A single intravenous injection of spores plus selected microtubule-interacting agents was able to cause regressions of several tumors in the absence of excessive toxicity.
摘要翻译：目前用于治疗癌症的方法部分地由于药物不能影响肿瘤血管化程度差的区域而受到限制。我们发现厌氧菌的孢子与微管相互作用的药物联合使用会导致肿瘤血管和血管腔的破坏。发现两类微管抑制剂发挥显着不同的作用。一些抑制微管合成的药物，如长春瑞滨，当与孢子结合使用时会引起快速，大量的出血性坏死。相反，稳定微管的药物，如紫杉类多西紫杉醇，则导致缓慢的肿瘤消退，从而杀死大多数肿瘤细胞。肿瘤灌注不足区域的剩余细胞可以被脊椎化细菌消灭。机理研究表明，微管去稳定剂，但不是微管稳定剂，从根本上减少了血液流向肿瘤，从而扩大了孢子可能发芽的缺氧生态位。单次静脉注射孢子加选定的微管相互作用剂能够在没有过度毒性的情况下引起几种肿瘤的消退。

63. 发明申请

WO02066684A3 GENOME-BASED PERSONALIZED MEDICINE 审中-公开
标题翻译：基于基因的个人化医学
公开(公告)号：WO02066684A3
公开(公告)日：2003-10-16
申请号：PCT/US0204686
申请日：2002-02-19
申请人： UNIV JOHNS HOPKINS , VOGELSTEIN BERT , KINZLER KENNETH W , YAN HAI , PAPADOPOULOS NICKOLAS
发明人： VOGELSTEIN BERT , KINZLER KENNETH W , YAN HAI , PAPADOPOULOS NICKOLAS
IPC分类号： C12Q1/68 , C12N5/12
CPC分类号： C12Q1/6876 , C12N2503/00 , C12Q2600/106 , C12Q2600/156
摘要： Individual alleles can be isolated from every chromosome within somatic cell hybrids generated from a single fusion event. Nucleic acids or proteins from the hybrids can be analyzed for polymorphisms to provide unambiguous determinations. Information thus obtained can be used to develop and implment personalized medical interventions for individuals having particular polymorphic markers.
摘要翻译：可以从单个融合事件产生的体细胞杂交体内的每个染色体分离个体等位基因。可以分析来自杂交体的核酸或蛋白质的多态性以提供明确的测定。由此获得的信息可用于为具有特定多态性标记的个体开发和隐含个性化医疗干预。

64. 发明申请

WO0168923A3 MITOCHONDRIAL DOSIMETER 审中-公开
公开(公告)号：WO0168923A3
公开(公告)日：2003-04-10
申请号：PCT/US0108253
申请日：2001-03-15
申请人： UNIV JOHNS HOPKINS , FLISS MAKIKO , SIDRANSKY DAVID , JEN JIN , POLYAK KOMELIA , VOGELSTEIN BERT , KINZLER KENNETH W
发明人： FLISS MAKIKO , SIDRANSKY DAVID , JEN JIN , POLYAK KOMELIA , VOGELSTEIN BERT , KINZLER KENNETH W
IPC分类号： G01N33/50 , C12N5/08 , C12N15/09 , C12Q1/68 , G01N37/00
CPC分类号： C12Q1/6809 , C12Q1/6883 , C12Q1/6886 , C12Q2600/156 , C12Q2600/158
摘要： Mitochondrial mutations occur as a product of contact of a person with an environmental pollutant. Mitochondrial mutations are readily detectable in body fluids. Measurement of mitochondrial mutations in body fluids can be used as a dosimeter to monitor exposure to the environmental pollutant. Mitochondrial mutations can also be detected in cancer patients. Probes and primers containing mutant mitochondrial sequences can be used to monitor patient condition.
摘要翻译：线粒体突变作为人与环境污染物接触的产物发生。线粒体突变在体液中容易检测到。体液中线粒体突变的测量可用作剂量计来监测对环境污染物的暴露。线粒体突变也可以在癌症患者中检测到。含有突变体线粒体序列的探针和引物可用于监测患者状况。

65. 发明申请

WO02064790A2 JFY1 PROTEIN INDUCES RAPID APOPTOSIS 审中-公开
标题翻译： JFY1蛋白诱导快速病变
公开(公告)号：WO02064790A2
公开(公告)日：2002-08-22
申请号：PCT/US0147455
申请日：2001-12-12
申请人： UNIV JOHNS HOPKINS , YU JIAN , KINZLER KENNETH W , VOGELSTEIN BERT
发明人： YU JIAN , KINZLER KENNETH W , VOGELSTEIN BERT
IPC分类号： A61K31/7088 , A61K48/00 , A61P35/00 , C07K14/47 , C07K19/00 , C12N1/15 , C12N1/19 , C12N1/21 , C12N5/10 , C12N15/09 , C12N15/12 , C12Q1/68 , G01N33/15 , G01N33/50 , G01N33/53 , G01N33/566 , C12N15/11 , C12N15/62
CPC分类号： G01N33/5011 , C07K14/4747 , C07K2319/00 , G01N2500/20
摘要： Through global profiling of genes that were expressed soon after p53 expression, we identified a gene termed (JFY1) . The protein encoded by (JFY1) was found to be exclusively mitochondri al and to bind to Bcl-2 and Bcl-XL through a BH3 domain. Exogenous expression of (JFY1) resul ted in an extremely rapid and profound apoptosis that occurred much earlier than that resulting from exogenous expression of p53. Based on its unique expression patterns, p53-dependence, and biochemical properties, (JFY1) is likely to be a dir ect mediator of p53-associated apoptosis.
摘要翻译：通过对p53表达后不久表达的基因的全球分析，我们鉴定了一个称为（JFY1）的基因。发现由（JFY1）编码的蛋白质是唯一的线粒体，并通过BH3结构域结合Bcl-2和Bcl-XL。（JFY1）的外源性表达发生了非常快速和深刻的凋亡，其发生早于p53外源表达产生的凋亡。基于其独特的表达模式，p53依赖性和生物化学性质，（JFY1）可能是p53相关凋亡的直接介导物。

66. 发明申请

WO0011195A9 C-MYC IS ACTIVATED BY BETA-CATENIN AND TCF-4 审中-公开
标题翻译： C-MYC是由卡培他滨和TCF-4激活的
公开(公告)号：WO0011195A9
公开(公告)日：2002-08-22
申请号：PCT/US9918774
申请日：1999-08-20
申请人： UNIV JOHNS HOPKINS MED , HE TONG-CHUAN , VOGELSTEIN BERT , KINZLER KENNETH W
发明人： HE TONG-CHUAN , VOGELSTEIN BERT , KINZLER KENNETH W
IPC分类号： C12N15/09 , A61K31/711 , A61K38/00 , A61K45/00 , A61K48/00 , A61P35/00 , C07K14/47 , C12N15/12 , C12Q1/02 , C12Q1/68 , G01N33/15 , G01N33/50 , C12N15/63 , C07K14/27
CPC分类号： C07K14/47 , A61K38/00 , A61K48/00 , C07K14/4705 , C12Q1/6897
摘要： The APC tumor suppressor protein binds to beta -catenin, a protein recently shown to interact with Tcf/Lef transcription factors. Here, the gene encoding a Tcf family member that is expressed in colonic epithelium (hTcf-4) was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta -catenin. Nuclei of APC colon carcinoma cells were found to contain a stable beta -catenin-hTCF-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta -catenin from hTcf4 and abrogated the transcriptional transactivation. Constitutive transcription of TCF target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium. It is also shown here that the products of mutant APC genes found in colorectal tumors are defective in regulating beta -catenin/Tcf-4 transcriptional activation. Furthermore, colorectal tumors with intact APC genes were shown to contain subtle activating mutations of beta -catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta -catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta -catenin.
摘要翻译： APC肿瘤抑制蛋白结合β-连环蛋白，最近显示出与Tcf / Lef转录因子相互作用的蛋白质。这里，克隆并表征编码在结肠上皮（hTcf-4）中表达的Tcf家族成员的基因。 hTcf-4仅在与β-连环蛋白相关时才转录转录。发现APC < - / - >结肠癌细胞的核含有一个稳定的β-连环蛋白-hTCF-4复合物，其通过Tcf报告基因的转录测量而具有组成型活性。重新引入APC从hTcf4中除去β-连环蛋白，并废除转录反式激活。由APC功能丧失引起的TCF靶基因的组成转录可能是结肠上皮早期转化的关键事件。这里还显示，在结肠直肠肿瘤中发现的突变APC基因的产物在调节β-连环蛋白/ Tcf-4转录激活中是缺陷的。此外，具有完整APC基因的结肠直肠肿瘤显示含有改变功能显着磷酸化位点的β-连环蛋白的微妙活化突变。这些结果表明，β-连环蛋白的调节对于APC的肿瘤抑制作用至关重要，并且该调节可以通过APC或β-连环蛋白的突变来规避。

67. 发明申请

WO0011219A9 SUBTLE MITOCHONDRIAL MUTATIONS AS TUMOR MARKERS 审中-公开
标题翻译：作为肿瘤标志物的小鼠MITOCHONDRON MUTATIONS
公开(公告)号：WO0011219A9
公开(公告)日：2001-04-26
申请号：PCT/US9918775
申请日：1999-08-20
申请人： UNIV JOHNS HOPKINS MED , VOGELSTEIN BERT , KINZLER KENNETH W , POLYAK KORNELIA
发明人： VOGELSTEIN BERT , KINZLER KENNETH W , POLYAK KORNELIA
IPC分类号： G01N33/53 , C12N5/08 , C12N15/09 , C12Q1/68 , G01N33/566
CPC分类号： C12Q1/6809 , C12Q1/6886 , C12Q2600/156
摘要： The accumulation of homoplasmic somatic mutations has been observed in the mitochondrial DNA of certain tumor cells. The presence or a recurrence of a tumor can be detected by determining the presence of single basepair mutations in the mitochondrial genome from a cell sample of a patient.
摘要翻译：已经在某些肿瘤细胞的线粒体DNA中观察到同质体细胞突变的积累。可以通过确定来自患者细胞样品的线粒体基因组中单个碱基对突变的存在来检测肿瘤的存在或复发。

68. 发明申请

WO0031300A2 GENOTYPING BY MASS SPECTROMETRIC ANALYSIS OF SHORT DNA FRAGMENTS 审中-公开
标题翻译：基因芯片技术用于短链DNA片段的质谱分析
公开(公告)号：WO0031300A2
公开(公告)日：2000-06-02
申请号：PCT/US9927523
申请日：1999-11-22
申请人： UNIV JOHNS HOPKINS , LAKEN STEVEN J , VOGELSTEIN BERT , KINZLER KENNETH W , GROOPMAN JOHN D , JACKSON PETA E , FRIESEN MARLIN D
发明人： LAKEN STEVEN J , VOGELSTEIN BERT , KINZLER KENNETH W , GROOPMAN JOHN D , JACKSON PETA E , FRIESEN MARLIN D
IPC分类号： C12Q1/68 , G01N30/72 , G01N33/50
CPC分类号： C12Q1/683 , C12Q1/6844 , C12Q1/6872 , C12Q2565/627 , C12Q2525/204 , C12Q2521/313 , C12Q2525/131
摘要： Genotyping can be accomplished by analysis of short, defined DNA segments using electrospray ionization mass spectrometry. The DNA segments are produced using specially designed primers to amplify a cDNA or genomic DNA template. The primers contain a recognition site for a restriction endonuclease. The amplification products are digested with the restriction endonuclease. Single nucleotide polymorphisms can be detected rapidly and reliably.
摘要翻译：基因分型可以通过使用电喷雾电离质谱法分析短的，确定的DNA片段来完成。使用特别设计的引物来产生DNA片段以扩增cDNA或基因组DNA模板。引物含有限制性内切核酸酶的识别位点。扩增产物用限制性内切酶消化。单核苷酸多态性可以快速可靠地检测到。

69. 发明申请

WO2005017182A3 MULTI-COLOR IN VITRO TRANSLATION 审中-公开
标题翻译：多色翻译
公开(公告)号：WO2005017182A3
公开(公告)日：2007-12-06
申请号：PCT/US2004019097
申请日：2004-07-21
申请人： JOHNS HOPINKS UNIVERSITY SCHOO , TRAVERSO CARLO GIOVANNI , DIEHL FRANK , KINZLER KENNETH W , VOGELSTEIN BERT
发明人： TRAVERSO CARLO GIOVANNI , DIEHL FRANK , KINZLER KENNETH W , VOGELSTEIN BERT
IPC分类号： C12Q1/68 , C07K14/00 , C12Q20060101
CPC分类号： G01N33/6845 , G01N33/542
摘要： In vitro <
摘要翻译：体外

70. 发明专利

ES2659209T3 Procedimiento para generar organismos hipermutables 未知
公开(公告)号：ES2659209T3
公开(公告)日：2018-03-14
申请号：ES01935403
申请日：2001-05-14
申请人： UNIV JOHNS HOPKINS , MORPHOTEK INC , NICOLAIDES NICHOLAS C , SASS PHILIP M , GRASSO LUIGI , VOGELSTEIN BERT , KINZLER KENNETH
发明人： NICOLAIDES NICHOLAS C , SASS PHILIP M , GRASSO LUIGI , VOGELSTEIN BERT , KINZLER KENNETH W
IPC分类号： A01K67/027 , C12N15/10 , C07K14/47 , C12N15/01 , C12N15/09 , C12Q1/02 , C12Q1/68 , G01N33/15 , G01N33/50 , G01N33/53 , G01N33/566
摘要： Procedimiento para generar una célula genéticamente estable in vitro que comprende una mutación en un gen de interés, comprendiendo dicho procedimiento las etapas de: cultivar una célula de mamífero hipermutable que comprende el gen de interés y un polinucleótido que codifica una proteína hPMS2 de reparación de errores de apareamiento del péptido truncado que consiste en los 133 aminoácidos N-terminales de HPMS2 (hPMS2-134); probar la célula para determinar si el gen de interés alberga una mutación y detectar la mutación; y restaurar la actividad de reparación de errores de apareamiento a la célula disminuyendo o suprimiendo la expresión del polinucleótido que codifica hPMS2-134, generando de ese modo una célula genéticamente estable que comprende una mutación en un gen de interés.

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