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1. 发明申请

US20100184100A1 Tyrosine Kinome 有权
标题翻译：酪氨酸激酶
公开(公告)号：US20100184100A1
公开(公告)日：2010-07-22
申请号：US12705760
申请日：2010-02-15
申请人： Alberto Bardelli , Will Parsons , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
发明人： Alberto Bardelli , Will Parsons , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
IPC分类号： G01N33/574 , C07H21/00
CPC分类号： C12Q1/6886 , A61K31/506 , C12N9/1205 , C12Q1/025 , C12Q1/485 , C12Q1/6809 , C12Q1/6827 , C12Q2600/136 , C12Q2600/156 , G01N33/574
摘要： Protein kinases are important signaling molecules involved in tumorigenesis. Mutational analysis of the human tyrosine kinase gene family (98 genes) identified somatic alterations in −20% of colorectal cancers, with the majority of mutations occurring in NTRK3, FES, GUCY2F and a previously uncharacterized tyrosine kinase gene called MCCK/MLK4. Most alterations were in conserved residues affecting key regions of the kinase domain. These data represent a paradigm for the unbiased analysis of signal transducing genes in cancer and provide useful targets for therapeutic intervention.
摘要翻译：蛋白激酶是参与肿瘤发生的重要信号分子。人类酪氨酸激酶基因家族（98个基因）的突变分析鉴定了-20％的结肠直肠癌的体细胞变化，大部分突变发生在NTRK3，FES，GUCY2F和以前称为MCCK / MLK4的未表征的酪氨酸激酶基因。大多数改变是保守的残基影响激酶结构域的关键区域。这些数据代表了癌症中信号转导基因的无偏见分析的范例，并为治疗干预提供了有用的目标。

2. 发明授权

US08394598B2 Tyrosine kinome 有权
标题翻译：酪氨酸激酶
公开(公告)号：US08394598B2
公开(公告)日：2013-03-12
申请号：US12705760
申请日：2010-02-15
申请人： Alberto Bardelli , Will Parsons , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
发明人： Alberto Bardelli , Will Parsons , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
IPC分类号： C12Q1/68 , G01N33/574
CPC分类号： C12Q1/6886 , A61K31/506 , C12N9/1205 , C12Q1/025 , C12Q1/485 , C12Q1/6809 , C12Q1/6827 , C12Q2600/136 , C12Q2600/156 , G01N33/574
摘要： Protein kinases are important signaling molecules involved in tumorigenesis. Mutational analysis of the human tyrosine kinase gene family (98 genes) identified somatic alterations in -20% of colorectal cancers, with the majority of mutations occurring in NTRK3, FES, GUCY2F and a previously uncharacterized tyrosine kinase gene called MCCK/MLK4. Most alterations were in conserved residues affecting key regions of the kinase domain. These data represent a paradigm for the unbiased analysis of signal transducing genes in cancer and provide useful targets for therapeutic intervention.
摘要翻译：蛋白激酶是参与肿瘤发生的重要信号分子。人类酪氨酸激酶基因家族（98个基因）的突变分析鉴定了-20％的结肠直肠癌的体细胞变化，大部分突变发生在NTRK3，FES，GUCY2F和以前称为MCCK / MLK4的未表征的酪氨酸激酶基因。大多数改变是保守的残基影响激酶结构域的关键区域。这些数据代表了癌症中信号转导基因的无偏见分析的范例，并为治疗干预提供了有用的目标。

3. 发明授权

US09580750B2 P13K pathway mutations in cancer 有权
标题翻译：癌症中P13K通路突变
公开(公告)号：US09580750B2
公开(公告)日：2017-02-28
申请号：US11920860
申请日：2006-05-23
申请人： Donald William Parsons , Tian-li Wang , Yardena Samuels , Alberto Bardelli , Christopher Lengauer , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
发明人： Donald William Parsons , Tian-li Wang , Yardena Samuels , Alberto Bardelli , Christopher Lengauer , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
IPC分类号： C12Q1/62 , G01N33/574 , C07K16/40 , C12Q1/68 , C12Q1/48 , G01N33/50
CPC分类号： C12Q1/6883 , C12Q1/485 , C12Q2600/136 , C12Q2600/156 , G01N33/5044 , G01N33/57419
摘要： Given the important role of protein kinases in pathways affecting cellular growth and invasion, we have analyzed 340 serine/threonine kinases for genetic mutations in colorectal cancers. Mutations in eight genes were identified, including three members of the phosphatidylinositol-3-kinase (PI3K) pathway; the alterations in the latter genes each occurred in different tumors and did not overlap with mutations in PIK3CA or other non-serine-threonine kinase (STK) members of the PI3K pathway, suggesting that mutations in any of these genes had equivalent tumorigenic effects. These data demonstrate that the PI3K pathway is a major target for mutational activation in colorectal cancers and provide new opportunities for therapeutic intervention.
摘要翻译：鉴于蛋白激酶在影响细胞生长和侵袭的途径中的重要作用，我们已经分析了340个丝氨酸/苏氨酸激酶在结肠直肠癌中的遗传突变。鉴定出8个基因的突变，包括磷脂酰肌醇-3-激酶（PI3K）通路的3个成员; 后一种基因的改变各自发生在不同的肿瘤中，并且不与PIK3CA或PI3K途径的其他非丝氨酸 - 苏氨酸激酶（STK）成员的突变重叠，这表明任何这些基因中的突变具有相等的致瘤作用。这些数据表明，PI3K途径是结肠直肠癌突变激活的主要靶标，为治疗干预提供新的机会。

4. 发明申请

US20110059434A1 P13k pathway mutations in cancer 有权
标题翻译：癌症中P13k通路突变
公开(公告)号：US20110059434A1
公开(公告)日：2011-03-10
申请号：US11920860
申请日：2006-05-23
申请人： Donald William Parsons , Tian-li Wang , Yardena Samuels , Alberto Bardelli , Christopher Lengauer , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
发明人： Donald William Parsons , Tian-li Wang , Yardena Samuels , Alberto Bardelli , Christopher Lengauer , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
IPC分类号： C12Q1/68 , C12Q1/48 , C12N9/12 , G01N33/574
CPC分类号： C12Q1/6883 , C12Q1/485 , C12Q2600/136 , C12Q2600/156 , G01N33/5044 , G01N33/57419
摘要： Given the important role of protein kinases in pathways affecting cellular growth and invasion, we have analyzed 340 serine/threonine kinases for genetic mutations in colorectal cancers. Mutations in eight genes were identified, including three members of the phosphatidylinositol-3-kinase (PI3K) pathway; the alterations in the latter genes each occurred in different tumors and did not overlap with mutations in PIK3CA or other non-serine-threonine kinase (STK) members of the PI3K pathway, suggesting that mutations in any of these genes had equivalent tumorigenic effects. These data demonstrate that the PI3K pathway is a major target for mutational activation in colorectal cancers and provide new opportunities for therapeutic intervention.
摘要翻译：鉴于蛋白激酶在影响细胞生长和侵袭的途径中的重要作用，我们已经分析了340个丝氨酸/苏氨酸激酶在结肠直肠癌中的遗传突变。鉴定出8个基因的突变，包括磷脂酰肌醇-3-激酶（PI3K）通路的3个成员; 后一种基因的改变各自发生在不同的肿瘤中，并且不与PIK3CA或PI3K途径的其他非丝氨酸 - 苏氨酸激酶（STK）成员的突变重叠，这表明任何这些基因中的突变具有相等的致瘤作用。这些数据表明，PI3K途径是结肠直肠癌突变激活的主要靶标，为治疗干预提供新的机会。

5. 发明授权

US07745165B2 Phosphatase associated with metastasis 有权
标题翻译：与转移相关的磷酸酶
公开(公告)号：US07745165B2
公开(公告)日：2010-06-29
申请号：US10868658
申请日：2004-06-16
申请人： Bert Vogelstein , Kenneth W. Kinzler , Saurabh Saha , Alberto Bardelli
发明人： Bert Vogelstein , Kenneth W. Kinzler , Saurabh Saha , Alberto Bardelli
IPC分类号： C12Q1/48 , G01N33/567
CPC分类号： C12N9/16 , A61K39/00 , C12Q1/6886 , C12Q2600/112 , C12Q2600/136 , C12Q2600/158
摘要： Among the genes identified, in a comparison of the global gene expression profile of metastatic colorectal cancer to that of primary cancers, benign colorectal tumors, and normal colorectal epithelium, the PRL-3 protein tyrosine phosphatase gene was of particular interest. It was expressed at high levels in each of 18 cancer metastases studied but at lower levels in non-metastatic tumors and normal colorectal epithelium. In three of twelve metastases examined, multiple copies of the PRL-3 gene were found within a small amplicon located at chromosome 8q24.3. These data suggest that the PRL-3 gene is important for colorectal cancer metastasis and provides a new therapeutic target for these intractable lesions.
摘要翻译：在确定的基因中，在转移性结肠直肠癌与原发性癌症，良性结肠直肠肿瘤和正常结肠直肠上皮的全球基因表达谱比较中，PRL-3蛋白酪氨酸磷酸酶基因特别引人关注。在所研究的18个癌症转移中的每一个中表达高水平，但在非转移性肿瘤和正常结肠直肠上皮中的水平较低。在检查的十二个转移中的三个中，在位于染色体8q24.3的小扩增子中发现了PRL-3基因的多个拷贝。这些数据表明，PRL-3基因对结肠直肠癌转移很重要，为这些难治性病变提供了新的治疗靶点。

6. 发明授权

US09637779B2 Antisense transcriptomes of cells 有权
公开(公告)号：US09637779B2
公开(公告)日：2017-05-02
申请号：US13131413
申请日：2009-12-02
申请人： Bert Vogelstein , Kenneth W. Kinzler , Yiping He , Victor Velculescu , Nickolas Papadopoulos
发明人： Bert Vogelstein , Kenneth W. Kinzler , Yiping He , Victor Velculescu , Nickolas Papadopoulos
IPC分类号： C12Q1/68 , G06F19/22
CPC分类号： C12Q1/6844 , G06F19/22 , C12Q2539/113 , C12Q2523/125 , C12Q2521/107
摘要： Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the Plus- or Minus-strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was non-random across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, suggesting that they are a fundamental component of gene regulation.

7. 发明申请

US20120009573A1 Antisense Transcriptomes of Cells 有权
标题翻译：细胞反义转录组
公开(公告)号：US20120009573A1
公开(公告)日：2012-01-12
申请号：US13131413
申请日：2009-12-02
申请人： Bert Vogelstein , Kenneth W. Kinzler , Yiping He , Victor Velculescu , Nickolas Papadopoulos
发明人： Bert Vogelstein , Kenneth W. Kinzler , Yiping He , Victor Velculescu , Nickolas Papadopoulos
IPC分类号： C12Q1/68
CPC分类号： C12Q1/6844 , G06F19/22 , C12Q2539/113 , C12Q2523/125 , C12Q2521/107
摘要： Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the Plus- or Minus-strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was non-random across the genome, and differed among cell types. Anti-sense transcripts thus appear to be a pervasive feature of human cells, suggesting that they are a fundamental component of gene regulation.
摘要翻译：哺乳动物细胞中的转录可以在全基因组范围内进行评估，但是难以可靠地确定个体转录本是否衍生自染色体的加号或阴影链。这种区别对于了解已知转录物（有义）和可能调节它们的互补反义转录物之间的关系可能是至关重要的。在这里，我们描述了一种可用于（i）识别任何特定RNA转录物的DNA链起源的技术，（ii）在全球范围内量化来自表达基因的正义和反义转录本的数量。我们检查了五种不同的人类细胞类型，并且在每种情况下都发现2900至6400个人类基因中的反义转录物的证据。反义转录物的分布与有义转录物的分布不同，在基因组中是非随机的，并且在细胞类型之间不同。因此，反义转录物似乎是人类细胞的普遍特征，表明它们是基因调控的基本组成部分。

8. 发明授权

US08039210B2 Protein tyrosine phosphatase mutations in cancers 有权
标题翻译：蛋白酪氨酸磷酸酶突变在癌症
公开(公告)号：US08039210B2
公开(公告)日：2011-10-18
申请号：US11596349
申请日：2005-05-16
申请人： Zhenghe Wang , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
发明人： Zhenghe Wang , Victor Velculescu , Kenneth W. Kinzler , Bert Vogelstein
IPC分类号： C12Q1/68
CPC分类号： C12Q1/6886 , C12N9/16 , C12Q2600/112 , C12Q2600/136 , C12Q2600/156 , C12Q2600/158 , C12Y301/03048 , G01N33/5011 , G01N2333/916
摘要： Tyrosine phosphorylation, regulated by protein tyrosine phosphatases (PTPs) and kinases (PTKs), is important in signaling pathways underlying tumorigenesis. A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14) affecting 26% of colorectal cancers and a smaller fraction of lung, breast and gastric cancers. Fifteen mutations were nonsense, frameshift or splice site alterations predicted to result in truncated proteins lacking phosphatase activity. Five missense mutations in the most commonly altered PTP (PTPRP) were biochemically examined and found to reduce phosphatase activity. Expression of wild-type but not a mutant PTPRT in human cancer cells inhibited cell growth. These observations suggest that the tyrosine phosphatase genes are tumor suppressor genes, regulating cellular pathways that may be amenable to therapeutic intervention.
摘要翻译：由蛋白酪氨酸磷酸酶（PTP）和激酶（PTK）调节的酪氨酸磷酸化在肿瘤发生的信号通路中是重要的。人类癌症中酪氨酸磷酸酶基因超家族的突变分析鉴定了影响26％结肠直肠癌和较小部分肺癌，乳腺癌和胃癌的6种PTPs（PTPRF，PTPRG，PTPRT，PTPN3，PTPN13，PTPN14）中的83个体细胞突变。十五个突变是无义，移位或剪接位点改变，预计会导致截短的蛋白质缺乏磷酸酶活性。在生物化学检查中发现最常改变的PTP（PTPRP）中的五个错义突变被发现可以降低磷酸酶活性。野生型但不是突变PTPRT在人类癌细胞中的表达抑制细胞生长。这些观察结果表明酪氨酸磷酸酶基因是肿瘤抑制基因，调节可能适合于治疗干预的细胞途径。

9. 发明申请

US20110229479A1 GENETIC ALTERATIONS IN ISOCITRATE DEHYDROGENASE AND OTHER GENES IN MALIGNANT GLIOMA 有权
标题翻译：异烟肼脱氢酶和其他基因在恶性胶质瘤中的遗传变异
公开(公告)号：US20110229479A1
公开(公告)日：2011-09-22
申请号：US13060191
申请日：2009-09-03
申请人： Bert Vogelstein , Kenneth W. Kinzler , D. Williams Parsons , Xiaosong Zhang , Jimmy Cheng-Ho Lin , Rebecca J. Leary , Philipp Angenendt , Nickolas Papadopoulos , Victor Velculescu , Giovanni Parmigiani , Rachel Karchin , Sian Jones , Hai Yan , Darell Bigner , Chien-Tsun Kuan
发明人： Bert Vogelstein , Kenneth W. Kinzler , D. Williams Parsons , Xiaosong Zhang , Jimmy Cheng-Ho Lin , Rebecca J. Leary , Philipp Angenendt , Nickolas Papadopoulos , Victor Velculescu , Giovanni Parmigiani , Rachel Karchin , Sian Jones , Hai Yan , Darell Bigner , Chien-Tsun Kuan
IPC分类号： A61K39/395 , C12Q1/68 , G01N33/574 , C07K16/32 , A61K39/00 , C12N9/04 , C07H21/04 , C12Q1/32 , A61P37/04 , A61P35/00
CPC分类号： C12Q1/6886 , C12Q2600/112 , C12Q2600/118 , C12Q2600/136 , C12Q2600/156
摘要： We found mutations of the R132 residue of isocitrate dehydrogenase 1 (IDH1) in the majority of grade II and III astrocytomas and oligodendrogliomas as well as in glioblastomas that develop from these lower grade lesions. Those tumors without mutations in IDH1 often had mutations at the analogous R172 residue of the closely related IDH2 gene. These findings have important implications for the pathogenesis and diagnosis of malignant gliomas.
摘要翻译：我们发现大多数II级和III级星形细胞瘤和少突胶质细胞瘤中异柠檬酸脱氢酶1（IDH1）的R132残基突变以及从这些较低级别病变发展的成胶质细胞瘤。那些没有IDH1突变的肿瘤在紧密相关的IDH2基因的类似R172残基中经常具有突变。这些发现对恶性胶质瘤的发病机制和诊断具有重要意义。

10. 发明授权

US08685660B2 Genetic alterations in isocitrate dehydrogenase and other genes in malignant glioma 有权
标题翻译：异柠檬酸脱氢酶和恶性胶质瘤中其他基因的遗传改变
公开(公告)号：US08685660B2
公开(公告)日：2014-04-01
申请号：US13060191
申请日：2009-09-03
申请人： Bert Vogelstein , Kenneth W. Kinzler , D. Williams Parsons , Xiaosong Zhang , Jimmy Cheng-Ho Lin , Rebecca J. Leary , Philipp Angenendt , Nickolas Papadopoulos , Victor Velculescu , Giovanni Parmigiani , Rachel Karchin , Sian Jones , Hai Yan , Darell Bigner , Chien-Tsun Kuan , Gregory J. Riggins
发明人： Bert Vogelstein , Kenneth W. Kinzler , D. Williams Parsons , Xiaosong Zhang , Jimmy Cheng-Ho Lin , Rebecca J. Leary , Philipp Angenendt , Nickolas Papadopoulos , Victor Velculescu , Giovanni Parmigiani , Rachel Karchin , Sian Jones , Hai Yan , Darell Bigner , Chien-Tsun Kuan , Gregory J. Riggins
IPC分类号： G01N33/574
CPC分类号： C12Q1/6886 , C12Q2600/112 , C12Q2600/118 , C12Q2600/136 , C12Q2600/156
摘要： We found mutations of the R132 residue of isocitrate dehydrogenase 1 (IDH1) in the majority of grade II and III astrocytomas and oligodendrogliomas as well as in glioblastomas that develop from these lower grade lesions. Those tumors without mutations in IDH1 often had mutations at the analogous R172 residue of the closely related IDH2 gene. These findings have important implications for the pathogenesis and diagnosis of malignant gliomas.
摘要翻译：我们发现大多数II级和III级星形细胞瘤和少突胶质细胞瘤中异柠檬酸脱氢酶1（IDH1）的R132残基突变以及从这些较低级别病变发展的成胶质细胞瘤。那些没有IDH1突变的肿瘤在紧密相关的IDH2基因的类似R172残基中经常具有突变。这些发现对恶性胶质瘤的发病机制和诊断具有重要意义。

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