排序方式: 共有18条查询结果,搜索用时 15 毫秒
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Roberto Sarnari Allison M. Blake Alexander Ruh Muhannad A. Abbasi Ashitha Pathrose Julie Blaisdell Ryan S. Dolan Kambiz Ghafourian Jane E. Wilcox Sadiya S. Khan Esther E. Vorovich Jonathan D. Rich Allen S. Anderson Clyde W. Yancy James C. Carr Michael Markl 《Journal of magnetic resonance imaging : JMRI》2020,52(3):920-929
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Androgens suppress osteoclast formation induced by RANKL and macrophage-colony stimulating factor 总被引:12,自引:0,他引:12
Huber DM Bendixen AC Pathrose P Srivastava S Dienger KM Shevde NK Pike JW 《Endocrinology》2001,142(9):3800-3808
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Lee Jeesoo El Hangouche Nadia Pathrose Ashitha Soulat Gilles Barker Alex J. Thomas James D. Markl Michael 《The international journal of cardiovascular imaging》2022,38(9):2047-2056
The International Journal of Cardiovascular Imaging - This study investigated the impact of bicuspid aortic valve (BAV) on valve morphology and motion as well as proximal and aortic hemodynamics... 相似文献
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Kishore Thekke Adiyat Kuriakose Milka James Pathrose Gregory Raveendran Vishn Kumar K. Vinod Unni V. Narayanan 《International urology and nephrology》2020,52(2):247-252
International Urology and Nephrology - The aim of this study was to assess the feasibility of robotic assisted kidney transplantation in graft with multiple vessels. Eighteen patients underwent... 相似文献
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Mammary-specific Ron receptor overexpression induces highly metastatic mammary tumors associated with beta-catenin activation 总被引:3,自引:0,他引:3
Zinser GM Leonis MA Toney K Pathrose P Thobe M Kader SA Peace BE Beauman SR Collins MH Waltz SE 《Cancer research》2006,66(24):11967-11974
Activated growth factor receptor tyrosine kinases (RTK) play pivotal roles in a variety of human cancers, including breast cancer. Ron, a member of the Met RTK proto-oncogene family, is overexpressed or constitutively active in 50% of human breast cancers. To define the significance of Ron overexpression and activation in vivo, we generated transgenic mice that overexpress a wild-type or constitutively active Ron receptor in the mammary epithelium. In these animals, Ron expression is significantly elevated in mammary glands and leads to a hyperplastic phenotype by 12 weeks of age. Ron overexpression is sufficient to induce mammary transformation in all transgenic animals and is associated with a high degree of metastasis, with metastatic foci detected in liver and lungs of >86% of all transgenic animals. Furthermore, we show that Ron overexpression leads to receptor phosphorylation and is associated with elevated levels of tyrosine phosphorylated beta-catenin and the up-regulation of genes, including cyclin D1 and c-myc, which are associated with poor prognosis in patients with human breast cancers. These studies suggest that Ron overexpression may be a causative factor in breast tumorigenesis and provides a model to dissect the mechanism by which the Ron induces transformation and metastasis. 相似文献
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Thobe MN Gray JK Gurusamy D Paluch AM Wagh PK Pathrose P Lentsch AB Waltz SE 《Oncogene》2011,30(50):4990-4998
The Ron receptor tyrosine kinase (TK) is overexpressed in many cancers, including prostate cancer. To examine the significance of Ron in prostate cancer in vivo, we utilized a genetically engineered mouse model, referred to as TRAMP mice, that is predisposed to develop prostate tumors. In this model, we show that prostate tumors from 30-week-old TRAMP mice have increased Ron expression compared with age-matched wild-type prostates. Based on the upregulation of Ron in human prostate cancers and in this murine model of prostate tumorigenesis, we hypothesized that this receptor has a functional role in the development of prostate tumors. To test this hypothesis, we crossed TRAMP mice with mice that are deficient in Ron signaling (TK-/-). Interestingly, TK-/- TRAMP+ mice show a significant decrease in prostate tumor mass relative to TRAMP mice containing functional Ron. Moreover, TK-/- TRAMP+ prostate tumors exhibited decreased tumor vascularization relative to TK+/+ TRAMP+ prostate tumors, which correlated with reduced levels of the angiogenic molecules vascular endothelial growth factor and CXCL2. Although Ron loss did not alter tumor cell proliferation, a significant decrease in cell survival was observed. Similarly, murine prostate cancer cell lines containing a Ron deficiency exhibited decreased levels of active nuclear factor-κB, suggesting that Ron may be important in regulating prostate cell survival at least partly through this pathway. In total, our data show for the first time that Ron promotes prostate tumor growth, prostate tumor angiogenesis and prostate cancer cell survival in vivo. 相似文献