排序方式: 共有16条查询结果,搜索用时 46 毫秒
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Franchi Francesco Schneider David J. Prats Jayne Fan Weihong Rollini Fabiana Been Latonya Taatjes-Sommer Heidi S. Bhatt Deepak L. Deliargyris Efthymios N. Angiolillo Dominick J. 《Journal of thrombosis and thrombolysis》2022,54(3):373-381
Journal of Thrombosis and Thrombolysis - Low dose enteric-coated aspirin (EC-ASA) is routinely used for secondary cardiovascular event prevention. However, absorption of EC tablets is poor, which... 相似文献
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Stroke and conversion to high risk in children screened with transcranial Doppler ultrasound during the STOP study
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Adams RJ Brambilla DJ Granger S Gallagher D Vichinsky E Abboud MR Pegelow CH Woods G Rohde EM Nichols FT Jones A Luden JP Bowman L Hagner S Morales KH Roach ES;STOP Study 《Blood》2004,103(10):3689-3694
The Stroke Prevention Trial in Sickle Cell Anemia (STOP) was a randomized multicenter controlled trial comparing prophylactic blood transfusion with standard care in sickle cell anemia (SCA) children aged 2 to 16 years selected for high stroke risk by transcranial Doppler (TCD). More than 2000 children were screened with TCD to identify the 130 high-risk children who entered the randomized trial. A total of 5613 TCD studies from 2324 children were evaluated. We also collected information on stroke. We describe the changes in TCD with repeated testing and report the outcome without transfusion in the STOP screened cohort. Risk of stroke was higher with abnormal TCD than with normal or conditional TCD (P <.001) or inadequate TCD (P =.002), and risk with conditional TCD was higher than with normal TCD (P <.001). Repeated TCD in 1215 children showed that the condition of 9.4% of children became abnormal during observation. Younger patients and those with higher initial flow velocities were most likely to convert to abnormal TCDs. Screening in STOP confirmed the predictive value of TCD for stroke. Substantial differences in the probability of conversion to abnormal TCD were observed, with younger children and those with higher velocity more likely to have an abnormal TCD with rescreening. 相似文献
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Carolyn G Marsden Mary Jo Wright Latonya Carrier Krzysztof Moroz Radhika Pochampally Brian G Rowan 《BMC cancer》2012,12(1):10
Background
The study of breast cancer metastasis depends on the use of established breast cancer cell lines that do not accurately represent the heterogeneity and complexity of human breast tumors. A tumor model was developed using primary breast tumor-initiating cells isolated from patient core biopsies that would more accurately reflect human breast cancer metastasis. 相似文献5.
Tamoxifen has efficacy as a breast cancer therapy and chemoprevention agent. However, toxicity and resistance to tamoxifen limit its clinical application. There is an urgent need to develop compounds that may be combined with tamoxifen to improve efficacy and overcome toxicity and resistance. We showed previously that the organoselenium compound methylseleninic acid (MSA) increased the growth-inhibitory effect of tamoxifen and reversed tamoxifen resistance in breast cancer cells. In this study, we examined the mechanism for induction of apoptosis by MSA combined with tamoxifen in tamoxifen-sensitive and tamoxifen-resistant breast cancer cells. 4-hydroxytamoxifen (TAM; 10(-7) mol/L) alone resulted in cell cycle arrest but no apoptosis, whereas MSA alone (10 mumol/L) induced apoptosis in tamoxifen-sensitive cells. Combination of MSA with TAM resulted in a synergistic apoptosis in both tamoxifen-sensitive and tamoxifen-resistant breast cancer cells compared with either agent alone. MSA and MSA combined with TAM induced apoptosis through the intrinsic, mitochondrial apoptotic pathway. MSA induced a sequential activation of caspase-9 and then caspase-8. These results indicate that the growth inhibition synergy and reversal of tamoxifen resistance by combination of selenium with tamoxifen occurs via a tamoxifen-induced cell cycle arrest, allowing more cells to enter the intrinsic apoptotic pathway elicited by selenium. [Mol Cancer Ther 2008;7(9):3056-63]. 相似文献
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M Anbalagan A Ali RK Jones CG Marsden M Sheng L Carrier Y Bu D Hangauer BG Rowan 《Molecular cancer therapeutics》2012,11(9):1936-1947
Src kinase is elevated in breast tumors that are ER/PR negative and do not overexpress HER2, but clinical trials with Src inhibitors have shown little activity. The present study evaluated preclinical efficacy of a novel peptidomimetic compound, KX-01 (KX2-391), that exhibits dual action as an Src and pretubulin inhibitor. KX-01 was evaluated as a single-agent and in combination with paclitaxel in MDA-MB-231, MDA-MB-157, and MDA-MB-468 human ER/PR/HER2-negative breast cancer cells. Treatments were evaluated by growth/apoptosis, isobologram analysis, migration/invasion assays, tumor xenograft volume, metastasis, and measurement of Src, focal adhesion kinase (FAK), microtubules, Ki67, and microvessel density. KX-01 inhibited cell growth in vitro and in combination with paclitaxel resulted in synergistic growth inhibition. KX-01 resulted in a dose-dependent inhibition of MDA-MB-231 and MDA-MB-157 tumor xenografts (1 and 5 mg/kg, twice daily). KX-01 inhibited activity of Src and downstream mediator FAK in tumors that was coincident with reduced proliferation and angiogenesis and increased apoptosis. KX01 also resulted in microtubule disruption in tumors. Combination of KX-01 with paclitaxel resulted in significant regression of MDA-MB-231 tumors and reduced metastasis to mouse lung and liver. KX-01 is a potently active Src/pretubulin inhibitor that inhibits breast tumor growth and metastasis. As ER/PR/HER2-negative patients are candidates for paclitaxel therapy, combination with KX-01 may potentiate antitumor efficacy in management of this aggressive breast cancer subtype. Mol Cancer Ther; 11(9); 1936-47. ?2012 AACR. 相似文献
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Li Z Carrier L Belame A Thiyagarajah A Salvo VA Burow ME Rowan BG 《Breast cancer research and treatment》2009,118(1):33-43
To investigate the therapeutic effect of methylselenocysteine (MSC) combined with tamoxifen in MCF-7 breast cancer xenograft
and the underlying mechanisms. MCF-7 breast cancer xenograft was established in ovariectomized female athymic nude mice and
treated with tamoxifen and/or MSC. Tumor size was measured twice a week. Immunohistochemistry and TUNEL assays were used to
measure ERα expression, ERα target genes (progesterone receptor (PR) and cyclin D1 expression), Ki-67 index, apoptosis and
microvessel density. Combined treatment with tamoxifen and MSC synergistically inhibited tumor growth compared to MSC alone
and tamoxifen alone. MSC alone or MSC + tamoxifen significantly reduced ERα, PR and cyclin D1, Ki67 index and microvessel
density while increasing apoptosis in tumor tissues. These findings demonstrate synergistic growth inhibition of ERα positive
breast cancer xenografts by combination of tamoxifen with organic selenium compounds. Organic selenium may provide added benefit
when combined with tamoxifen in adjuvant therapy or prevention. 相似文献
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