SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Cox Peter M.) "

Sökning: WFRF:(Cox Peter M.)

  • Resultat 101-103 av 103
  • Föregående 1...5678910[11]
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
101.
  • Lim, Soon Tjin, et al. (författare)
  • Platelet function/reactivity testing and prediction of risk of recurrent vascular events and outcomes after TIA or ischaemic stroke : systematic review and meta-analysis
  • 2020
  • Ingår i: Journal of Neurology. - : Steinkopff. - 0340-5354. ; 267:10, s. 3021-3037
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The prevalence of ex vivo ‘high on-treatment platelet reactivity (HTPR)’ and its relationship with recurrent vascular events/outcomes in patients with ischaemic cerebrovascular disease (CVD) is unclear. Methods: A systematic review and meta-analysis was performed in accordance with the PRISMA statement. MEDLINE, EMBASE and Cochrane Library were searched for completed manuscripts until May 2019 on TIA/ischaemic stroke patients, ≥ 18 years, treated with commonly-prescribed antiplatelet therapy, who had platelet function/reactivity testing and prospective follow-up data on recurrent stroke/TIA, myocardial infarction, vascular death or other cerebrovascular outcomes. Data were pooled using random-effects meta-analysis. Primary outcome was the composite risk of recurrent stroke/TIA, myocardial infarction or vascular death. Secondary outcomes were recurrent stroke/TIA, severe stroke (NIHSS > 16) or disability/impairment (modified Rankin scale ≥ 3) during follow-up. Results: Antiplatelet–HTPR prevalence was 3–65% with aspirin, 8–56% with clopidogrel and 1.8–35% with aspirin–clopidogrel therapy. Twenty studies (4989 patients) were included in our meta-analysis. There was a higher risk of the composite primary outcome (OR 2.93, 95% CI 1.90–4.51) and recurrent ischaemic stroke/TIA (OR 2.43, 95% CI 1.51–3.91) in patients with vs. those without ‘antiplatelet–HTPR’ on any antiplatelet regimen. These risks were also more than twofold higher in patients with vs. those without ‘aspirin–HTPR’ and ‘dual antiplatelet–HTPR’, respectively. Clopidogrel–HTPR status did not significantly predict outcomes, but the number of eligible studies was small. The risk of severe stroke was higher in those with vs. without antiplatelet–HTPR (OR 2.65, 95% CI 1.00–7.01). Discussion: Antiplatelet–HTPR may predict risks of recurrent vascular events/outcomes in CVD patients. Given the heterogeneity between studies, further prospective, multi-centre studies are warranted.
  •  
102.
  • Roghanian, Ali, et al. (författare)
  • Antagonistic Human FcγRIIB (CD32B) Antibodies Have Anti-Tumor Activity and Overcome Resistance to Antibody Therapy In Vivo.
  • 2015
  • Ingår i: Cancer Cell. - : Cell Press. - 1878-3686. ; 27:4, s. 473-488
  • Tidskriftsartikel (refereegranskat)abstract
    • Therapeutic antibodies have transformed cancer therapy, unlocking mechanisms of action by engaging the immune system. Unfortunately, cures rarely occur and patients display intrinsic or acquired resistance. Here, we demonstrate the therapeutic potential of targeting human (h) FcγRIIB (CD32B), a receptor implicated in immune cell desensitization and tumor cell resistance. FcγRIIB-blocking antibodies prevented internalization of the CD20-specific antibody rituximab, thereby maximizing cell surface accessibility and immune effector cell mediated antitumor activity. In hFcγRIIB-transgenic (Tg) mice, FcγRIIB-blocking antibodies effectively deleted target cells in combination with rituximab, and other therapeutic antibodies, from resistance-prone stromal compartments. Similar efficacy was seen in primary human tumor xenografts, including with cells from patients with relapsed/refractory disease. These data support the further development of hFcγRIIB antibodies for clinical assessment.
  •  
103.
  • Setiawan, Veronica Wendy, et al. (författare)
  • CYP17 genetic variation and risk of breast and prostate cancer from the national Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3)
  • 2007
  • Ingår i: Cancer Epidemiology Biomarkers & Prevention. - : American Association for Cancer Research. - 1538-7755. ; 16:11, s. 2237-2246
  • Tidskriftsartikel (refereegranskat)abstract
    • CYP17 encodes cytochrome p450c17 alpha, which mediates activities essential for the production of sex steroids. Common germ line variation in the CYP17 gene has been related to inconsistent results in breast and prostate cancer, with most studies focusing on the nonsynonymous single nucleotide polymorphism (SNP) T27C (rs743572). We comprehensively characterized variation in CYP17 by direct sequencing of exons followed by dense genotyping across the 58 kb region around CYP17 in five racial/ethnic populations. Two blocks of strong linkage disequilibrium were identified and nine haplotype-tagging SNPs, including T27C, were chosen to predict common haplotypes (R-h(2) >= 0.85). These haplotype-tagging SNPs were genotyped in 8,138 prostate cancer cases and 9,033 controls, and 5,333 breast cancer cases and 7,069 controls from the Breast and Prostate Cancer Cohort Consortium. We observed borderline significant associations with prostate cancer for rs2486758 [TC versus TT, odds ratios (OR), 1.07; 95% confidence intervals (95% Cl), 1.00-1.14; CC versus TT, OR, 1.09; 95% CI, 0.95-1.26; P trend = 0.04] and rs6892 (AG versus AA, OR, 1.08; 95% CI, 1.00-1.15; GG versus AA, OR, 1.11; 95% CI, 0.95-1.30; P trend = 0.03). We also observed marginally significant associations with breast cancer for rs4919687 (GA versus GG, OR, 1.04; 95% CI, 0.97-1.12, AA versus GG, OR, 1.17; 95% CI, 1.03-1.34; P trend = 0.03) and rs4919682 (CT versus CC, OR, 1.04; 95% CI, 0.97-1.12; TT versus CC, OR, 1.16; 95% CI, 1.01-1.33; P trend = 0.04). Common variation at CYP17 was not associated with circulating sex steroid hormones in men or postmenopausal women. Our findings do not support the hypothesis that common germ line variation in CYP17 makes a substantial contribution to postmenopausal breast or prostate cancer susceptibility.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 101-103 av 103
  • Föregående 1...5678910[11]
Typ av publikation
tidskriftsartikel (99)
forskningsöversikt (3)
bokkapitel (1)
Typ av innehåll
refereegranskat (103)
Författare/redaktör
Giles, Graham G (52)
Easton, Douglas F. (50)
Giles, GG (46)
Cox, A (44)
Southey, Melissa C. (43)
Dunning, Alison M. (42)
visa fler...
Chang-Claude, Jenny (41)
Chanock, Stephen J (41)
Southey, MC (41)
Chang-Claude, J (41)
Kraft, Peter (41)
Cox, Angela (41)
Haiman, Christopher ... (40)
Schmidt, Marjanka K. (40)
Easton, DF (39)
Hopper, John L. (39)
Andrulis, Irene L. (39)
Nevanlinna, H (38)
Brauch, H (38)
Hamann, U (38)
Couch, FJ (38)
Bojesen, Stig E. (38)
Fasching, Peter A. (38)
Nevanlinna, Heli (37)
Hall, P (37)
Hopper, JL (37)
Hamann, Ute (37)
Milne, Roger L. (37)
Brauch, Hiltrud (37)
Garcia-Closas, M (36)
Hall, Per (36)
Garcia-Closas, Monts ... (36)
Milne, RL (35)
Fasching, PA (35)
Chenevix-Trench, G (35)
Hunter, David J. (35)
Blomqvist, C (34)
Benitez, J. (34)
Dunning, AM (34)
Mannermaa, A (34)
Lambrechts, D (34)
Kraft, P (34)
Chenevix-Trench, Geo ... (34)
Benitez, Javier (34)
Blomqvist, Carl (33)
Czene, K (33)
Schmidt, MK (33)
Mannermaa, Arto (33)
Pharoah, Paul D. P. (33)
Bolla, Manjeet K. (33)
visa färre...
Lärosäte
Uppsala universitet (52)
Lunds universitet (39)
Karolinska Institutet (38)
Umeå universitet (26)
Göteborgs universitet (6)
Stockholms universitet (6)
visa fler...
Linköpings universitet (6)
Naturhistoriska riksmuseet (2)
Kungliga Tekniska Högskolan (1)
Örebro universitet (1)
Jönköping University (1)
Högskolan i Skövde (1)
Chalmers tekniska högskola (1)
visa färre...
Språk
Engelska (103)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (84)
Naturvetenskap (15)
Samhällsvetenskap (3)
Teknik (1)
Lantbruksvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy