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Sökning: WFRF:(Stampfer Meir J) > Genetic variation i...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00006302naa a2200517 4500
001oai:DiVA.org:oru-41449
003SwePub
008150114s2010 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:121239655
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-414492 URI
0247 a https://doi.org/10.1093/carcin/bgq1322 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1212396552 URI
040 a (SwePub)orud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Meyer, Mara S.u Department of Epidemiology, Harvard School of Public Health, Boston, USA4 aut
2451 0a Genetic variation in RNASEL associated with prostate cancer risk and progression
264 c 2010-06-24
264 1a Oxford, United Kingdom :b Oxford University Press,c 2010
338 a print2 rdacarrier
520 a Variation in genes contributing to the host immune response may mediate the relationship between inflammation and prostate carcinogenesis. RNASEL at chromosome 1q25 encodes ribonuclease L, part of the interferon-mediated immune response to viral infection. We therefore investigated the association between variation in RNASEL and prostate cancer risk and progression in a study of 1286 cases and 1264 controls nested within the prospective Physicians' Health Study. Eleven single-nucleotide polymorphisms (SNPs) were selected using the web-based 'Tagger' in the HapMap CEPH panel (Utah residents of Northern and Western European Ancestry). Unconditional logistic regression models assessed the relationship between each SNP and incident advanced stage (T(3)/T(4), T(0)-T(4)/M(1) and lethal disease) and high Gleason grade (>/=7) prostate cancer. Further analyses were stratified by calendar year of diagnosis. Cox proportional hazards models examined the relationship between genotype and prostate cancer-specific survival. We also explored associations between genotype and serum inflammatory biomarkers interleukin-6 (IL-6), C-reactive protein (CRP) and tumor necrosis factor-alpha receptor 2 using linear regression. Individuals homozygous for the variant allele of rs12757998 had an increased risk of prostate cancer [AA versus GG; odds ratio (OR): 1.63, 95% confidence interval (CI): 1.18-2.25), and more specifically, high-grade tumors (OR: 1.90, 95% CI: 1.25-2.89). The same genotype was associated with increased CRP (P = 0.02) and IL-6 (P = 0.05) levels. Missense mutations R462Q and D541E were associated with an increased risk of advanced stage disease only in the pre-prostate-specific antigen era. There were no significant associations with survival. The results of this study support a link between RNASEL and prostate cancer and suggest that the association may be mediated through inflammation. These novel findings warrant replication in future studies.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Cancer och onkologi0 (SwePub)302032 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cancer and Oncology0 (SwePub)302032 hsv//eng
7001 a Penney, Kathryn L.u Department of Epidemiology, Harvard School of Public Health, Boston, USA4 aut
7001 a Stark, Jennifer R.u Department of Epidemiology, Harvard School of Public Health, Boston, USA4 aut
7001 a Schumacher, Fredrick R.u Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA4 aut
7001 a Sesso, Howard D.u Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, USA4 aut
7001 a Loda, Massimou Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA4 aut
7001 a Fiorentino, Michelangelou Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA4 aut
7001 a Finn, Stephenu Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA4 aut
7001 a Flavin, Richard J.u Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA4 aut
7001 a Kurth, Tobiasu Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, USA4 aut
7001 a Price, Alkes L.u Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Biostatistics, Harvard School of Public Health, Boston, USA4 aut
7001 a Giovannucci, Edward L.u Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Nutrition, Harvard School of Public Health, Boston,USA4 aut
7001 a Fall, Katja,d 1971-u Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden4 aut0 (Swepub:oru)kafl
7001 a Stampfer, Meir J.u Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA4 aut
7001 a Ma, Jingu Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA4 aut
7001 a Mucci, Lorelei A.u Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA4 aut
7102 a Department of Epidemiology, Harvard School of Public Health, Boston, USAb Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA4 org
7730 t Carcinogenesisd Oxford, United Kingdom : Oxford University Pressg 31:9, s. 1597-603q 31:9<1597-603x 0143-3334x 1460-2180
8564 u https://academic.oup.com/carcin/article-pdf/31/9/1597/17289397/bgq132.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-41449
8564 8u https://doi.org/10.1093/carcin/bgq132
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:121239655

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