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Beskow, Anna H.
Alternative names
Publications (9 of 9) Show all publications
Baron, T., Beskow, A. H., James, S. K. & Lindahl, B. (2019). Biobank linked to SWEDEHEART quality registry-routine blood sample collection opens new opportunities for cardiovascular research. Upsala Journal of Medical Sciences, 124(1), 12-15
Open this publication in new window or tab >>Biobank linked to SWEDEHEART quality registry-routine blood sample collection opens new opportunities for cardiovascular research
2019 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 124, no 1, p. 12-15Article in journal (Refereed) Published
Abstract [en]

High-quality biobanking within routine health services, through the use of existing health-care practices and infrastructure, with respect to safety and integrity of patients in line with the Swedish Biobank Act, enables large-scale collection of biological material at reasonable costs. Complementing the extensive information on myocardial infarction patients from a national registry gives unique opportunities for research focusing on better understanding of cardiovascular disease occurrence and prognosis, developing of new diagnostic methods, and personalized treatments with greater efficacy and fewer side effects.

Keywords
Biobank, SWEDEHEART, cardiovascular research, quality registry
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-374224 (URN)10.1080/03009734.2018.1498957 (DOI)000461811100004 ()30251587 (PubMedID)
Available from: 2019-01-18 Created: 2019-01-18 Last updated: 2019-04-17Bibliographically approved
Beskow, A. H. (2019). Uppsala Biobank-the development of a biobank organization in a local, regional, and national setting. Upsala Journal of Medical Sciences, 124(1), 6-8
Open this publication in new window or tab >>Uppsala Biobank-the development of a biobank organization in a local, regional, and national setting
2019 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 124, no 1, p. 6-8Article in journal (Refereed) Published
Abstract [en]

A biobank is generally in an international setting considered as a sample collection with linked data. In Sweden we have a lot of sample collections, but the definition of a biobank has changed, and it has become an organization that administrates many sample collections as well as an infrastructure to support research. Uppsala Biobank was started in September 2008 as a joint biobank organization between Uppsala County Council and Uppsala University. At the start there were 138 registered biobanks in Uppsala for these two principals. The decision was to have only one biobank, where all previous biobanks would be transformed to be sample collections. Uppsala Biobank has gone from the wish to centralize biobanking administration to be a research infrastructure, a national model for hospital-integrated biobanking, a support structure for biobanking activities in the health care region, and the local competence center for all biobank issues in Uppsala.

Place, publisher, year, edition, pages
TAYLOR & FRANCIS LTD, 2019
Keywords
Biobank, cancer, infrastructure, organization
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-381203 (URN)10.1080/03009734.2018.1547992 (DOI)000461811100002 ()30706759 (PubMedID)
Available from: 2019-04-10 Created: 2019-04-10 Last updated: 2019-04-10Bibliographically approved
Glimelius, B., Melin, B., Enblad, G., Alafuzoff, I., Beskow, A. H., Ahlström, H., . . . Sjöblom, T. (2018). U-CAN: a prospective longitudinal collection of biomaterials and clinical information from adult cancer patients in Sweden.. Acta Oncologica, 57(2), 187-194
Open this publication in new window or tab >>U-CAN: a prospective longitudinal collection of biomaterials and clinical information from adult cancer patients in Sweden.
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2018 (English)In: Acta Oncologica, ISSN 0284-186X, E-ISSN 1651-226X, Vol. 57, no 2, p. 187-194Article in journal (Refereed) Published
Abstract [en]

Background: Progress in cancer biomarker discovery is dependent on access to high-quality biological materials and high-resolution clinical data from the same cases. To overcome current limitations, a systematic prospective longitudinal sampling of multidisciplinary clinical data, blood and tissue from cancer patients was therefore initiated in 2010 by Uppsala and Umeå Universities and involving their corresponding University Hospitals, which are referral centers for one third of the Swedish population.

Material and Methods: Patients with cancer of selected types who are treated at one of the participating hospitals are eligible for inclusion. The healthcare-integrated sampling scheme encompasses clinical data, questionnaires, blood, fresh frozen and formalin-fixed paraffin-embedded tissue specimens, diagnostic slides and radiology bioimaging data.

Results: In this ongoing effort, 12,265 patients with brain tumors, breast cancers, colorectal cancers, gynecological cancers, hematological malignancies, lung cancers, neuroendocrine tumors or prostate cancers have been included until the end of 2016. From the 6914 patients included during the first five years, 98% were sampled for blood at diagnosis, 83% had paraffin-embedded and 58% had fresh frozen tissues collected. For Uppsala County, 55% of all cancer patients were included in the cohort.

Conclusions: Close collaboration between participating hospitals and universities enabled prospective, longitudinal biobanking of blood and tissues and collection of multidisciplinary clinical data from cancer patients in the U-CAN cohort. Here, we summarize the first five years of operations, present U-CAN as a highly valuable cohort that will contribute to enhanced cancer research and describe the procedures to access samples and data.

National Category
Cancer and Oncology Urology and Nephrology Clinical Laboratory Medicine
Research subject
Pathology
Identifiers
urn:nbn:se:uu:diva-325565 (URN)10.1080/0284186X.2017.1337926 (DOI)000423473200003 ()28631533 (PubMedID)
Funder
Swedish Cancer Society
Available from: 2017-06-26 Created: 2017-06-26 Last updated: 2019-03-29Bibliographically approved
Baron, T., Beskow, A., James, S. & Lindahl, B. (2013). Biobank kopplad till Swedeheart en resurs för framtida forskning: Erfarenheter av insamling av blodprov i hjärtsjukvården i Uppsala. Läkartidningen, 110, CF43
Open this publication in new window or tab >>Biobank kopplad till Swedeheart en resurs för framtida forskning: Erfarenheter av insamling av blodprov i hjärtsjukvården i Uppsala
2013 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, p. CF43-Article in journal (Refereed) Published
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-241182 (URN)
Note

[Biobank linked to Swedeheart, a resource for future research]

Available from: 2015-01-08 Created: 2015-01-08 Last updated: 2019-04-17Bibliographically approved
Engelmark, M. T., Ivansson, E. L., Magnusson, J. J., Gustavsson, I. M., Beskow, A. H., Magnusson, P. K. E. & Gyllensten, U. B. (2006). Identification of susceptibility loci for cervical carcinoma by genome scan of affected sib-pairs. Human Molecular Genetics, 15(22), 3351-3360
Open this publication in new window or tab >>Identification of susceptibility loci for cervical carcinoma by genome scan of affected sib-pairs
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2006 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 15, no 22, p. 3351-3360Article in journal (Refereed) Published
Abstract [en]

Cervical cancer is caused by a combination of environmental and genetic risk factors. Infection by oncogenic types of human papillomavirus is recognized as the major environmental risk factor and epidemiological studies indicate that host genetic factors predispose to disease development. A number of genetic susceptibility factors have been proposed, but with exception of the human leukocyte antigen CHLA, class II, have not shown consistent results among studies. We have performed the first genomewide linkage scan using 278 affected sib-pairs to identify loci involved in susceptibility to cervical cancer. A two-step qualitative non-parametric linkage analysis using 387 microsatellites with an average spacing of 10.5 cM revealed excess allelic sharing at nine regions on eight chromosomes. These regions were further analysed with 125 markers to increase the map density to 1.28 cM. Nominal significant linkage was found for three of the nine loci [9q32 (maximum lod-score, MLS) =1.95, P < 0.002), 12q24 (MLS=1.25, P < 0.015) and 16q24 (MLS=1.35, P < 0.012)]. These three regions have previously been connected to human cancers that share characteristics with cervical carcinoma, such as esophageal cancer and Hodgkin's lymphoma. A number of candidate genes involved in defence against viral infections, immune response and tumour suppression are found in these regions. One such gene is the thymic stromal co-transporter (TSCOT). Analyses of TSCOT single nucleotide polymorphisms further strengthen the linkage to this region (MLS=2.40, P < 0.001). We propose that the 9q32 region contains susceptibility locus for cervical cancer and that TSCOT is a candidate gene potentially involved in the genetic predisposition to this disease.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-10741 (URN)10.1093/hmg/ddl411 (DOI)000241629900009 ()17035246 (PubMedID)
Available from: 2007-04-23 Created: 2007-04-23 Last updated: 2017-12-11Bibliographically approved
Beskow, A. H., Moberg, M. & Gyllensten, U. B. (2005). HLA class II allele control of HPV load in carcinoma in situ of the cervix uteri.. Int J Cancer, 117(3), 510-4
Open this publication in new window or tab >>HLA class II allele control of HPV load in carcinoma in situ of the cervix uteri.
2005 (English)In: Int J Cancer, ISSN 0020-7136, Vol. 117, no 3, p. 510-4Article in journal (Refereed) Published
Keywords
Adult, Cervical Intraepithelial Neoplasia/*immunology/*virology, Cohort Studies, Female, HLA-D Antigens/*genetics, Histocompatibility Testing, Humans, Middle Aged, Papillomaviridae/genetics/*isolation & purification, Patient Selection, Vaginal Smears, Viral Load
Identifiers
urn:nbn:se:uu:diva-10749 (URN)15906352 (PubMedID)
Available from: 2007-04-23 Created: 2007-04-23
Beskow, A. H., Engelmark, M. T., Magnusson, J. J. & Gyllensten, U. B. (2005). Interaction of host and viral risk factors for development of cervical carcinoma in situ. International Journal of Cancer, 117(4), 690-692
Open this publication in new window or tab >>Interaction of host and viral risk factors for development of cervical carcinoma in situ
2005 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 117, no 4, p. 690-692Article in journal (Other academic) Published
Abstract [en]

Infection by oncogenic human papillomavirus (HPV) is a necessary but not sufficient cause of cervical carcinoma. Several host genetic and viral factors have been reported to increase the risk of carcinoma development given an HPV infection. In our study, we have analysed the contribution of HPV 16 E6 sequence subtype and allelic variation at human leukocyte antigen (HLA) class II loci to the risk of developing cervical carcinoma in situ. Non-European-like HPV 16 E6 sequence subtypes were not found to be associated with an increased risk of cervical carcinoma, as compared to European-like variants. However, an association was found between the HPV 16 E6 L83V variant and the DR*04-DQ*03 haplotype. This association has been observed in several independent studies and shows that both the host HLA class II genotype and viral subtype will affect the risk of an infection progressing into cervical carcinoma.

Keywords
cervical carcinoma, HLA, HPV 16 E6
Identifiers
urn:nbn:se:uu:diva-73377 (URN)10.1002/ijc.21212 (DOI)15929080 (PubMedID)
Available from: 2005-06-02 Created: 2005-06-02 Last updated: 2017-12-14Bibliographically approved
Engelmark, M., Beskow, A., Magnusson, J., Erlich, H. & Gyllensten, U. (2004). Affected sib-pair analysis of the contribution of HLA class I and class II loci to development of cervical cancer.. Hum Mol Genet, 13(17), 1951-8
Open this publication in new window or tab >>Affected sib-pair analysis of the contribution of HLA class I and class II loci to development of cervical cancer.
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2004 (English)In: Hum Mol Genet, ISSN 0964-6906, Vol. 13, no 17, p. 1951-8Article in journal (Other academic) Published
Keywords
Cervix Neoplasms/*genetics, Cohort Studies, Comparative Study, Female, Gene Frequency, Genes; MHC Class I/*genetics, Genes; MHC Class II/*genetics, Genetic Predisposition to Disease, Genotype, Haplotypes/genetics, Humans, Research Support; Non-U.S. Gov't, Siblings, Sweden
Identifiers
urn:nbn:se:uu:diva-73379 (URN)15238505 (PubMedID)
Available from: 2005-06-02 Created: 2005-06-02
Beskow, A., Rönnholm, J., Magnusson, P. K. & Gyllensten, U. B. (2001). Susceptibility locus for epidermodysplasia verruciformis not linked to cervical cancer in situ. Hereditas, 135(1), 61-63
Open this publication in new window or tab >>Susceptibility locus for epidermodysplasia verruciformis not linked to cervical cancer in situ
2001 (English)In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 135, no 1, p. 61-63Article in journal (Refereed) Published
Abstract [en]

Cervical cancer is strongly associated with infection by oncogenic forms of human papillomavirus (HPV), mainly HPV 16 and HPV 18. The aim of this study was to test if a locus previously mapped to a region on chromosome 17 qter in patients with epidermodysplasia verucciformis (EV) and psoriasis and considered to be responsible for an increased susceptibility to HPV 5, also is linked to increased HPV susceptibility in cervical cancer in situ. We also wanted to test whether HPV 16 positivity cluster in families with cervical cancer. DNA was extracted from formalin fixed biopsies of 224 affected from 77 families diagnosed with cervical cancer in situ. Two microsatellite markers (D17S939 and D17S802) containing the locus were genotyped and linkage analysis was performed. No linkage was found to any of the two markers, neither when considering all cancer cases as affected nor when only considering HPV 16 infected cancer cases as affected in the analysis. We conclude that the susceptibility locus for HPV 5 infections associated with EV and psoriasis does not seem to affect susceptibility to HPV 16, frequently detected in cervical cancer. Also, positivity for HPV 16 did not show a significant clustering in families.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-65678 (URN)10.1111/j.1601-5223.2001.00061.x (DOI)12035615 (PubMedID)
Available from: 2005-06-01 Created: 2005-06-01 Last updated: 2017-11-28Bibliographically approved
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