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Sund, Malin
Publications (10 of 107) Show all publications
Stepien, M., Duarte-Salles, T., Fedirko, V., Floegel, A., Barupal, D. K., Rinaldi, S., . . . Jenab, M. (2016). Alteration of amino acid and biogenic amine metabolism in hepatobiliary cancers: findings from a prospective cohort study. International Journal of Cancer, 138(2), 348-360.
Open this publication in new window or tab >>Alteration of amino acid and biogenic amine metabolism in hepatobiliary cancers: findings from a prospective cohort study
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2016 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 138, no 2, 348-360 p.Article in journal (Refereed) Published
Abstract [en]

Perturbations in levels of amino acids (AA) and their derivatives are observed in hepatocellular carcinoma (HCC). Yet, it is unclear whether these alterations precede or are a consequence of the disease, nor whether they pertain to anatomically related cancers of the intrahepatic bile duct (IHBC), and gallbladder and extrahepatic biliary tract (GBTC). Circulating standard AA, biogenic amines and hexoses were measured (Biocrates AbsoluteIDQ-p180Kit) in a case-control study nested within a large prospective cohort (147 HCC, 43 IHBC and 134 GBTC cases). Liver function and hepatitis status biomarkers were determined separately. Multivariable conditional logistic regression was used to calculate odds ratios and 95% confidence intervals (OR; 95%CI) for log-transformed standardised (mean = 0, SD = 1) serum metabolite levels and relevant ratios in relation to HCC, IHBC or GBTC risk. Fourteen metabolites were significantly associated with HCC risk, of which seven metabolites and four ratios were the strongest predictors in continuous models. Leucine, lysine, glutamine and the ratio of branched chain to aromatic AA (Fischer's ratio) were inversely, while phenylalanine, tyrosine and their ratio, glutamate, glutamate/glutamine ratio, kynurenine and its ratio to tryptophan were positively associated with HCC risk. Confounding by hepatitis status and liver enzyme levels was observed. For the other cancers no significant associations were observed. In conclusion, imbalances of specific AA and biogenic amines may be involved in HCC development.

Place, publisher, year, edition, pages
John Wiley & Sons, 2016
Keyword
hepatocellular carcinoma, biliary tract cancers, prospective cohort, targeted metabolomics, amino acids
National Category
Cancer and Oncology Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-107518 (URN)10.1002/ijc.29718 (DOI)000369161200010 ()26238458 (PubMedID)
Available from: 2015-08-24 Created: 2015-08-24 Last updated: 2017-12-04Bibliographically approved
Molina-Montes, E., Sanchez, M.-J., Zamora-Ros, R., Bueno-de-Mesquita, H. B., Wark, P. A., Obon-Santacana, M., . . . Duell, E. J. (2016). Flavonoid and lignan intake and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort. International Journal of Cancer, 139(7), 1480-1492.
Open this publication in new window or tab >>Flavonoid and lignan intake and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort
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2016 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 139, no 7, 1480-1492 p.Article in journal (Refereed) Published
Abstract [en]

Despite the potential cancer preventive effects of flavonoids and lignans, their ability to reduce pancreatic cancer risk has not been demonstrated in epidemiological studies. Our aim was to examine the association between dietary intakes of flavonoids and lignans and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 865 exocrine pancreatic cancer cases occurred after 11.3 years of follow-up of 477,309 cohort members. Dietary flavonoid and lignan intake was estimated through validated dietary questionnaires and the US Department of Agriculture (USDA) and Phenol Explorer databases. Hazard ratios (HR) and 95% confidence intervals (CIs) were calculated using age, sex and center-stratified Cox proportional hazards models, adjusted for energy intake, body mass index (BMI), smoking, alcohol and diabetes status. Our results showed that neither overall dietary intake of flavonoids nor of lignans were associated with pancreatic cancer risk (multivariable-adjusted HR for a doubling of intake=1.03, 95% CI: 0.95-1.11 and 1.02; 95% CI: 0.89-1.17, respectively). Statistically significant associations were also not observed by flavonoid subclasses. An inverse association between intake of flavanones and pancreatic cancer risk was apparent, without reaching statistical significance, in microscopically confirmed cases (HR for a doubling of intake=0.96, 95% CI: 0.91-1.00). In conclusion, we did not observe an association between intake of flavonoids, flavonoid subclasses or lignans and pancreatic cancer risk in the EPIC cohort. What's new? Flavonoids and lignans found in plant-based foods are potent cancer chemopreventive agents but little is known about their effects on pancreatic cancer risk. Here the authors address this question in a large prospective epidemiological study using comprehensively derived dietary data. Their results support growing evidence that there is no association between food-based consumption of both substances with pancreatic cancer risk.

Keyword
diet, flavonoids, lignans, pancreatic cancer, cohort
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-124682 (URN)10.1002/ijc.30190 (DOI)000379977200005 ()27184434 (PubMedID)
Available from: 2016-08-22 Created: 2016-08-22 Last updated: 2017-11-28Bibliographically approved
Gaudet, M. M., Barrdahl, M., Lindstroem, S., Travis, R. C., Auer, P. L., Buring, J. E., . . . Kraft, P. (2016). Interactions between breast cancer susceptibility loci and menopausal hormone therapy in relationship to breast cancer in the Breast and Prostate Cancer Cohort Consortium. Breast Cancer Research and Treatment, 155(3), 531-540.
Open this publication in new window or tab >>Interactions between breast cancer susceptibility loci and menopausal hormone therapy in relationship to breast cancer in the Breast and Prostate Cancer Cohort Consortium
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2016 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 155, no 3, 531-540 p.Article in journal (Refereed) Published
Abstract [en]

Current use of menopausal hormone therapy (MHT) has important implications for postmenopausal breast cancer risk, and observed associations might be modified by known breast cancer susceptibility loci. To provide the most comprehensive assessment of interactions of prospectively collected data on MHT and 17 confirmed susceptibility loci with invasive breast cancer risk, a nested case-control design among eight cohorts within the NCI Breast and Prostate Cancer Cohort Consortium was used. Based on data from 13,304 cases and 15,622 controls, multivariable-adjusted logistic regression analyses were used to estimate odds ratios (OR) and 95 % confidence intervals (CI). Effect modification of current and past use was evaluated on the multiplicative scale. P values < 1.5 x 10(-3) were considered statistically significant. The strongest evidence of effect modification was observed for current MHT by 9q31-rs865686. Compared to never users of MHT with the rs865686 GG genotype, the association between current MHT use and breast cancer risk for the TT genotype (OR 1.79, 95 % CI 1.43-2.24; P (interaction) = 1.2 x 10(-4)) was less than expected on the multiplicative scale. There are no biological implications of the sub-multiplicative interaction between MHT and rs865686. Menopausal hormone therapy is unlikely to have a strong interaction with the common genetic variants associated with invasive breast cancer.

Keyword
Breast cancer, Menopausal hormone therapy, Genetic variation
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-118401 (URN)10.1007/s10549-016-3681-7 (DOI)000371055100014 ()26802016 (PubMedID)
Available from: 2016-04-13 Created: 2016-03-18 Last updated: 2017-11-30Bibliographically approved
Bakker, M. F., Peeters, P. H. M., Klaasen, V. M., Bueno-de-Mesquita, H. B., Jansen, E. H. J., Ros, M. M., . . . van Gils, C. H. (2016). Plasma carotenoids, vitamin C, tocopherols, and retinol and the risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition cohort. American Journal of Clinical Nutrition, 103(2), 454-464.
Open this publication in new window or tab >>Plasma carotenoids, vitamin C, tocopherols, and retinol and the risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition cohort
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2016 (English)In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 103, no 2, 454-464 p.Article in journal (Refereed) Published
Abstract [en]

Background: Carotenoids and vitamin C are thought to be associated with reduced cancer risk because of their antioxidative capacity.

Objective: This study evaluated the associations of plasma carotenoid, retinol, tocopherol, and vitamin C concentrations and risk of breast cancer.

Design: In a nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort, 1502 female incident breast cancer cases were included, with an oversampling of premenopausal (n = 582) and estrogen receptor-negative (ER-) cases (n = 462). Controls (n = 1502) were individually matched to cases by using incidence density sampling. Prediagnostic samples were analyzed for alpha-carotene, beta-carotene, lycopene, lutein, zeaxanthin, beta-cryptoxanthin, retinol, alpha-tocopherol, gamma-tocopherol, and 454 vitamin C. Breast cancer risk was computed according to hormone receptor status and age at diagnosis (proxy for menopausal status) by using conditional logistic regression and was further stratified by smoking status, alcohol consumption, and body mass index (BMI). All statistical tests were 2-sided.

Results: In quintile 5 compared with quintile 1, alpha-carotene (OR: 0.61; 95% CI: 0.39, 0.98) and beta-carotene (OR: 0.41; 95% CI: 0.26, 0.65) were inversely associated with risk of ER- breast tumors. The other analytes were not statistically associated with ER- breast cancer. For estrogen receptor-positive (ER+) tumors, no statistically significant associations were found. The test for heterogeneity between ER- and ER+ tumors was statistically significant only for beta-carotene (P-heterogeneity = 0.03). A higher risk of breast cancer was found for retinol in relation to ER-/progesterone receptor-negative tumors (OR: 2.37; 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06). We observed no statistically significant interaction between smoking, alcohol, or BMI and all investigated plasma analytes (based on tertile distribution).

Conclusion: Our results indicate that higher concentrations of plasma beta-carotene and alpha-carotene are associated with lower breast cancer risk of ER tumors.

Keyword
breast cancer, EPIC, antioxidants, carotenoids, plasma
National Category
Cancer and Oncology Nutrition and Dietetics
Identifiers
urn:nbn:se:umu:diva-117384 (URN)10.3945/ajcn.114.101659 (DOI)000369465400021 ()26791185 (PubMedID)
Available from: 2016-03-21 Created: 2016-02-29 Last updated: 2017-11-30Bibliographically approved
Le, N., Sund, M. & Vinci, A. (2016). Prognostic and predictive markers in pancreatic adenocarcinoma. Digestive and Liver Disease, 48(3), 223-230.
Open this publication in new window or tab >>Prognostic and predictive markers in pancreatic adenocarcinoma
2016 (English)In: Digestive and Liver Disease, ISSN 1590-8658, E-ISSN 1878-3562, Vol. 48, no 3, 223-230 p.Article, review/survey (Refereed) Published
Abstract [en]

Pancreatic ductal adenocarcinoma is characterized by a poor prognosis and a low median survival, despite improvements observed for many other solid tumours. Intensive research efforts have been undertaken during the last decades to discover new prognostic and treatment predictive biomarkers for pancreatic ductal adenocarcinoma. The mainstay of medical treatment for the disease has been the well-tolerated nucleoside analogue, gemcitabine. The only targeted agent currently used in pancreatic ductal adenocarcinoma patients is the epithelial growth factor receptor inhibitor erlotinib in combination with gemcitabine. Recently, treatment regimens such as a combination of fluorouracilleucovorin-irinotecan-oxaliplatin (FOLFIRINOX) and the combination of nab-paclitaxel with gemcitabine have been introduced for metastatic pancreatic ductal adenocarcinoma. Although these treatment regimens significantly improve survival of patients, there are no good predictive biomarkers available that can be used to identify who would benefit most from them. Therefore, the search for predictive biomarkers that would facilitate personalization of chemotherapy is highly relevant.

Keyword
Chemotherapy, Metastatic pancreatic cancer, Predictive marker, Prognostic marker
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-117805 (URN)10.1016/j.dld.2015.11.001 (DOI)000369840400002 ()
Available from: 2016-04-11 Created: 2016-03-04 Last updated: 2017-11-30Bibliographically approved
Georgoudaki, A.-M., Prokopec, K. E., Boura, V. F., Hellqvist, E., Sohn, S., Ostling, J., . . . Karlsson, M. C. I. (2016). Reprogramming Tumor-Associated Macrophages by Antibody Targeting Inhibits Cancer Progression and Metastasis. Cell reports, 15(9), 2000-2011.
Open this publication in new window or tab >>Reprogramming Tumor-Associated Macrophages by Antibody Targeting Inhibits Cancer Progression and Metastasis
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2016 (English)In: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 15, no 9, 2000-2011 p.Article in journal (Refereed) Published
Abstract [en]

Tumors are composed of multiple cell types besides the tumor cells themselves, including innate immune cells such as macrophages. Tumor-associated macrophages (TAMs) are a heterogeneous population of myeloid cells present in the tumor microenvironment (TME). Here, they contribute to immunosuppression, enabling the establishment and persistence of solid tumors as well as metastatic dissemination. We have found that the pattern recognition scavenger receptor MARCO defines a subtype of suppressive TAMs and is linked to clinical outcome. An anti-MARCO monoclonal antibody was developed, which induces anti-tumor activity in breast and colon carcinoma, as well as in melanoma models through reprogramming-TAM-populations to a pro-inflammatory phenotype and increasing tumor immunogenicity. This anti-tumor activity is dependent on the inhibitory Fc-receptor, Fc gamma RIIB, and also enhances the efficacy of checkpoint therapy. These results demonstrate that immunotherapies using antibodies designed to modify myeloid cells of the TME represent a promising mode of cancer treatment.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-123070 (URN)10.1016/j.celrep.2016.04.084 (DOI)000376887500014 ()27210762 (PubMedID)
Available from: 2016-06-27 Created: 2016-06-27 Last updated: 2017-11-28Bibliographically approved
Pang, M.-F., Georgoudaki, A.-M., Lambut, L., Johansson, J., Tabor, V., Hagikura, K., . . . Fuxe, J. (2016). TGF-beta 1-induced EMT promotes targeted migration of breast cancer cells through the lymphatic system by the activation of CCR7/CCL21-mediated chemotaxis. Oncogene, 35(6), 748-760.
Open this publication in new window or tab >>TGF-beta 1-induced EMT promotes targeted migration of breast cancer cells through the lymphatic system by the activation of CCR7/CCL21-mediated chemotaxis
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2016 (English)In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 35, no 6, 748-760 p.Article in journal (Refereed) Published
Abstract [en]

Tumor cells frequently disseminate through the lymphatic system during metastatic spread of breast cancer and many other types of cancer. Yet it is not clear how tumor cells make their way into the lymphatic system and how they choose between lymphatic and blood vessels for migration. Here we report that mammary tumor cells undergoing epithelial-mesenchymal transition (EMT) in response to transforming growth factor-beta (TGF-beta 1) become activated for targeted migration through the lymphatic system, similar to dendritic cells (DCs) during inflammation. EMT cells preferentially migrated toward lymphatic vessels compared with blood vessels, both in vivo and in 3D cultures. A mechanism of this targeted migration was traced to the capacity of TGF-beta 1 to promote CCR7/CCL21-mediated crosstalk between tumor cells and lymphatic endothelial cells. On one hand, TGF-beta 1 promoted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcription factor. Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic dissemination of EMT cells in syngeneic mice. On the other hand, TGF-beta 1 promoted CCL21 expression in lymphatic endothelial cells. CCL21 acted in a paracrine fashion to mediate chemotactic migration of EMT cells toward lymphatic endothelial cells. The results identify TGF-beta 1-induced EMT as a mechanism, which activates tumor cells for targeted, DC-like migration through the lymphatic system. Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to inhibit EMT and lymphogenic spread of tumor cells.

Place, publisher, year, edition, pages
Nature Publishing Group, 2016
National Category
Cancer and Oncology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:umu:diva-118253 (URN)10.1038/onc.2015.133 (DOI)000370331300008 ()25961925 (PubMedID)
Available from: 2016-03-17 Created: 2016-03-14 Last updated: 2017-11-30Bibliographically approved
Wadsten, C., Heyman, H., Holmqvist, M., Ahlgren, J., Lambe, M., Sund, M. & Warnberg, F. (2016). Treatment and prognosis of DCIS during twenty years. A population-based register study from a Swedish cohort. Paper presented at 38th Annual CTRC-AACR San Antonio Breast Cancer Symposium, DEC 08-12, 2015, San Antonio, TX. Cancer Research, 76.
Open this publication in new window or tab >>Treatment and prognosis of DCIS during twenty years. A population-based register study from a Swedish cohort
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2016 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76Article in journal, Meeting abstract (Other academic) Published
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-123385 (URN)10.1158/1538-7445.SABCS15-P5-17-02 (DOI)000375622403267 ()
Conference
38th Annual CTRC-AACR San Antonio Breast Cancer Symposium, DEC 08-12, 2015, San Antonio, TX
Note

Supplement: 4

Meeting Abstract: P5-17-02

Available from: 2016-07-04 Created: 2016-07-01 Last updated: 2017-11-28Bibliographically approved
Sampson, J. N., Wheeler, W. A., Yeager, M., Panagiotou, O., Wang, Z., Berndt, S. I., . . . Chatterjee, N. (2015). Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types. Journal of the National Cancer Institute, 107(12), Article ID djv279.
Open this publication in new window or tab >>Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
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2015 (English)In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 107, no 12, djv279Article in journal (Refereed) Published
Abstract [en]

Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.

Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.

Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.

Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-114630 (URN)10.1093/jnci/djv279 (DOI)000366970900015 ()26464424 (PubMedID)
Available from: 2016-02-05 Created: 2016-01-25 Last updated: 2017-11-30Bibliographically approved
Barrdahl, M., Canzian, F., Lindström, S., Shui, I., Black, A., Hoover, R. N., . . . Campa, D. (2015). Association of breast cancer risk loci with breast cancer survival. International Journal of Cancer, 137(12), 2837-2845.
Open this publication in new window or tab >>Association of breast cancer risk loci with breast cancer survival
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2015 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 137, no 12, 2837-2845 p.Article in journal (Refereed) Published
Abstract [en]

The survival of breast cancer patients is largely influenced by tumor characteristics, such as TNM stage, tumor grade and hormone receptor status. However, there is growing evidence that inherited genetic variation might affect the disease prognosis and response to treatment. Several lines of evidence suggest that alleles influencing breast cancer risk might also be associated with breast cancer survival. We examined the associations between 35 breast cancer susceptibility loci and the disease over-all survival (OS) in 10,255 breast cancer patients from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3) of which 1,379 died, including 754 of breast cancer. We also conducted a meta-analysis of almost 35,000 patients and 5,000 deaths, combining results from BPC3 and the Breast Cancer Association Consortium (BCAC) and performed in silico analyses of SNPs with significant associations. In BPC3, the C allele of LSP1-rs3817198 was significantly associated with improved OS (HRper-allele=0.70; 95% CI: 0.58-0.85; ptrend=2.84 x 10-4; HRheterozygotes=0.71; 95% CI: 0.55-0.92; HRhomozygotes=0.48; 95% CI: 0.31-0.76; p2DF=1.45 x 10-3). In silico, the C allele of LSP1-rs3817198 was predicted to increase expression of the tumor suppressor cyclin-dependent kinase inhibitor 1C (CDKN1C). In the meta-analysis, TNRC9-rs3803662 was significantly associated with increased death hazard (HRMETA =1.09; 95% CI: 1.04-1.15; ptrend=6.6 x 10-4; HRheterozygotes=0.96 95% CI: 0.90-1.03; HRhomozygotes=1.21; 95% CI: 1.09-1.35; p2DF=1.25 x 10-4). In conclusion, we show that there is little overlap between the breast cancer risk single nucleotide polymorphisms (SNPs) identified so far and the SNPs associated with breast cancer prognosis, with the possible exceptions of LSP1-rs3817198 and TNRC9-rs3803662.

What's new? Genetic factors are known to influence the risk of breast cancer, but inherited genetic variation may also affect disease prognosis and response to treatment. In this study, the we investigated whether single nucleotide polymorphisms (SNPs) that are known to be associated with breast cancer risk might also influence the survival of breast-cancer patients. While two of the investigated SNPs may influence survival, there was otherwise no indication that SNP alleles related to breast cancer risk also play a role in the survival of breast cancer patients.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2015
Keyword
breast cancer, SNP, survival, BPC3, meta-analysis
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-111131 (URN)10.1002/ijc.29446 (DOI)000362843300010 ()25611573 (PubMedID)
Available from: 2015-11-13 Created: 2015-11-06 Last updated: 2017-12-01Bibliographically approved
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