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Melin, Beatrice S.
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Publications (10 of 163) Show all publications
Disney-Hogg, L., Cornish, A. J., Sud, A., Law, P. J., Kinnersley, B., Jacobs, D. I., . . . Houlston, R. S. (2018). Impact of atopy on risk of glioma: a Mendelian randomisation study. BMC Medicine, 16, Article ID 42.
Open this publication in new window or tab >>Impact of atopy on risk of glioma: a Mendelian randomisation study
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2018 (English)In: BMC Medicine, ISSN 1741-7015, E-ISSN 1741-7015, Vol. 16, article id 42Article in journal (Refereed) Published
Abstract [en]

Background: An inverse relationship between allergies with glioma risk has been reported in several but not all epidemiological observational studies. We performed an analysis of genetic variants associated with atopy to assess the relationship with glioma risk using Mendelian randomisation (MR), an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations.

Methods: Two-sample MR was undertaken using genome-wide association study data. We used single nucleotide polymorphisms (SNPs) associated with atopic dermatitis, asthma and hay fever, IgE levels, and self-reported allergy as instrumental variables. We calculated MR estimates for the odds ratio (OR) for each risk factor with glioma using SNP-glioma estimates from 12,488 cases and 18,169 controls, using inverse-variance weighting (IVW), maximum likelihood estimation (MLE), weighted median estimate (WME) and mode-based estimate (MBE) methods. Violation of MR assumptions due to directional pleiotropy were sought using MR-Egger regression and HEIDI-outlier analysis.

Results: Under IVW, MLE, WME and MBE methods, associations between glioma risk with asthma and hay fever, self-reported allergy and IgE levels were non-significant. An inverse relationship between atopic dermatitis and glioma risk was found by IVW (OR 0.96, 95% confidence interval (CI) 0.93-1.00, P = 0.041) and MLE (OR 0.96, 95% CI 0.94-0.99, P = 0.003), but not by WME (OR 0.96, 95% CI 0.91-1.01, P = 0.114) or MBE (OR 0.97, 95% CI 0.92-1.02, P = 0.194).

Conclusions: Our investigation does not provide strong evidence for relationship between atopy and the risk of developing glioma, but findings do not preclude a small effect in relation to atopic dermatitis. Our analysis also serves to illustrate the value of using several MR methods to derive robust conclusions.

Place, publisher, year, edition, pages
BioMed Central, 2018
Keywords
Mendelian randomisation, Allergy, Cancer, Glioma, Risk
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-146437 (URN)10.1186/s12916-018-1027-5 (DOI)000427993600001 ()29540232 (PubMedID)
Available from: 2018-05-08 Created: 2018-05-08 Last updated: 2018-06-09Bibliographically approved
Disney-Hogg, L., Sud, A., Law, P. J., Cornish, A. J., Kinnersley, B., Ostrom, Q. T., . . . Houlston, R. S. (2018). Influence of obesity-related risk factors in the aetiology of glioma. British Journal of Cancer, 118(7), 1020-1027
Open this publication in new window or tab >>Influence of obesity-related risk factors in the aetiology of glioma
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2018 (English)In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 118, no 7, p. 1020-1027Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Obesity and related factors have been implicated as possible aetiological factors for the development of glioma in epidemiological observation studies. We used genetic markers in a Mendelian randomisation framework to examine whether obesity-related traits influence glioma risk. This methodology reduces bias from confounding and is not affected by reverse causation. METHODS: Genetic instruments were identified for 10 key obesity-related risk factors, and their association with glioma risk was evaluated using data from a genome-wide association study of 12,488 glioma patients and 18,169 controls. The estimated odds ratio of glioma associated with each of the genetically defined obesity-related traits was used to infer evidence for a causal relationship. RESULTS: No convincing association with glioma risk was seen for genetic instruments for body mass index, waist-to-hip ratio, lipids, type-2 diabetes, hyperglycaemia or insulin resistance. Similarly, we found no evidence to support a relationship between obesity-related traits with subtypes of glioma-glioblastoma (GBM) or non-GBM tumours. CONCLUSIONS: This study provides no evidence to implicate obesity-related factors as causes of glioma.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:umu:diva-148648 (URN)10.1038/s41416-018-0009-x (DOI)000429279300013 ()29531326 (PubMedID)2-s2.0-85043501357 (Scopus ID)
Available from: 2018-06-25 Created: 2018-06-25 Last updated: 2018-06-25Bibliographically approved
Takahashi, H., Cornish, A. J., Sud, A., Law, P. J., Kinnersley, B., Ostrom, Q. T., . . . Houlston, R. S. (2018). Mendelian randomisation study of the relationship between vitamin D and risk of glioma. Scientific Reports, 8, Article ID 2339.
Open this publication in new window or tab >>Mendelian randomisation study of the relationship between vitamin D and risk of glioma
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2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 2339Article in journal (Refereed) Published
Abstract [en]

To examine for a causal relationship between vitamin D and glioma risk we performed an analysis of genetic variants associated with serum 25-hydroxyvitamin D (25(OH) D) levels using Mendelian randomisation (MR), an approach unaffected by biases from confounding. Two-sample MR was undertaken using genome-wide association study data. Single nucleotide polymorphisms (SNPs) associated with 25(OH) D levels were used as instrumental variables (IVs). We calculated MR estimates for the odds ratio (OR) for 25(OH) D levels with glioma using SNP-glioma estimates from 12,488 cases and 18,169 controls, using inverse-variance weighted (IVW) and maximum likelihood estimation (MLE) methods. A non-significant association between 25(OH) D levels and glioma risk was shown using both the IVW (OR = 1.21, 95% confidence interval [CI] = 0.90-1.62, P = 0.201) and MLE (OR = 1.20, 95% CI = 0.98-1.48, P = 0.083) methods. In an exploratory analysis of tumour subtype, an inverse relationship between 25(OH)D levels and glioblastoma (GBM) risk was identified using the MLE method (OR = 0.62, 95% CI = 0.43-0.89, P = 0.010), but not the IVW method (OR = 0.62, 95% CI = 0.37-1.04, P = 0.070). No statistically significant association was shown between 25(OH) D levels and non-GBM glioma. Our results do not provide evidence for a causal relationship between 25(OH) D levels and all forms of glioma risk. More evidence is required to explore the relationship between 25(OH) D levels and risk of GBM.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Occupational Health and Environmental Health Medical Genetics Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-145147 (URN)10.1038/s41598-018-20844-w (DOI)000424087700011 ()29402980 (PubMedID)
Available from: 2018-03-02 Created: 2018-03-02 Last updated: 2018-06-09Bibliographically approved
Ruiz, V. Y., Praska, C. E., Armstrong, G., Kollmeyer, T. M., Yamada, S., Decker, P. A., . . . Jenkins, R. B. (2018). Molecular subtyping of tumors from patients with familial glioma. Neuro-Oncology, 20(6), 810-817
Open this publication in new window or tab >>Molecular subtyping of tumors from patients with familial glioma
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2018 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 20, no 6, p. 810-817Article in journal (Refereed) Published
Abstract [en]

Background. Single-gene mutation syndromes account for some familial glioma (FG); however, they make up only a small fraction of glioma families. Gliomas can be classified into 3 major molecular subtypes based on isocitrate dehydrogenase (IDH) mutation and 1p/19q codeletion. We hypothesized that the prevalence of molecular subtypes might differ in familial versus sporadic gliomas and that tumors in the same family should have the same molecular subtype. Methods. Participants in the FG study (Gliogene) provided samples for germline DNA analysis. Formalin-fixed, paraffin-embedded tumors were obtained from a subset of FG cases, and DNA was extracted. We analyzed tissue from 75 families, including 10 families containing a second affected family member. Copy number variation data were obtained using a first-generation Affymetrix molecular inversion probe (MIP) array. Results. Samples from 62 of 75 (83%) FG cases could be classified into the 3 subtypes. The prevalence of the molecular subtypes was: 30 (48%) IDH-wildtype, 21 (34%) IDH-mutant non-codeleted, and 11 (19%) IDH-mutant and 1p/19q codeleted. This distribution of molecular subtypes was not statistically different from that of sporadic gliomas (P = 0.54). Of 10 paired FG samples, molecular subtypes were concordant for 7 (kappa = 0.59): 3 IDH-mutant non-codeleted, 2 IDH-wildtype, and 2 IDH-mutant and 1p/19q codeleted gliomas. Conclusions. Our data suggest that within individual families, patients develop gliomas of the same molecular subtype. However, we did not observe differences in the prevalence of the molecular subtypes in FG compared with sporadic gliomas. These observations provide further insight into the distribution of molecular subtypes in FG.

Place, publisher, year, edition, pages
Oxford University Press, 2018
Keywords
familial glioma (FG), IDH-mutant and 1p/19q-codeleted, IDH-mutant non-codeleted, IDH-wild type, lecular inversion probe (MIP)
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-148725 (URN)10.1093/neuonc/nox192 (DOI)000432685600010 ()29040662 (PubMedID)2-s2.0-85047765948 (Scopus ID)
Available from: 2018-06-21 Created: 2018-06-21 Last updated: 2018-06-21Bibliographically approved
Vermeulen, R., Saberi Hosnijeh, F., Bodinier, B., Portengen, L., Liquet, B., Garrido-Manriquez, J., . . . Liao, S.-F. (2018). Pre-diagnostic blood immune markers, incidence and progression of B-cell lymphoma and multiple myeloma: univariate and functionally informed multivariate analyses. International Journal of Cancer
Open this publication in new window or tab >>Pre-diagnostic blood immune markers, incidence and progression of B-cell lymphoma and multiple myeloma: univariate and functionally informed multivariate analyses
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2018 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215Article in journal (Refereed) Epub ahead of print
Abstract [en]

Recent prospective studies have shown that dysregulation of the immune system may precede the development of B‐cell lymphomas (BCL) in immunocompetent individuals. However, to date, the studies were restricted to a few immune markers, which were considered separately. Using a nested case–control study within two European prospective cohorts, we measured plasma levels of 28 immune markers in samples collected a median of 6 years before diagnosis (range 2.01–15.97) in 268 incident cases of BCL (including multiple myeloma [MM]) and matched controls. Linear mixed models and partial least square analyses were used to analyze the association between levels of immune marker and the incidence of BCL and its main histological subtypes and to investigate potential biomarkers predictive of the time to diagnosis. Linear mixed model analyses identified associations linking lower levels of fibroblast growth factor‐2 (FGF‐2 p = 7.2 × 10−4) and transforming growth factor alpha (TGF‐α, p = 6.5 × 10−5) and BCL incidence. Analyses stratified by histological subtypes identified inverse associations for MM subtype including FGF‐2 (p = 7.8 × 10−7), TGF‐α (p = 4.08 × 10−5), fractalkine (p = 1.12 × 10−3), monocyte chemotactic protein‐3 (p = 1.36 × 10−4), macrophage inflammatory protein 1‐alpha (p = 4.6 × 10−4) and vascular endothelial growth factor (p = 4.23 × 10−5). Our results also provided marginal support for already reported associations between chemokines and diffuse large BCL (DLBCL) and cytokines and chronic lymphocytic leukemia (CLL). Case‐only analyses showed that Granulocyte‐macrophage colony stimulating factor levels were consistently higher closer to diagnosis, which provides further evidence of its role in tumor progression. In conclusion, our study suggests a role of growth‐factors in the incidence of MM and of chemokine and cytokine regulation in DLBCL and CLL.

Keywords
cytokine, lymphoma, mixed-effect modeling, multiple myeloma, multivariate models, prospective cohort, time to diagnosis
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-147948 (URN)10.1002/ijc.31536 (DOI)29667176 (PubMedID)
Available from: 2018-05-23 Created: 2018-05-23 Last updated: 2018-06-09
Glimelius, B., Melin, B., Enblad, G., Alafuzoff, I., Beskow, A., 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 Umea 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.

Place, publisher, year, edition, pages
Taylor & Francis, 2018
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-144850 (URN)10.1080/0284186X.2017.1337926 (DOI)000423473200003 ()28631533 (PubMedID)
Available from: 2018-02-23 Created: 2018-02-23 Last updated: 2018-06-09Bibliographically approved
Spaeth, F., Wibom, C., Krop, E. J. M., Johansson, A.-S., Bergdahl, I. A., Vermeulen, R. & Melin, B. (2017). Biomarker Dynamics in B-cell Lymphoma: A Longitudinal Prospective Study of Plasma Samples Up to 25 Years before Diagnosis. Cancer Research, 77(6), 1408-1415
Open this publication in new window or tab >>Biomarker Dynamics in B-cell Lymphoma: A Longitudinal Prospective Study of Plasma Samples Up to 25 Years before Diagnosis
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2017 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 77, no 6, p. 1408-1415Article in journal (Refereed) Published
Abstract [en]

The B-cell activation markers CXCL13, sCD23, (S)CD27, and sCD30 are associated with future lymphoma risk. However, a lack of information about the individual dynamics of markerdisease association hampers interpretation. In this study, we identified 170 individuals who had donated two prediagnostic blood samples before B-cell lymphoma diagnosis, along with 170 matched cancer-free controls from the Northern Sweden Health and Disease Study. Lymphoma risk associations were investigated by subtype and marker levels measured at baseline, at the time of the repeated sample, and with the rate of change in the marker level. Notably, we observed strong associations between CXCL13, sCD23, sCD27, and sCD30 and lymphoma risk in blood samples collected 15 to 25 years before diagnosis. B-cell activation marker levels increased among future lympho-ma cases over time, while remaining stable among controls. Associations between slope and risk were strongest for indolent lymphoma subtypes. We noted a marked association of sCD23 with chronic lymphocytic leukemia (ORSlope - 28, Ptrend(-)7.279 x 10 (-10)). Among aggressive lymphomas, the association between diffuse large B-cell lymphoma risk and slope was restricted to CXCL13. B-cell activation seemed to play a role in B-cell lymphoma development at early stages across different subtypes. Furthermore, B-cell activation presented differential trajectories in future lymphoma patients, mainly driven by indolent subtypes. Our results suggest a utility of these markers in predicting the presence of early occult disease and/or the screening and monitoring of indolent lymphoma in individual patients. 

Place, publisher, year, edition, pages
American Association for Cancer Research, 2017
National Category
Cancer and Oncology Hematology
Identifiers
urn:nbn:se:umu:diva-140249 (URN)10.1158/0008-5472.CAN-16-2345 (DOI)000396845600015 ()28108506 (PubMedID)
Available from: 2017-10-17 Created: 2017-10-17 Last updated: 2018-06-09Bibliographically approved
Sjöström, O., Lindholm, L. & Melin, B. (2017). Colonoscopic surveillance - a cost-effective method to prevent hereditary and familial colorectal cancer. Scandinavian Journal of Gastroenterology, 52(9), 1002-1007
Open this publication in new window or tab >>Colonoscopic surveillance - a cost-effective method to prevent hereditary and familial colorectal cancer
2017 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 52, no 9, p. 1002-1007Article in journal (Refereed) Published
Abstract [en]

Objective: Approximately 20-30% of all colorectal cancer (CRC) cases may have a familial contribution. The family history of CRC can be prominent (e.g., hereditary colorectal cancer (HCRC)) or more moderate (e.g., familial colorectal cancer (FCRC)). For family members at risk, colonoscopic surveillance is a well-established method to prevent both HCRC and FCRC, although the evidence for the exact procedures of the surveillance is limited. Surveillance can come at a high price if individuals are frequently examined, as this may result in unnecessary colonoscopies in relation to actual risk for CRC. This study analyses the cost-effectiveness of a surveillance programme implemented in the Northern Sweden Health Care Region.

Methods: The study includes 259 individuals prospectively recorded in the colonoscopic surveillance programme registry at the Cancer Prevention Clinic, Umea University Hospital. We performed a cost-utility analysis with a contrafactual design: we compared observed costs and loss of quality-adjusted life years (QALYs) due to CRC with the surveillance programme to an expected outcome without surveillance. The main measure was the incremental cost-effectiveness ratio (ICER) between surveillance and non-surveillance. Scenario analysis was used to explore uncertainty.

Results: The ICER between surveillance and non-surveillance in the base model was 3596Euro/QALY. The ICER varied from -4620Euro in the best-case scenario to 33,779Euro in the worst-case scenario.

Conclusion: Colonoscopic surveillance is a very cost-effective method to prevent HCRC and FCRC compared to current thresholds for cost-effectiveness and other cancer preventive interventions.

Keywords
Colonic disorders, health economy, endoscopy general
National Category
Public Health, Global Health, Social Medicine and Epidemiology Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-137901 (URN)10.1080/00365521.2017.1327615 (DOI)000404368000013 ()28587529 (PubMedID)
Available from: 2017-07-31 Created: 2017-07-31 Last updated: 2018-06-09Bibliographically approved
Bengtsson, D., Joost, P., Aravidis, C., Stenmark, M. A., Backman, A.-S., Melin, B., . . . Burman, P. (2017). Corticotroph Pituitary Carcinoma in a Patient With Lynch Syndrome (LS) and Pituitary Tumors in a Nationwide LS Cohort. Journal of Clinical Endocrinology and Metabolism, 102(11), 3928-3932
Open this publication in new window or tab >>Corticotroph Pituitary Carcinoma in a Patient With Lynch Syndrome (LS) and Pituitary Tumors in a Nationwide LS Cohort
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2017 (English)In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 102, no 11, p. 3928-3932Article in journal (Refereed) Published
Abstract [en]

Context: Lynch syndrome (LS) is a cancer-predisposing syndrome caused by germline mutations in genes involved in DNA mismatch repair (MMR). Patients are at high risk for several types of cancer, but pituitary tumors have not previously been reported.

Case: A 51-year-old man with LS (MSH2 mutation) and a history of colon carcinoma presented with severe Cushing disease and a locally aggressive pituitary tumor. The tumor harbored a mutation consistent with the patient’s germline mutation and displayed defect MMR function. Sixteen months later, the tumor had developed into a carcinoma with widespread liver metastases. The patient prompted us to perform a nationwide study in LS.

Nationwide Study: A diagnosis consistent with a pituitary tumor was sought for in the Swedish National Patient Registry. In 910 patients with LS, representing all known cases in Sweden, another two clinically relevant pituitary tumors were found: an invasive nonsecreting macroadenoma and a microprolactinoma (i.e., in total three tumors vs. one expected).

Conclusion: Germline mutations in MMR genes may contribute to the development and/or the clinical course of pituitary tumors. Because tumors with MMR mutations are susceptible to treatment with immune checkpoint inhibitors, we suggest to actively ask for a family history of LS in the workup of patients with aggressive pituitary tumors.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS INC, 2017
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-142255 (URN)10.1210/jc.2017-01401 (DOI)000414558500005 ()
Available from: 2017-12-08 Created: 2017-12-08 Last updated: 2018-06-09Bibliographically approved
Georgiadis, P., Liampa, I., Hebels, D. G., Krauskopf, J., Chatziioannou, A., Valavanis, I., . . . Kyrtopoulos, S. A. (2017). Evolving DNA methylation and gene expression markers of B-cell chronic lymphocytic leukemia are present in pre-diagnostic blood samples more than 10 years prior to diagnosis. BMC Genomics, 18, Article ID 728.
Open this publication in new window or tab >>Evolving DNA methylation and gene expression markers of B-cell chronic lymphocytic leukemia are present in pre-diagnostic blood samples more than 10 years prior to diagnosis
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2017 (English)In: BMC Genomics, ISSN 1471-2164, E-ISSN 1471-2164, Vol. 18, article id 728Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: B-cell chronic lymphocytic leukemia (CLL) is a common type of adult leukemia. It often follows an indolent course and is preceded by monoclonal B-cell lymphocytosis, an asymptomatic condition, however it is not known what causes subjects with this condition to progress to CLL. Hence the discovery of prediagnostic markers has the potential to improve the identification of subjects likely to develop CLL and may also provide insights into the pathogenesis of the disease of potential clinical relevance.

RESULTS: We employed peripheral blood buffy coats of 347 apparently healthy subjects, of whom 28 were diagnosed with CLL 2.0-15.7 years after enrollment, to derive for the first time genome-wide DNA methylation, as well as gene and miRNA expression, profiles associated with the risk of future disease. After adjustment for white blood cell composition, we identified 722 differentially methylated CpG sites and 15 differentially expressed genes (Bonferroni-corrected p < 0.05) as well as 2 miRNAs (FDR < 0.05) which were associated with the risk of future CLL. The majority of these signals have also been observed in clinical CLL, suggesting the presence in prediagnostic blood of CLL-like cells. Future CLL cases who, at enrollment, had a relatively low B-cell fraction (<10%), and were therefore less likely to have been suffering from undiagnosed CLL or a precursor condition, showed profiles involving smaller numbers of the same differential signals with intensities, after adjusting for B-cell content, generally smaller than those observed in the full set of cases. A similar picture was obtained when the differential profiles of cases with time-to-diagnosis above the overall median period of 7.4 years were compared with those with shorted time-to-disease. Differentially methylated genes of major functional significance include numerous genes that encode for transcription factors, especially members of the homeobox family, while differentially expressed genes include, among others, multiple genes related to WNT signaling as well as the miRNAs miR-150-5p and miR-155-5p.

CONCLUSIONS: Our findings demonstrate the presence in prediagnostic blood of future CLL patients, more than 10 years before diagnosis, of CLL-like cells which evolve as preclinical disease progresses, and point to early molecular alterations with a pathogenetic potential.

Keywords
Biomarkers of risk, Epigenomics, Molecular epidemiology, Prospective cohort, Transcriptomics, miRNA
National Category
Medical Genetics Hematology Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-139600 (URN)10.1186/s12864-017-4117-4 (DOI)000410587900002 ()28903739 (PubMedID)
Available from: 2017-09-19 Created: 2017-09-19 Last updated: 2018-06-09Bibliographically approved
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