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Melin, Beatrice S.
Alternative names
Publications (10 of 166) Show all publications
Berntsson, S. G., Merrell, R. T., Amirian, E. S., Armstrong, G. N., Lachance, D., Smits, A., . . . Melin, B. S. (2018). Glioma-related seizures in relation to histopathological subtypes: a report from the glioma international case-control study. Journal of Neurology, 265(6), 1432-1442
Open this publication in new window or tab >>Glioma-related seizures in relation to histopathological subtypes: a report from the glioma international case-control study
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2018 (English)In: Journal of Neurology, ISSN 0340-5354, E-ISSN 1432-1459, Vol. 265, no 6, p. 1432-1442Article in journal (Refereed) Published
Abstract [en]

Background: The purpose of this study was to evaluate the distribution of glioma-related seizures and seizure control at the time of tumor diagnosis with respect to tumor histologic subtypes, tumor treatment and patient characteristics, and to compare seizure history preceding tumor diagnosis (or study enrollment) between glioma patients and healthy controls.

Methods: The Glioma International Case Control study (GICC) risk factor questionnaire collected information on demographics, past medical/medication history, and occupational history. Cases from eight centers were also asked detailed questions on seizures in relation to glioma diagnosis; cases (n = 4533) and controls (n = 4171) were also asked about seizures less than 2 years from diagnosis and previous seizure history more than 2 years prior to tumor diagnosis, including childhood seizures.

Results: Low-grade gliomas (LGGs), particularly oligodendrogliomas/oligoastrocytomas, had the highest proportion of glioma-related seizures. Patients with low-grade astrocytoma demonstrated the most medically refractory seizures. A total of 83% of patients were using only one antiepileptic drug (AED), which was levetiracetam in 71% of cases. Gross total resection was strongly associated with reduced seizure frequency (p < 0.009). No significant difference was found between glioma cases and controls in terms of seizure occurring more than 2 years before diagnosis or during childhood.

Conclusions: Our study showed that glioma-related seizures were most common in low-grade gliomas. Gross total resection was associated with lower seizure frequency. Additionally, having a history of childhood seizures is not a risk factor ***for developing glioma-related seizures or glioma.

Place, publisher, year, edition, pages
Springer, 2018
Keywords
Observational study (cohort, case-control), Epileptic seizures, Primary brain tumor, Glioma-related seizures
National Category
Neurology
Identifiers
urn:nbn:se:umu:diva-150883 (URN)10.1007/s00415-018-8857-0 (DOI)000434462300023 ()29687214 (PubMedID)2-s2.0-85045844511 (Scopus ID)
Available from: 2018-08-31 Created: 2018-08-31 Last updated: 2018-08-31Bibliographically approved
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
Ward, H. A., Gayle, A., Jakszyn, P., Merritt, M., Melin, B., Freisling, H., . . . Cross, A. J. (2018). Meat and haem iron intake in relation to glioma in the European Prospective Investigation into Cancer and Nutrition study. European Journal of Cancer Prevention, 27(4), 379-383
Open this publication in new window or tab >>Meat and haem iron intake in relation to glioma in the European Prospective Investigation into Cancer and Nutrition study
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2018 (English)In: European Journal of Cancer Prevention, ISSN 0959-8278, E-ISSN 1473-5709, Vol. 27, no 4, p. 379-383Article in journal (Refereed) Published
Abstract [en]

Diets high in red or processed meat have been associated positively with some cancers, and several possible underlying mechanisms have been proposed, including iron-related pathways. However, the role of meat intake in adult glioma risk has yielded conflicting findings because of small sample sizes and heterogeneous tumour classifications. The aim of this study was to examine red meat, processed meat and iron intake in relation to glioma risk in the European Prospective Investigation into Cancer and Nutrition study. In this prospective cohort study, 408751 individuals from nine European countries completed demographic and dietary questionnaires at recruitment. Multivariable Cox proportional hazards models were used to examine intake of red meat, processed meat, total dietary iron and haem iron in relation to incident glioma. During an average follow-up of 14.1 years, 688 incident glioma cases were diagnosed. There was no evidence that any of the meat variables (red, processed meat or subtypes of meat) or iron (total or haem) were associated with glioma; results were unchanged when the first 2 years of follow-up were excluded. This study suggests that there is no association between meat or iron intake and adult glioma. This is the largest prospective analysis of meat and iron in relation to glioma and as such provides a substantial contribution to a limited and inconsistent literature.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2018
Keywords
brain cancer, dietary iron, European Prospective Investigation into Cancer and Nutrition, glioma, haem iron, N-nitroso compounds, processed meat, red meat
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-150758 (URN)10.1097/CEJ.0000000000000331 (DOI)000435653600014 ()27845960 (PubMedID)
Available from: 2018-08-31 Created: 2018-08-31 Last updated: 2018-08-31Bibliographically 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, 143(6), 1335-1347
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 1097-0215, Vol. 143, no 6, p. 1335-1347Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
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)000441128700007 ()29667176 (PubMedID)
Available from: 2018-05-23 Created: 2018-05-23 Last updated: 2018-09-13Bibliographically approved
Ostrom, Q. T., Kinnersley, B., Wrensch, M. R., Eckel-Passow, J. E., Armstrong, G., Rice, T., . . . Barnholtz-Sloan, J. S. S. (2018). Sex-specific glioma genome-wide association study identifies new risk locus at 3p21.31 in females, and finds sex-differences in risk at 8q24.21. Scientific Reports, 8, Article ID 7352.
Open this publication in new window or tab >>Sex-specific glioma genome-wide association study identifies new risk locus at 3p21.31 in females, and finds sex-differences in risk at 8q24.21
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2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 7352Article in journal (Refereed) Published
Abstract [en]

Incidence of glioma is approximately 50% higher in males. Previous analyses have examined exposures related to sex hormones in women as potential protective factors for these tumors, with inconsistent results. Previous glioma genome-wide association studies (GWAS) have not stratified by sex. Potential sex-specific genetic effects were assessed in autosomal SNPs and sex chromosome variants for all glioma, GBM and non-GBM patients using data from four previous glioma GWAS. Datasets were analyzed using sex-stratified logistic regression models and combined using meta-analysis. There were 4,831 male cases, 5,216 male controls, 3,206 female cases and 5,470 female controls. A significant association was detected at rs11979158 (7p11.2) in males only. Association at rs55705857 (8q24.21) was stronger in females than in males. A large region on 3p21.31 was identified with significant association in females only. The identified differences in effect of risk variants do not fully explain the observed incidence difference in glioma by sex.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2018
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-150697 (URN)10.1038/s41598-018-24580-z (DOI)000431737300038 ()29743610 (PubMedID)
Available from: 2018-09-06 Created: 2018-09-06 Last updated: 2018-09-06Bibliographically approved
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
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