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| 2. |
- Nielsen, Kari, et al.
(författare)
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Swedish CDKN2A mutation carriers do not present the atypical mole syndrome phenotype.
- 2010
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Ingår i: Melanoma Research. - 0960-8931. ; Jul 1, s. 266-272
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Tidskriftsartikel (refereegranskat)abstract
- Phenotypic characteristics were examined in melanoma-prone southern Swedish CDKN2A (p16-113insArg/p14ARF-128insSer) mutation families, in relation to the CDKN2A genotype, nevi, clinically atypical nevi (CAN) and melanoma. Individuals from eight melanoma-prone families, with index patients carrying the CDKN2A mutation, were offered skin examinations and genotyping (CDKN2A and MC1R). Ninety-three individuals above 18 years of age participated; 29 invasive melanomas in 16 patients were recorded, all in the 38 verified CDKN2A mutation carriers. Median age at diagnosis was 36 years. Several MC1R variants were observed. A significant correlation to CAN (P=0.01) and red hair colour (P=0.02) could be confirmed in melanoma patients. A positive mutation status (CDKN2A) was correlated to one or more CAN (P=0.007) but neither to blue eyes, red hair colour, heavy freckling nor high number of nevi. For mutation carriers, median total naevus count was 24 and interquartile range was 12-47 (mean 31); whereas for the whole cohort, median total naevus count was 12 and interquartile range was 5-25 (mean 22). No participant fulfilled the atypical mole syndrome phenotype criteria. Melanomas were diagnosed only in mutation carriers, and melanoma diagnosis was statistically correlated to the presence of one or more CAN and red hair colour, supporting the possible synergistic effect of a MC1R mutation on increased risk of melanoma in patients with a CDKN2A mutation. Family history, with verified tumour diagnoses, remains an important clinical tool for finding mutation carriers for referral to clinical geneticists and simultaneous presence of CAN in probable mutation carriers might strengthen this indication. The atypical mole syndrome phenotype was, however, not verified in the studied families and total naevus counts were low.
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| 3. |
- Beral, V., et al.
(författare)
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Ovarian Cancer and Body Size : Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies
- 2012
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Ingår i: PLoS Medicine. - : PUBLIC LIBRARY SCIENCE. - 1549-1277 .- 1549-1676. ; 9:4
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Tidskriftsartikel (refereegranskat)abstract
- Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade.
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| 4. |
- Björner, Sofie, et al.
(författare)
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Epithelial and Stromal MicroRNA Signatures of Columnar Cell Hyperplasia Linking Let-7c to Precancerous and Cancerous Breast Cancer Cell Proliferation
- 2014
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Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 9:8
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Tidskriftsartikel (refereegranskat)abstract
- Columnar cell hyperplasia (CCH) is the earliest histologically identifiable breast lesion linked to cancer progression and is characterized by increased proliferation, decreased apoptosis and elevated oestrogen receptor alpha (ER alpha) expression. The mechanisms underlying the initiation of these lesions have not been clarified but might involve early and fundamental changes in cancer progression. MiRNAs are key regulators of several biological processes, acting by influencing the post-transcriptional regulation of numerous targets, thus making miRNAs potential candidates in cancer initiation. Here we have defined novel epithelial as well as stromal miRNA signatures from columnar cell hyperplasia lesions compared to normal terminal duct lobular units by using microdissection and miRNA microarrays. Let-7c were among the identified downregulated epithelial miRNAs and its functions were delineated in unique CCH derived cells and breast cancer cell line MCF-7 suggesting anti-proliferative traits potentially due to effects on Myb and ER alpha. MiR-132 was upregulated in the stroma surrounding CCH compared to stoma surrounding normal terminal duct lobular units (TDLUs), and overexpression of miR-132 in immortalized fibroblasts and in fibroblasts co-cultured with epithelial CCH cells caused substantial expression changes of genes involved in metabolism, DNA damage and cell motility. The miRNA signatures identified in CCH indicate early changes in the epithelial and stromal compartment of CCH and could represent early key alterations in breast cancer progression that potentially could be targeted in novel prevention or treatment schedules.
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| 5. |
- Lahmann, P. H., et al.
(författare)
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Measures of birth size in relation to risk of prostate cancer: the Malmo Diet and Cancer Study, Sweden
- 2012
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Ingår i: Journal of Developmental Origins of Health and Disease. - 2040-1752 .- 2040-1744. ; 3:6, s. 442-449
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Tidskriftsartikel (refereegranskat)abstract
- There is some evidence that perinatal factors, specifically birth weight (BW), may be related to the onset of prostate cancer (PRCA). This case-control study, nested within the Malmo Diet and Cancer Cohort Study, used archived birth record data from 308 incident PRCA cases diagnosed between 1991 and 2005, and 637 age-matched controls among 4781 men born (1923-1945) in Malmo and Lund, Sweden. We applied conditional logistic regression to examine the birth size-PRCA association, including tumour subtypes, adjusting for perinatal and adult factors. Compared with controls, cases had a non-significantly higher mean BW and were more likely to have high (> 4000 g) BW (21% v. 18%), but did not differ in other birth size measures, nor in mean adult body mass index. We observed a non-linear association between BW and PRCA risk. Compared with BWs between 3000 and 3500 g (reference), the fully adjusted odds ratios (OR, 95% CI) were 0.55 (0.33-0.91) for < 3000 g, 0.86 (0.61-1.22) for 3500-4000 g and 0.98 (0.64-1.50) for > 4000 g. Among men with aggressive tumours, the reduction in risk for those with BWs < 3000 g (OR 0.26, 95% CI 0.09-0.72) was stronger than the rate of risk for PRCA overall. Crude risk estimates were minimally attenuated when adjusted for gestational age, maternal age, birth order and adult factors. Birth length, head circumference and placental weight were not associated with prostate cancer. Our results indicate a protective effect of lower BW on risk of total and aggressive prostate cancer, rather than any direct effect of larger birth size.
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| 6. |
- Sjövall, Katarina, et al.
(författare)
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Sick leave of spouses to cancer patients before and after diagnosis
- 2010
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Ingår i: Acta Oncologica. - : Taylor & Francis. - 0284-186X .- 1651-226X. ; 49:4, s. 467-473
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Tidskriftsartikel (refereegranskat)abstract
- Background. The impact of cancer on spouses of cancer patients may be considerable in many aspects. Our objective was to evaluate sick leave in spouses of cancer patients before and after the diagnosis. Material and methods. Using Swedish population-based registries, we studied sick leave of spouses to patients with newly diagnosed colon, rectal, lung, prostate, or breast cancer. We identified the cancer patients via the Swedish Cancer Registry and obtained information of their spouse through linkage with the population register. We assessed the number of sick leave episodes and sick days one year before until one year after the spouses' cancer diagnosis by cross-referencing with Swedish Social Insurance Agency data. We also compared the number of sick days of spouses with the general population adjusted for age, sex and partner status. Results. In general, spouses (N=1 923) to cancer patients had an increase in the frequency of new episodes of sick leave in the months before and after the cancer diagnosis. Spouses of lung cancer patients had most sick leave episodes, and the largest number of sick days per person. In comparison to the general population, spouses in the lung cancer group also had the highest standardised sick day ratio 1.76; 95% confidence interval 1.24, 2.40. The corresponding risk for spouses in other groups of cancer was not significantly increased. Discussion. In Sweden there is often increased sick leave of spouses to cancer patients. It may be due to emotional stress and physical reactions that follow with cancer which needs to be further explored in order to provide adequate support and care.
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| 7. |
- Sjövall, Katarina, et al.
(författare)
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Sickness absence among cancer patients in the pre-diagnostic and the post-diagnostic phases of five common forms of cancer
- 2012
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Ingår i: Supportive Care in Cancer. - : Springer. - 0941-4355 .- 1433-7339. ; 20:4, s. 741-747
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Tidskriftsartikel (refereegranskat)abstract
- Purpose The purpose of this study was to observe sickness absence before and after the cancer diagnosis among cancer patients with five common forms of cancer.Methods Using cohort data, we observed sick leave in the pre- and post-diagnostic phase among patients with colon, rectal, breast, prostate, or lung cancer (n = 2,738). We also identified reference subjects without cancer (total n = 12,246) who were individually matched for age and gender for each specific cancer cohort in order to compare sickness absence between patients with a specific form of cancer and the background population without cancer.Results Lung cancer patients had the highest increase in sick days both pre- and post-diagnosis and prostate cancer patients had the lowest increase. Irrespective of the form of cancer, cancer patients had significantly more sick days in the post-diagnostic phase compared to their reference subjects, ranging from 5 (prostate cancer) to 12 times the amount of sick days (colon and lung cancer). One year post-diagnosis, less than half of the cancer patients were on sick leave, except for lung cancer patients where 63% were still on sick leave.Conclusion Sick leave among cancer patients seems related not only to the cancer diagnosis and its treatment but also to the prodromal illness in the pre-diagnostic phase, especially for forms of cancer with heavier symptom burden such as colon and lung cancer. Although cancer results in substantial increase in sick leave, it is important to acknowledge that a major part of cancer patients return to work within 1 year after the cancer diagnosis.
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| 8. |
- Sundström, Johan, Professor, 1971-, et al.
(författare)
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Risk factors for subarachnoid haemorrhage : a nationwide cohort of 950 000 adults
- 2019
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Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 48:6, s. 2018-2025
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Subarachnoid haemorrhage (SAH) is a devastating disease, with high mortality rate and substantial disability among survivors. Its causes are poorly understood. We aimed to investigate risk factors for SAH using a novel nationwide cohort consortium.METHODS: We obtained individual participant data of 949 683 persons (330 334 women) between 25 and 90 years old, with no history of SAH at baseline, from 21 population-based cohorts. Outcomes were obtained from the Swedish Patient and Causes of Death Registries.RESULTS: During 13 704 959 person-years of follow-up, 2659 cases of first-ever fatal or non-fatal SAH occurred, with an age-standardized incidence rate of 9.0 [95% confidence interval (CI) (7.4-10.6)/100 000 person-years] in men and 13.8 [(11.4-16.2)/100 000 person-years] in women. The incidence rate increased exponentially with higher age. In multivariable-adjusted Poisson models, marked sex interactions for current smoking and body mass index (BMI) were observed. Current smoking conferred a rate ratio (RR) of 2.24 (95% CI 1.95-2.57) in women and 1.62 (1.47-1.79) in men. One standard deviation higher BMI was associated with an RR of 0.86 (0.81-0.92) in women and 1.02 (0.96-1.08) in men. Higher blood pressure and lower education level were also associated with higher risk of SAH.CONCLUSIONS: The risk of SAH is 45% higher in women than in men, with substantial sex differences in risk factor strengths. In particular, a markedly stronger adverse effect of smoking in women may motivate targeted public health initiatives.
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| 9. |
- Baldetorp, Bo, et al.
(författare)
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Analysis of protein expression in pure cell nuclei populations isolated from human breast cancer tissue by DNA flow cytometric sorting.
- 2010
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Ingår i: Journal of Proteomics. - : Elsevier BV. - 1874-3919. ; 73, s. 1111-1116
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Tidskriftsartikel (refereegranskat)abstract
- In this study, cell nuclei from aneuploid breast cancer samples were sorted with respect to DNA content into pure diploid and aneuploid fractions using flow cytometry. The nuclear proteins were then separated by one-dimensional gel electrophoresis (1D-PAGE) and differences in protein expression patterns, between diploid and aneuploid nuclei from the same tumours, were compared. Using a combination of peptide finger printing and peptide identification by MALDI-TOF mass spectrometry, we identified proteins and confirmed that the proteins were of nuclear origins. The results in this study add further information to the knowledge about the breast cancer disease complexity and heterogeneity at molecular level. For some of the tumours studied different nuclei protein patterns were obtained, in the diploid respective aneuploid nuclei populations, whilst other tumours did not show these differences.
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| 10. |
- Barrett, Jennifer H., et al.
(författare)
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Genome-wide association study identifies three new melanoma susceptibility loci
- 2011
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 43:11, s. 1108-1113
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Tidskriftsartikel (refereegranskat)abstract
- We report a genome-wide association study for melanoma that was conducted by the GenoMEL Consortium. Our discovery phase included 2,981 individuals with melanoma and 1,982 study-specific control individuals of European ancestry, as well as an additional 6,426 control subjects from French or British populations, all of whom were genotyped for 317,000 or 610,000 single-nucleotide polymorphisms (SNPs). Our analysis replicated previously known melanoma susceptibility loci. Seven new regions with at least one SNP with P < 10(-5) and further local imputed or genotyped support were selected for replication using two other genome-wide studies (from Australia and Texas, USA). Additional replication came from case-control series from the UK and The Netherlands. Variants at three of the seven loci replicated at P < 10(-3): an SNP in ATM (rs1801516, overall P = 3.4 x 10(-9)), an SNP in MX2 (rs45430, P = 2.9 x 10-9) and an SNP adjacent to CASP8 (rs13016963, P = 8.6 x 10(-10)). A fourth locus near CCND1 remains of potential interest, showing suggestive but inconclusive evidence of replication (rs1485993, overall P = 4.6 x 10(-7) under a fixed-effects model and P = 1.2 x 10(-3) under a random-effects model). These newly associated variants showed no association with nevus or pigmentation phenotypes in a large British case-control series.
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