ORCID Profile
0000-0003-0118-0341
Current Organisations
University of Louisville
,
Karolinska Institutet
,
Uppsala University
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Publisher: Elsevier BV
Date: 11-2017
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814641.V1
Abstract: supplementary materials
Publisher: Springer Science and Business Media LLC
Date: 24-05-2018
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814635.V1
Abstract: Selected characteristics of the participants.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 26-02-2019
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 15-02-2019
Publisher: Springer Science and Business Media LLC
Date: 16-08-2019
Publisher: Elsevier BV
Date: 04-2020
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/0008-5472.22421684.V1
Abstract: This file contains Supplementary tables 1 - 7 and the text for Supplementary Figure 1A-D.
Publisher: Springer Science and Business Media LLC
Date: 26-06-2023
DOI: 10.1038/S41416-023-02312-Z
Abstract: Diabetes is an established risk factor for colorectal cancer. However, the mechanisms underlying this relationship still require investigation and it is not known if the association is modified by genetic variants. To address these questions, we undertook a genome-wide gene-environment interaction analysis. We used data from 3 genetic consortia (CCFR, CORECT, GECCO 31,318 colorectal cancer cases/41,499 controls) and undertook genome-wide gene-environment interaction analyses with colorectal cancer risk, including interaction tests of genetics(G)xdiabetes (1-degree of freedom d.f.) and joint testing of Gxdiabetes, G-colorectal cancer association (2-d.f. joint test) and G-diabetes correlation (3-d.f. joint test). Based on the joint tests, we found that the association of diabetes with colorectal cancer risk is modified by loci on chromosomes 8q24.11 (rs3802177, SLC30A8 – OR AA : 1.62, 95% CI: 1.34–1.96 OR AG : 1.41, 95% CI: 1.30–1.54 OR GG : 1.22, 95% CI: 1.13–1.31 p -value 3-d.f. : 5.46 × 10 −11 ) and 13q14.13 (rs9526201, LRCH1 – OR GG : 2.11, 95% CI: 1.56–2.83 OR GA : 1.52, 95% CI: 1.38–1.68 OR AA : 1.13, 95% CI: 1.06–1.21 p -value 2-d.f. : 7.84 × 10 −09 ). These results suggest that variation in genes related to insulin signaling ( SLC30A8 ) and immune function ( LRCH1 ) may modify the association of diabetes with colorectal cancer risk and provide novel insights into the biology underlying the diabetes and colorectal cancer relationship.
Publisher: Springer Science and Business Media LLC
Date: 09-06-2017
DOI: 10.1038/NCOMMS15724
Abstract: Previous genome-wide association studies (GWAS) have identified six risk loci for renal cell carcinoma (RCC). We conducted a meta-analysis of two new scans of 5,198 cases and 7,331 controls together with four existing scans, totalling 10,784 cases and 20,406 controls of European ancestry. Twenty-four loci were tested in an additional 3,182 cases and 6,301 controls. We confirm the six known RCC risk loci and identify seven new loci at 1p32.3 (rs4381241, P =3.1 × 10 −10 ), 3p22.1 (rs67311347, P =2.5 × 10 −8 ), 3q26.2 (rs10936602, P =8.8 × 10 −9 ), 8p21.3 (rs2241261, P =5.8 × 10 −9 ), 10q24.33-q25.1 (rs11813268, P =3.9 × 10 −8 ), 11q22.3 (rs74911261, P =2.1 × 10 −10 ) and 14q24.2 (rs4903064, P =2.2 × 10 −24 ). Expression quantitative trait analyses suggest plausible candidate genes at these regions that may contribute to RCC susceptibility.
Publisher: Oxford University Press (OUP)
Date: 05-05-2022
DOI: 10.1093/JNCI/DJAC094
Abstract: The use of menopausal hormone therapy (MHT) may interact with genetic variants to influence colorectal cancer (CRC) risk. We conducted a genome-wide, gene-environment interaction between single nucleotide polymorphisms and the use of any MHT, estrogen only, and combined estrogen-progestogen therapy with CRC risk, among 28 486 postmenopausal women (11 519 CRC patients and 16 967 participants without CRC) from 38 studies, using logistic regression, 2-step method, and 2– or 3–degree-of-freedom joint test. A set-based score test was applied for rare genetic variants. The use of any MHT, estrogen only and estrogen-progestogen were associated with a reduced CRC risk (odds ratio [OR] = 0.71, 95% confidence interval [CI] = 0.64 to 0.78 OR = 0.65, 95% CI = 0.53 to 0.79 and OR = 0.73, 95% CI = 0.59 to 0.90, respectively). The 2-step method identified a statistically significant interaction between a GRIN2B variant rs117868593 and MHT use, whereby MHT-associated CRC risk was statistically significantly reduced in women with the GG genotype (OR = 0.68, 95% CI = 0.64 to 0.72) but not within strata of GC or CC genotypes. A statistically significant interaction between a DCBLD1 intronic variant at 6q22.1 (rs10782186) and MHT use was identified by the 2–degree-of-freedom joint test. The MHT-associated CRC risk was reduced with increasing number of rs10782186-C alleles, showing odds ratios of 0.78 (95% CI = 0.70 to 0.87) for TT, 0.68 (95% CI = 0.63 to 0.73) for TC, and 0.66 (95% CI = 0.60 to 0.74) for CC genotypes. In addition, 5 genes in rare variant analysis showed suggestive interactions with MHT (2-sided P & 1.2 × 10−4). Genetic variants that modify the association between MHT and CRC risk were identified, offering new insights into pathways of CRC carcinogenesis and potential mechanisms involved.
Publisher: American Association for Cancer Research (AACR)
Date: 24-02-2022
DOI: 10.1158/1055-9965.EPI-21-1003
Abstract: Currently known associations between common genetic variants and colorectal cancer explain less than half of its heritability of 25%. As alcohol consumption has a J-shape association with colorectal cancer risk, nondrinking and heavy drinking are both risk factors for colorectal cancer. In idual-level data was pooled from the Colon Cancer Family Registry, Colorectal Transdisciplinary Study, and Genetics and Epidemiology of Colorectal Cancer Consortium to compare nondrinkers (≤1 g/day) and heavy drinkers (& g/day) with light-to-moderate drinkers (1–28 g/day) in GxE analyses. To improve power, we implemented joint 2df and 3df tests and a novel two-step method that modifies the weighted hypothesis testing framework. We prioritized putative causal variants by predicting allelic effects using support vector machine models. For nondrinking as compared with light-to-moderate drinking, the hybrid two-step approach identified 13 significant SNPs with pairwise r2 & 0.9 in the 10q24.2/COX15 region. When stratified by alcohol intake, the A allele of lead SNP rs2300985 has a dose–response increase in risk of colorectal cancer as compared with the G allele in light-to-moderate drinkers [OR for GA genotype = 1.11 95% confidence interval (CI), 1.06–1.17 OR for AA genotype = 1.22 95% CI, 1.14–1.31], but not in nondrinkers or heavy drinkers. Among the correlated candidate SNPs in the 10q24.2/COX15 region, rs1318920 was predicted to disrupt an HNF4 transcription factor binding motif. Our study suggests that the association with colorectal cancer in 10q24.2/COX15 observed in genome-wide association study is strongest in nondrinkers. We also identified rs1318920 as the putative causal regulatory variant for the region. The study identifies multifaceted evidence of a possible functional effect for rs1318920.
Publisher: Elsevier BV
Date: 06-2021
DOI: 10.1093/AJCN/NQAB003
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814635
Abstract: Selected characteristics of the participants.
Publisher: Springer Science and Business Media LLC
Date: 03-12-2018
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 13-01-2017
DOI: 10.1212/WNL.0000000000003617
Abstract: To determine the natural history of dissecting aneurysm (DA) and whether DA is associated with an increased recurrent stroke risk and whether type of antithrombotic drugs (antiplatelets vs anticoagulants) modifies the persistence or development of DA. We included 264 patients with extracranial cervical artery dissection (CAD) from the Cervical Artery Dissection in Stroke Study (CADISS), a multicenter prospective study that compared antiplatelet with anticoagulation therapy. Logistic regression was used to estimate age- and sex-adjusted odds ratios. We conducted a systematic review of published studies assessing the natural history of DA and stroke risk in patients with non-surgically-treated extracranial CAD with DA. In CADISS, DA was present in 24 of 264 patients at baseline. In 36 of 248 patients with follow-up neuroimaging at 3 months, 12 of the 24 baseline DAs persisted, and 24 new DA had developed. There was no association between treatment allocation (antiplatelets vs anticoagulants) and whether DA at baseline persisted at follow-up or whether new DA developed. During 12 months of follow-up, stroke occurred in 1 of 48 patients with DA and in 7 of 216 patients without DA (age- and sex-adjusted odds ratio 0.84 95% confidence interval 0.10–7.31 p = 0.88). Published studies, mainly retrospective, showed a similarly low risk of stroke and no evidence of an increased stroke rate in patients with DA. The results of CADISS provide evidence suggesting that DAs may have benign prognosis and therefore medical treatment should be considered.
Publisher: Springer Science and Business Media LLC
Date: 23-06-2019
Publisher: Public Library of Science (PLoS)
Date: 03-01-2019
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814632.V1
Abstract: Summary of G × BMI analyses using 1DF, two-step, and 3DF analyses.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769316
Abstract: Abstract Colorectal cancer risk can be impacted by genetic, environmental, and lifestyle factors, including diet and obesity. Gene-environment interactions (G × E) can provide biological insights into the effects of obesity on colorectal cancer risk. Here, we assessed potential genome-wide G × E interactions between body mass index (BMI) and common SNPs for colorectal cancer risk using data from 36,415 colorectal cancer cases and 48,451 controls from three international colorectal cancer consortia (CCFR, CORECT, and GECCO). The G × E tests included the conventional logistic regression using multiplicative terms (one degree of freedom, 1DF test), the two-step EDGE method, and the joint 3DF test, each of which is powerful for detecting G × E interactions under specific conditions. BMI was associated with higher colorectal cancer risk. The two-step approach revealed a statistically significant G×BMI interaction located within the Formin 1/Gremlin 1 ( i FMN1/GREM1 /i ) gene region (rs58349661). This SNP was also identified by the 3DF test, with a suggestive statistical significance in the 1DF test. Among participants with the CC genotype of rs58349661, overweight and obesity categories were associated with higher colorectal cancer risk, whereas null associations were observed across BMI categories in those with the TT genotype. Using data from three large international consortia, this study discovered a locus in the i FMN1/GREM1 /i gene region that interacts with BMI on the association with colorectal cancer risk. Further studies should examine the potential mechanisms through which this locus modifies the etiologic link between obesity and colorectal cancer. Significance: This gene-environment interaction analysis revealed a genetic locus in FMN1/GREM1 that interacts with body mass index in colorectal cancer risk, suggesting potential implications for precision prevention strategies. /
Publisher: American Association for Cancer Research (AACR)
Date: 09-2005
DOI: 10.1158/1055-9965.EPI-05-0218
Abstract: Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food-frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk—the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21 P value, test for trend = 0.73 P value, test for between-studies heterogeneity = 0.74]. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90 95% CI, 0.78-1.04, for the highest versus the lowest quartile P value, test for trend = 0.06 P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and in idual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814632
Abstract: Summary of G × BMI analyses using 1DF, two-step, and 3DF analyses.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/0008-5472.22421684
Abstract: This file contains Supplementary tables 1 - 7 and the text for Supplementary Figure 1A-D.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/0008-5472.22421687
Abstract: This file contains Supplementary Figure 1, parts A - D, and the figure description.
Publisher: Elsevier BV
Date: 09-2018
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2020
DOI: 10.1161/STROKEAHA.120.031707
Abstract: The risks of stroke and dementia increase steeply with age, and both are preventable. At present, the best way to preserve cognitive function is to prevent stroke. Therapeutic nihilism based on age is common and unwarranted. We address recent advances in stroke prevention that could contribute greatly to prevention of stroke and dementia at a time when the aging of the population threatens to markedly increase the incidence of both. Issues discussed: (1) old patients benefit even more from lipid-lowering therapy than do younger patients (2) patients with stiff arteries are at risk from a target systolic blood pressure mm Hg (3) the interaction of the intestinal microbiome, age, and renal function has important dietary implications for older adults (4) anticoagulation with direct-acting oral anticoagulants should be prescribed more to old patients with atrial fibrillation (5) B vitamins to lower homocysteine prevent stroke and (6) most old patients in whom intervention is warranted for carotid stenosis would benefit more from endarterectomy than from stenting. An 80-year-old person has much to lose from a stroke and should not have effective therapy withheld on account of age. Lipid-lowering therapy, a more plant-based diet, appropriate anticoagulation or antiplatelet therapy, appropriate blood pressure control, B vitamins to lower homocysteine, and judicious intervention for carotid stenosis could do much to reduce the growing burden of stroke and dementia.
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/0008-5472.C.6510986.V1
Abstract: Abstract Biliary tract cancers are rare but highly fatal with poorly understood etiology. Identifying potentially modifiable risk factors for these cancers is essential for prevention. Here we estimated the relationship between adiposity and cancer across the biliary tract, including cancers of the gallbladder (GBC), intrahepatic bile ducts (IHBDC), extrahepatic bile ducts (EHBDC), and the ulla of Vater (AVC). We pooled data from 27 prospective cohorts with over 2.7 million adults. Adiposity was measured using baseline body mass index (BMI), waist circumference, hip circumference, waist-to-hip, and waist-to-height ratios. HRs and 95% confidence intervals (95% CI) were estimated using Cox proportional hazards models adjusted for sex, education, race, smoking, and alcohol consumption with age as the time metric and the baseline hazard stratified by study. During 37,883,648 person-years of follow-up, 1,343 GBC cases, 1,194 EHBDC cases, 784 IHBDC cases, and 623 AVC cases occurred. For each 5 kg/m sup /sup increase in BMI, there were risk increases for GBC (HR = 1.27 95% CI, 1.19–1.36), IHBDC (HR = 1.32 95% CI, 1.21–1.45), and EHBDC (HR = 1.13 95% CI, 1.03–1.23), but not AVC (HR = 0.99 95% CI, 0.88–1.11). Increasing waist circumference, hip circumference, waist-to-hip ratio, and waist-to-height ratio were associated with GBC and IHBDC but not EHBDC or AVC. These results indicate that adult adiposity is associated with an increased risk of biliary tract cancer, particularly GBC and IHBDC. Moreover, they provide evidence for recommending weight maintenance programs to reduce the risk of developing these cancers. Significance: These findings identify a correlation between adiposity and biliary tract cancers, indicating that weight management programs may help minimize the risk of these diseases. /
Publisher: Springer Science and Business Media LLC
Date: 04-2006
Publisher: American Association for Cancer Research (AACR)
Date: 31-03-2023
DOI: 10.1158/0008-5472.22421687.V1
Abstract: This file contains Supplementary Figure 1, parts A - D, and the figure description.
Publisher: Wiley
Date: 09-11-2018
DOI: 10.1111/ENE.13840
Publisher: Elsevier BV
Date: 03-2012
Publisher: American Association for Cancer Research (AACR)
Date: 08-2019
DOI: 10.1158/0008-5472.CAN-19-0459
Abstract: These findings identify a correlation between adiposity and biliary tract cancers, indicating that weight management programs may help minimize the risk of these diseases.
Publisher: Wiley
Date: 04-03-2011
DOI: 10.1002/IJC.25794
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.23814641
Abstract: supplementary materials
Publisher: American Association for Cancer Research (AACR)
Date: 08-2023
DOI: 10.1158/0008-5472.C.6769316.V1
Abstract: Abstract Colorectal cancer risk can be impacted by genetic, environmental, and lifestyle factors, including diet and obesity. Gene-environment interactions (G × E) can provide biological insights into the effects of obesity on colorectal cancer risk. Here, we assessed potential genome-wide G × E interactions between body mass index (BMI) and common SNPs for colorectal cancer risk using data from 36,415 colorectal cancer cases and 48,451 controls from three international colorectal cancer consortia (CCFR, CORECT, and GECCO). The G × E tests included the conventional logistic regression using multiplicative terms (one degree of freedom, 1DF test), the two-step EDGE method, and the joint 3DF test, each of which is powerful for detecting G × E interactions under specific conditions. BMI was associated with higher colorectal cancer risk. The two-step approach revealed a statistically significant G×BMI interaction located within the Formin 1/Gremlin 1 ( i FMN1/GREM1 /i ) gene region (rs58349661). This SNP was also identified by the 3DF test, with a suggestive statistical significance in the 1DF test. Among participants with the CC genotype of rs58349661, overweight and obesity categories were associated with higher colorectal cancer risk, whereas null associations were observed across BMI categories in those with the TT genotype. Using data from three large international consortia, this study discovered a locus in the i FMN1/GREM1 /i gene region that interacts with BMI on the association with colorectal cancer risk. Further studies should examine the potential mechanisms through which this locus modifies the etiologic link between obesity and colorectal cancer. Significance: This gene-environment interaction analysis revealed a genetic locus in FMN1/GREM1 that interacts with body mass index in colorectal cancer risk, suggesting potential implications for precision prevention strategies. /
Publisher: American Association for Cancer Research (AACR)
Date: 30-05-2023
DOI: 10.1158/0008-5472.CAN-22-3713
Abstract: This gene-environment interaction analysis revealed a genetic locus in FMN1/GREM1 that interacts with body mass index in colorectal cancer risk, suggesting potential implications for precision prevention strategies.
Location: United States of America
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Susanna Larsson.