scholarly journals Population-based, Case-Control-Family Design to Investigate Genetic and Environmental Influences on Melanoma Risk: Australian Melanoma Family Study

2009 ◽  
Vol 170 (12) ◽  
pp. 1541-1554 ◽  
Author(s):  
A. E. Cust ◽  
H. Schmid ◽  
J. A. Maskiell ◽  
J. Jetann ◽  
M. Ferguson ◽  
...  
2012 ◽  
Vol 131 (3) ◽  
pp. E269-E281 ◽  
Author(s):  
Anne E. Cust ◽  
Chris Goumas ◽  
Elizabeth A. Holland ◽  
Chantelle Agha-Hamilton ◽  
Joanne F. Aitken ◽  
...  

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Simon Cheah ◽  
Roger Milne ◽  
Simon Harrison ◽  
Dallas English ◽  
Graham Giles

Abstract Background Although responsible for significant mortality and morbidity, our knowledge of modifiable causes of multiple myeloma (MM) remains limited. This analysis of an Australian population-based case-control family study investigated associations between smoking and alcohol consumption and MM risk. Methods Incident cases (n = 789) of MM were recruited mainly via cancer registries in Victoria and NSW. The controls included in the analysis (n = 1,113) were either family members of cases (n = 696) or recruited as part of a similarly designed case-control family study of renal cancer (n = 417). Unconditional multivariable logistic regression was used to estimate ORs, 95% CIs and p-values for associations between alcohol- and tobacco-related exposures and risk of MM. Results Heavy drinkers of alcohol had lower MM risk compared with non-drinkers (OR = 0.68, 95% CI = 0.50 – 0.93), and there was an inverse dose-response relationship for alcohol intake (OR per 10g ethanol per day = 0.92, 95% CI: 0.86 – 0.99); there was no evidence of interaction with sex (p = 0.27). There was no evidence of association between smoking-related exposures and MM risk. Conclusions These findings extend the knowledge of MM risk factor epidemiology. Further research into the causality of the association of alcohol with MM risk and potential underlying mechanisms is recommended. Key messages We found alcohol consumption to be inversely associated with risk of multiple myeloma.


PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e108391 ◽  
Author(s):  
Li Liu ◽  
Lixia Li ◽  
Shudong Zhou ◽  
Qingwu Jiang ◽  
Sidong Chen ◽  
...  

2009 ◽  
Vol 19 (8) ◽  
pp. 560-566 ◽  
Author(s):  
Yongzhong Zhang ◽  
Xiong Guo ◽  
Zhiguang Ping ◽  
Min Yu ◽  
Xiaowei Shi ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1378
Author(s):  
Tú Nguyen-Dumont ◽  
James G. Dowty ◽  
Jason A. Steen ◽  
Anne-Laure Renault ◽  
Fleur Hammet ◽  
...  

Case-control studies of breast cancer have consistently shown that pathogenic variants in CHEK2 are associated with about a 3-fold increased risk of breast cancer. Information about the recurrent protein-truncating variant CHEK2 c.1100delC dominates this estimate. There have been no formal estimates of age-specific cumulative risk of breast cancer for all CHEK2 pathogenic (including likely pathogenic) variants combined. We conducted a population-based case-control-family study of pathogenic CHEK2 variants (26 families, 1071 relatives) and estimated the age-specific cumulative risk of breast cancer using segregation analysis. The estimated hazard ratio for carriers of pathogenic CHEK2 variants (combined) was 4.9 (95% CI 2.5–9.5) relative to non-carriers. The HR for carriers of the CHEK2 c.1100delC variant was estimated to be 3.5 (95% CI 1.02–11.6) and the HR for carriers of all other CHEK2 variants combined was estimated to be 5.7 (95% CI 2.5–12.9). The age-specific cumulative risk of breast cancer was estimated to be 18% (95% CI 11–30%) and 33% (95% CI 21–48%) to age 60 and 80 years, respectively. These findings provide important information for the clinical management of breast cancer risk for women carrying pathogenic variants in CHEK2.


2017 ◽  
Vol 117 (3) ◽  
pp. 432-438 ◽  
Author(s):  
Marcella Malavolti ◽  
Carlotta Malagoli ◽  
Catherine M. Crespi ◽  
Furio Brighenti ◽  
Claudia Agnoli ◽  
...  

AbstractGlycaemic index (GI) and glycaemic load (GL) are indicators of dietary carbohydrate quantity and quality and have been associated with increased risk of certain cancers and type 2 diabetes. Insulin resistance has been associated with increased melanoma risk. However, GI and GL have not been investigated for melanoma. We present the first study to examine the possible association of GI and GL with melanoma risk. We carried out a population-based, case–control study involving 380 incident cases of cutaneous melanoma and 719 age- and sex-matched controls in a northern Italian region. Dietary GI and GL were computed for each subject using data from a self-administered, semi-quantitative food frequency questionnaire. We computed the odds ratio (OR) for melanoma according to quintiles of distribution of GL and GL among controls. A direct association between melanoma risk and GL emerged in females (OR 2·38; 95 % CI 1·25, 4·52 for the highest v. the lowest quintile of GL score, Pfor trend 0·070) but not in males. The association in females persisted in the multivariable analysis after adjusting for several potential confounders. There was no evidence of an association between GI and melanoma risk. GL might be associated with melanoma risk in females.


2014 ◽  
Vol 5 (2) ◽  
pp. 152-158 ◽  
Author(s):  
K. P. J. Wijnands ◽  
S. A. Obermann-Borst ◽  
E. J. G. Sijbrands ◽  
M. F. Wildhagen ◽  
W. A. Helbing ◽  
...  

Hyperglycemia, dyslipidemia and hyperhomocysteinemia are associated with both adult cardiovascular disease (CVD) and having a child with a congenital heart disease (CHD). We investigated associations between CVD in grandparents and the risk of CHD in grandchildren. In a case–control family study, we obtained detailed questionnaire information on CVD and CHD in 247 families with a CHD child and 203 families without a CHD child. Grandparents with CVD or intermittent claudication (IC) were significantly associated with an increased risk for CHD in grandchildren [OR 1.39 (95% CI 1.03–1.89) and OR 2.77 (95% CI 1.02–7.56), respectively]. The risk of CHD grandchildren was particularly increased in paternal grandfathers with CVD [OR 1.85 (95% CI 1.01–3.37)]. Overall, having a grandparent with CVD increased the risk for CHD in the grandchild by 1.65 (95% CI 1.12–2.41). After adjustment for potential maternal confounders, this risk was 1.44 (95% CI 0.94–2.21). Having two or more grandparents with CVD was associated with an approximately threefold risk for CHD grandchildren [OR adjusted 2.72 (95% CI 1.08–6.89)]. Our data suggest that CVD and IC in grandparents are associated with an increased risk of having a CHD grandchild. These first findings may be explained by shared causality of derangements in metabolic pathways and are in line with the fetal origins of health and disease.


2004 ◽  
Vol 15 (8) ◽  
pp. 845-850 ◽  
Author(s):  
Yanhui Gao ◽  
Qingwu Jiang ◽  
Xuefu Zhou ◽  
Baoguo Ding ◽  
Ruhong Wang ◽  
...  

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