scholarly journals Association studies in thyroid cancer susceptibility: are we on the right track?

2011 ◽  
Vol 47 (1) ◽  
pp. R43-R58 ◽  
Author(s):  
Iñigo Landa ◽  
Mercedes Robledo

It is widely accepted that thyroid cancer is strongly determined by the individual genetic background. In this regard, it is expected that sporadic thyroid cancer is the result of multiple low- to moderate-penetrance genes interacting with each other and with the environment, thus modulating individual susceptibility. In the last years, an important number of association studies on thyroid cancer have been published, trying to determine this genetic contribution. The aim of this review is to provide a comprehensive and critical evaluation of the associations reported so far in thyroid cancer susceptibility in case–control studies performed in both non-medullary (papillary and follicular) and medullary thyroid cancers, including their potential strengths and pitfalls. We summarize the genetic variants reported to date, and stress the importance of validating the results in independent series and assessing the functional role of the associated loci.

2016 ◽  
Vol 1 (4) ◽  
pp. 89-95
Author(s):  
Jamal Jafari Nedooshan ◽  
Mohammad Forat Yazdi ◽  
Hossein Neamatzadeh ◽  
Masoud Zare Shehneh ◽  
Saeed Kargar ◽  
...  

Objective: Many published data on the association between p53 codon 72 G>C polymorphism and thyroid carcinoma risk showed inconclusive results. The aim this study was to assess the association between p53 codon 72 G>C polymorphism and thyroid cancer risk. Methods: A literature search of PubMed, EMBASE, Google scholar and Web of Science databases for case–control studies examining the association between p53 codon 72 G>C polymorphism and thyroid cancer susceptibility up October 2016 was performed. Odds ratios (OR) with 95 % confidence intervals (95 % CI) were used to assess the strength of the association. Results: A total of 12 case–control studies involving 2,062 thyroid cancer patients and 3,027 controls were included. There was a significant association between the p53 codon 72 G>C polymorphism and thyroid cancer susceptibility in the overall populations under homozygote (CC vs. GG: OR = 1.18, 95% CI 1.12-3.05, P = 0.01) and recessive model (CC vs. GC+GG: OR = 1.73, 95% CI 1.16-2.59, P = 0.007). Subgroup analysis by ethnicity showed that there was no significant association between p53 codon 72 G>C polymorphism and thyroid cancer risk in Caucasians, Asians and mixed Brazilian. No significant publication bias was observed by using Begg’s funnel plot and Egger’s test. Conclusion: Present meta-analysis indicated that the p53 codon 72 G>C polymorphism may be associated with thyroid cancer risk. However, more studies with large sample size are needed to further assess the associations.


PLoS ONE ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. e0228187
Author(s):  
Catherine Tcheandjieu ◽  
Emilie Cordina-Duverger ◽  
Claire Mulot ◽  
Dominique Baron-Dubourdieu ◽  
Anne-Valérie Guizard ◽  
...  

2018 ◽  
Vol 64 (10) ◽  
pp. 942-951 ◽  
Author(s):  
Mohammad Zare ◽  
Jamal Jafari-Nedooshan ◽  
Mohammadali Jafari ◽  
Hossein Neamatzadeh ◽  
Seyed Mojtaba Abolbaghaei ◽  
...  

SUMMARY OBJECTIVE: There has been increasing interest in the study of the association between human mutL homolog 1 (hMLH1) gene polymorphisms and risk of colorectal cancer (CRC). However, results from previous studies are inconclusive. Thus, a meta-analysis was conducted to derive a more precise estimation of the effects of this gene. METHODS: A comprehensive search was conducted in the PubMed, EMBASE, Chinese Biomedical Literature databases until January 1, 2018. Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of the association. RESULTS: Finally, 38 case-control studies in 32 publications were identified met our inclusion criteria. There were 14 studies with 20668 cases and 19533 controls on hMLH1 −93G>A, 11 studies with 5,786 cases and 8,867 controls on 655A>G and 5 studies with 1409 cases and 1637 controls on 1151T>A polymorphism. The combined results showed that 655A>G and 1151T>A polymorphisms were significantly associated with CRC risk, whereas −93G>A polymorphism was not significantly associated with CRC risk. As for ethnicity, −93G>A and 655A>G polymorphisms were associated with increased risk of CRC among Asians, but not among Caucasians. More interestingly, subgroup analysis indicated that 655A>G might raise CRC risk in PCR-RFLP and HB subgroups. CONCLUSION: Inconsistent with previous meta-analyses, this meta-analysis shows that the hMLH1 655A>G and 1151T>A polymorphisms might be risk factors for CRC. Moreover, the −93G>A polymorphism is associated with the susceptibility of CRC in Asian population.


2009 ◽  
Vol 30 (5) ◽  
pp. 480-483 ◽  
Author(s):  
Elizabeth Cerceo ◽  
Ebbing Lautenbach ◽  
Darren R. Linkin ◽  
Warren B. Bilker ◽  
Ingi Lee

Of 57 case-control studies of antimicrobial resistance, matching was used in 23 (40%). Matched variables differed substantially across studies. Of these 23 matched case-control studies, 12 (52%) justified the use of matching, and 9 (39%) noted the strengths or limitations of this approach. Analysis that accounted for matching was performed in only 52% of the case-control studies.


2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Juhyun Song ◽  
Won Taek Lee ◽  
Kyung Ah Park ◽  
Jong Eun Lee

Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.


Nutrition ◽  
2019 ◽  
Vol 57 ◽  
pp. 5-11 ◽  
Author(s):  
Junyu Zhao ◽  
Haipeng Wang ◽  
Zhongwen Zhang ◽  
Xiaojun Zhou ◽  
Jinming Yao ◽  
...  

Author(s):  
Christopher R. Holroyd ◽  
Nicholas C. Harvey ◽  
Mark H. Edwards ◽  
Cyrus Cooper

Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.


2020 ◽  
Vol 34 (5) ◽  
pp. 703-714
Author(s):  
Xiaoping Gao ◽  
Mei Yin ◽  
Pei Yang ◽  
Xia Li ◽  
Lingling Di ◽  
...  

Background Controversies persist regarding whether exposure to cat or dog increases the risk of asthma and allergic rhinitis. Objective This meta-analysis aimed to assess the associations between exposure to cats or dogs and the development of asthma and allergic rhinitis. Methods A systematic review was performed to identify case-control and cohort studies before May 2019, evaluating the association between exposure to cats and dogs and the risk of asthma and rhinitis. The risk of bias was assessed using the Newcastle–Ottawa Scale. The odds ratios (ORs) and risk ratios (RRs) were pooled for case-control and cohort studies, respectively. Subgroup analyses were performed on prespecified study-level characteristics. Results The meta-analysis of 34 cohort studies showed a protective role of exposure to cats [RR: 0.88, 95% confidence interval (CI): 0.77–0.99] or dogs (RR: 0.85, 95% CI: 0.73–0.97) in the development of asthma. The subgroup analysis of birth cohort (RR: 0.74, 95% CI: 0.56–0.93) and children population (RR: 0.83, 95% CI: 0.70–0.96) also suggested a favorable role of exposure to dogs in the development of asthma. Pooled evidence from 13 case-control studies indicated no significant impact of cats (OR: 1.66, 95% CI: 0.39–2.94) and dogs (OR: 1.22, 95% CI: 0.92–1.52) on the development of asthma. A pooled analysis of five cohort studies showed a favorable effect of exposure to cats (RR: 0.60, 95% CI: 0.33–0.86) or dogs (RR: 0.68, 95% CI 0.44–0.90) on the development of allergic rhinitis. Conclusion The findings indicated a protective effect of exposure to cats and dogs, especially ownership, on the development of asthma and allergic rhinitis.


Hegel's Value ◽  
2021 ◽  
pp. 222-275
Author(s):  
Dean Moyar

This chapter utilizes the structure of life and valid inference to analyze the internal structure of Civil Society and the State as well as the relationship between the two institutional spheres. The chapter unpacks the passage from the Logic in which Hegel describes the State as a totality of inferences with the three terms of individuals, their needs, and the government. It is shown that the “system of needs” itself forms a quasi-living institutional system of estates centered on the division of labor. This system’s inadequacy motivates the role of the “police” and corporation as ethical agencies, forms of the Good, within Civil Society. While the move to the State overcomes the individualism of “needs,” the right of the individual remains in the dynamics of “settling one’s own account” in receiving from the State a return on one’s duty to the State. Hegel treats the State proper as a constitution consisting of three powers of government that form a totality of inferential relations that has the full structure of a living organism. The executive power is examined in detail as the particularizing element in the system.


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