| Title |
Effect of genetic variants and traits related to glucose metabolism and their interaction with obesity on breast and colorectal cancer risk among postmenopausal women
|
|---|---|
| Published in |
BMC Cancer, April 2017
|
| DOI | 10.1186/s12885-017-3284-7 |
| Pubmed ID | |
| Authors |
Su Yon Jung, Eric M. Sobel, Jeanette C. Papp, Zuo-Feng Zhang |
| Abstract |
Impaired glucose metabolism-related genetic variants and traits likely interact with obesity and related lifestyle factors, influencing postmenopausal breast and colorectal cancer (CRC), but their interconnected pathways are not fully understood. By stratifying via obesity and lifestyles, we partitioned the total effect of glucose metabolism genetic variants on cancer risk into two putative mechanisms: 1) indirect (risk-associated glucose metabolism genetic variants mediated by glucose metabolism traits) and 2) direct (risk-associated glucose metabolism genetic variants through pathways other than glucose metabolism traits) effects. Using 16 single-nucleotide polymorphisms (SNPs) associated with glucose metabolism and data from 5379 postmenopausal women in the Women's Health Initiative Harmonized and Imputed Genome-Wide Association Studies, we retrospectively assessed the indirect and direct effects of glucose metabolism-traits (fasting glucose, insulin, and homeostatic model assessment-insulin resistance [HOMA-IR]) using two quantitative tests. Several SNPs were associated with breast cancer and CRC risk, and these SNP-cancer associations differed between non-obese and obese women. In both strata, the direct effect of cancer risk associated with the SNP accounted for the majority of the total effect for most SNPs, with roughly 10% of cancer risk due to the SNP that was from an indirect effect mediated by glucose metabolism traits. No apparent differences in the indirect (glucose metabolism-mediated) effects were seen between non-obese and obese women. It is notable that among obese women, 50% of cancer risk was mediated via glucose metabolism trait, owing to two SNPs: in breast cancer, in relation to GCKR through glucose, and in CRC, in relation to DGKB/TMEM195 through HOMA-IR. Our findings suggest that glucose metabolism genetic variants interact with obesity, resulting in altered cancer risk through pathways other than those mediated by glucose metabolism traits. |
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 67 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 67 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Master | 11 | 16% |
| Student > Bachelor | 11 | 16% |
| Other | 7 | 10% |
| Researcher | 4 | 6% |
| Student > Postgraduate | 3 | 4% |
| Other | 7 | 10% |
| Unknown | 24 | 36% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 22 | 33% |
| Nursing and Health Professions | 6 | 9% |
| Pharmacology, Toxicology and Pharmaceutical Science | 4 | 6% |
| Biochemistry, Genetics and Molecular Biology | 3 | 4% |
| Agricultural and Biological Sciences | 3 | 4% |
| Other | 4 | 6% |
| Unknown | 25 | 37% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 28 April 2017.
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#20,418,183
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Outputs from BMC Cancer
#6,523
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Outputs of similar age from BMC Cancer
#101
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