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Research article
Yashuang Zhao
Harbin Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-7425-5773
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Studies have shown that abnormal changes of specific-gene DNA methylation in leukocytes may be associated with elevated risk of cancer. However, associations between the methylation of zinc-related genes, WT1 and CA10, and breast cancer risk, and interactions between WT1, CA10 methylation and dietary zinc intake on breast cancer risk remain unknown.
Methods
The methylation of WT1, CA10 was analyzed by methylation-sensitive high-resolution-melting (MS-HRM) in a case-control study with female subjects (N = 959). Logistic regression was used to analyze the associations and propensity score (PS) method was used to adjust confounders.
Results
The results showed that WT1 hypermethylation was associated with an increased risk of breast cancer with an odds ratio (OR) of 3.069 [95% confidence interval (CI): 1.669–5.643, P < 0.001]. Subgroup analyses showed that WT1 hypermethylation was specifically associated with an elevated risk of Luminal A subtype (OR = 2.620, 95%CI: 1.107-6.200, P = 0.029) and Luminal B subtype (OR = 3.231, 95%CI: 1.339–7.796, P = 0.009). CA10 hypermethylation was associated with an increased risk of Luminal B subtype (OR = 1.798, 95%CI: 1.085–2.982, P = 0.023). Furthermore, the joint effects of methylation of WT1, CA10 and lower dietary zinc intake were associated a strongly elevated risk of breast cancer with ORs of 11.220 (95%CI: 4.057–31.032, P < 0.001) and 4.145 (95%CI: 2.717–6.324, P < 0.001), respectively.
Conclusion
The study suggested the hypermethylation of WT1 methylation in leukocytes was significantly associated with an increased risk of breast cancer. Notably, the joint effects of WT1, CA10 methylation and lower dietary zinc intake might significantly associate with breast cancer risk.
Keywords
breast cancer, CA10, WT1, DNA methylation, leukocytes, zinc
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CURRENT STATUS: Published
View the published article at BMC Cancer.
No community comments so far
Editorial decision: Accept
On 14 Jul, 2020
Reviewers invited
Invitations sent on 07 Jul, 2020
Reviewer #1 agreed
On 07 Jul, 2020
Reviewer #2 agreed
On 07 Jul, 2020
Review #1 received
Received 07 Jul, 2020
Review #2 received
Received 07 Jul, 2020
Editor assigned
On 07 Jul, 2020
Submission checks complete
On 06 Jul, 2020
Editor invited
On 06 Jul, 2020
Version 1
Posted 27 May, 2020
No comments provided
Review #1 received
Received 06 Jun, 2020
Editorial decision: Major revision
On 06 Jun, 2020
Review #2 received
Received 02 Jun, 2020
Reviewer #2 agreed
On 27 May, 2020
Editor assigned
On 17 May, 2020
Reviewers invited
Invitations sent on 17 May, 2020
Reviewer #1 agreed
On 17 May, 2020
Submission checks complete
On 16 May, 2020
Editor invited
On 16 May, 2020
First submitted
On 05 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
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See the published version of this preprint at BMC Cancer.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Yashuang Zhao
Harbin Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-7425-5773
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Cancer.
No community comments so far
Editorial decision: Accept
On 14 Jul, 2020
Reviewers invited
Invitations sent on 07 Jul, 2020
Reviewer #1 agreed
On 07 Jul, 2020
Reviewer #2 agreed
On 07 Jul, 2020
Review #1 received
Received 07 Jul, 2020
Review #2 received
Received 07 Jul, 2020
Editor assigned
On 07 Jul, 2020
Submission checks complete
On 06 Jul, 2020
Editor invited
On 06 Jul, 2020
Version 1
Posted 27 May, 2020
No comments provided
Review #1 received
Received 06 Jun, 2020
Editorial decision: Major revision
On 06 Jun, 2020
Review #2 received
Received 02 Jun, 2020
Reviewer #2 agreed
On 27 May, 2020
Editor assigned
On 17 May, 2020
Reviewers invited
Invitations sent on 17 May, 2020
Reviewer #1 agreed
On 17 May, 2020
Submission checks complete
On 16 May, 2020
Editor invited
On 16 May, 2020
First submitted
On 05 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Cancer.
Background
Studies have shown that abnormal changes of specific-gene DNA methylation in leukocytes may be associated with elevated risk of cancer. However, associations between the methylation of zinc-related genes, WT1 and CA10, and breast cancer risk, and interactions between WT1, CA10 methylation and dietary zinc intake on breast cancer risk remain unknown.
Methods
The methylation of WT1, CA10 was analyzed by methylation-sensitive high-resolution-melting (MS-HRM) in a case-control study with female subjects (N = 959). Logistic regression was used to analyze the associations and propensity score (PS) method was used to adjust confounders.
Results
The results showed that WT1 hypermethylation was associated with an increased risk of breast cancer with an odds ratio (OR) of 3.069 [95% confidence interval (CI): 1.669–5.643, P < 0.001]. Subgroup analyses showed that WT1 hypermethylation was specifically associated with an elevated risk of Luminal A subtype (OR = 2.620, 95%CI: 1.107-6.200, P = 0.029) and Luminal B subtype (OR = 3.231, 95%CI: 1.339–7.796, P = 0.009). CA10 hypermethylation was associated with an increased risk of Luminal B subtype (OR = 1.798, 95%CI: 1.085–2.982, P = 0.023). Furthermore, the joint effects of methylation of WT1, CA10 and lower dietary zinc intake were associated a strongly elevated risk of breast cancer with ORs of 11.220 (95%CI: 4.057–31.032, P < 0.001) and 4.145 (95%CI: 2.717–6.324, P < 0.001), respectively.
Conclusion
The study suggested the hypermethylation of WT1 methylation in leukocytes was significantly associated with an increased risk of breast cancer. Notably, the joint effects of WT1, CA10 methylation and lower dietary zinc intake might significantly associate with breast cancer risk.
Figure 1
Figure 2
This is a list of supplementary files associated with this preprint. Click to download.
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