APOBEC3 deletion polymorphism is associated with epithelial ovarian cancer risk among Chinese women
Ovarian cancer remains the leading cause of death from gynecological malignancies and the second most common gynecological malignancy among women worldwide. However, the etiology still remains largely unknown. Previous studies identified APOBEC3 gene deletions were significantly associated with high...
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Published in | Tumor biology Vol. 35; no. 6; pp. 5723 - 5726 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Netherlands
01.06.2014
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 1010-4283 1423-0380 1423-0380 |
DOI | 10.1007/s13277-014-1758-7 |
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Summary: | Ovarian cancer remains the leading cause of death from gynecological malignancies and the second most common gynecological malignancy among women worldwide. However, the etiology still remains largely unknown. Previous studies identified
APOBEC3
gene deletions were significantly associated with higher breast cancer risk in both European and Chinese women. Considering both breast and ovarian cancers being hormonally driven and sharing multiple risk factors, we performed this case–control study to evaluate the association between
APOBEC3
deletion and epithelial ovarian cancer (EOC) risk. We analyzed the
APOBEC3
deletion in a case–control study of 2,938 Chinese women (including 1,374 EOC cases and 1,564 healthy controls). All participants were genotyped using real-time qualitative PCR (qPCR).
APOBEC3
deletion was significant associated with EOC risk, with ORs (95 % CIs) of 1.46 (1.14–1.86) associated with one copy deletion and 2.53 (0.91–7.06) associated with two copy deletion compared with subjects with no deletion (
P
for trend =1.50 × 10
−3
). Additional adjustments and stratified analyses did not change the results materially. Our data suggests that the loss genotypes of
APOBEC3
deletion predispose their carriers to EOC. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1010-4283 1423-0380 1423-0380 |
DOI: | 10.1007/s13277-014-1758-7 |