IFN-gamma and IL-12B polymorphisms in women with cervical intraepithellial neoplasia caused by human papillomavirus
The Human Papillomavirus (HPV) is a sexually transmitted organism associated with Cervical Intraepithelial Neoplasia (CIN) and cervical cancer, the second main cause of malignancy in women worldwide. The virus itself, however, is not enough to cause lesions on the cervix. Several studies suggest tha...
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Published in: | Molecular biology reports Vol. 39; no. 7; pp. 7627 - 7634 |
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Main Authors: | , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Dordrecht
Springer Netherlands
01-07-2012
Springer Nature B.V |
Subjects: | |
Online Access: | Get full text |
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Summary: | The Human Papillomavirus (HPV) is a sexually transmitted organism associated with Cervical Intraepithelial Neoplasia (CIN) and cervical cancer, the second main cause of malignancy in women worldwide. The virus itself, however, is not enough to cause lesions on the cervix. Several studies suggest that some polymorphic sites changes the cytokines levels and influence the cancer development in HPV infected patients. In this study, we evaluated the presence of functional polymorphisms at +874 (T/A)
IFNG
and +1188 (A/C)
IL
-
12B
genes in cervical smears samples from 76 healthy women and 162 women, HPV positive, with CIN lesion—CIN I (45), CIN II (55), CIN III (53) and cervical cancer (9)—in Brazilian population. There was no significant differences in genotype (
p
= 0.4192) and allele (
p
= 0.370; OR = 1.20) distributions between CIN patients and control groups on
IFNG
allelic polymorphism. Moreover, for
IL
-
12B
gene, there was a significant difference in genotype (
p
= 0.015) and allele distribution (
p
= 0.014; OR = 0.5754) between the groups. When samples were stratified according to grade of cervical lesion, the AA genotype and A allele were less frequent in the group with low-grade cervical lesions than in group with high-grade cervical lesions (
p
= 0.0036 and
p
= 0.0010; OR = 0.3819, respectively), suggesting that the C allele (mutant) may protect against the emergence of CIN lesions and its progression. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0301-4851 1573-4978 |
DOI: | 10.1007/s11033-012-1597-9 |