APOBEC3B high expression status is associated with aggressive phenotype in Japanese breast cancers
Background The members of AID/APOBEC protein family possess cytidine deaminase activity that converts cytidine residue to uridine on DNA and RNA. Recent studies have shown the possible influence of APOBEC3B ( A3B ) as DNA mutators of breast cancer genome. However, the clinical significance of A3B ex...
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Veröffentlicht in: | Breast cancer (Tokyo, Japan) Japan), 2016-09, Vol.23 (5), p.780-788 |
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Zusammenfassung: | Background
The members of AID/APOBEC protein family possess cytidine deaminase activity that converts cytidine residue to uridine on DNA and RNA. Recent studies have shown the possible influence of
APOBEC3B
(
A3B
) as DNA mutators of breast cancer genome. However, the clinical significance of
A3B
expression in Japanese breast cancer has not been studied in detail.
Methods
Ninety-three primary breast cancer tissues (74 estrogen-receptor (ER) positive, 3 ER and HER2 positive, 6 HER2 positive, and 10 triple negative) including 37 tumor-normal pairs were assessed for
A3B
mRNA expression using quantitative real-time RT-PCR. We analyzed the relation between
A3B
expression, mutation analysis of
TP53
and
PIK3CA
by direct sequencing, polymorphic
A3B
deletion allele and human papillomavirus (HPV) infection in tumors.
Results
A3B
mRNA was overexpressed in tumors compared with normal tissue. Patients with high
A3B
expression were associated with subtype and progression of lymph node metastasis and pathological nuclear grade. However, the expression was not related to any other clinicopathological factors, including mutation of
TP53
and
PIK3CA
, polymorphic
A3B
deletion allele, HPV infection and survival time.
Conclusion
The expression of
A3B
in breast cancer was higher than in non-cancerous tissues and was related to the lymph node metastasis and nuclear grade, which are reliable aggressive phenotype markers in breast cancer. Evaluation of
A3B
expression in tumor may be a marker for breast cancer with malignant potential. |
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ISSN: | 1340-6868 1880-4233 |
DOI: | 10.1007/s12282-015-0641-8 |