BackgroundGenetic variations in key DNA repair genes may influence DNA repair capacity, DNA damage and breast carcinogenesis. The current study aimed to estimate the association of APEX1 and OGG1 polymorphisms with the risk of breast cancer development.MethodsA total of 518 patients with histopathologically confirmed breast cancer and 921 region- and age-matched cancer-free controls were genotyped for the APEX1 polymorphisms rs3136817 and rs1130409 and the OGG1 polymorphisms rs1052133 and rs2072668 using a QuantStudio™ 12 K Flex Real-Time PCR System.ResultsThe rs3136817 heterozygous TC genotype along with the rs3136817 dominant model (TC + CC) was strongly associated with breast cancer susceptibility (odds ratio [OR] = 0.670, 95% confidence interval [95% CI]: 0.513 - 0.873, P = 0.003; OR = 0.682, 95% CI: 0.526 - 0.883, P = 0.004, respectively). No significant associations were observed among rs1130409, rs1052133, rs2072668 and breast cancer risk. Furthermore, an allele combination analysis revealed that APEX1 haplotypes containing C-T (alleles rs3136817 and rs1130409) conferred a significantly lower risk (corrected P < 0.001).ConclusionThis research is the latest report showing that an APEX1 rs3136817 heterozygous genotype may have a positive influence on DNA repair capacity in patients with breast cancer and thus may have a potential protective effect for Chinese Han women.Electronic supplementary materialThe online version of this article (10.1186/s12881-018-0578-9) contains supplementary material, which is available to authorized users.

Background. Axillary lymph node (ALN) staging is the most effective method to evaluate the condition of patients with breast cancer, their choice of treatment options, and prognosis. The sentinel lymph node (SLN) status assessment is the key to sentinel lymph node biopsy (SLNB) in patients with breast cancer. The choice of tracer and tracer injection sites affects SLNB. Objective. This study mainly analyzes the best tracer for SLNB and the best choice of tracer injection site. Methods. A total of 165 breast cancer patients who underwent SLNB were selected and injected with methylene blue or 99mTc-labeled sodium phytate or nanocarbon 20 min before biopsy. The number of SLNs detected by different tracers in different injection sites such as peritumoral tissue (PT) and subareolar area (SA) was counted, and the sensitivity, specificity, and positive/negative prediction rates were recorded and compared. Results. The detection success rate, average detection number of SLNs, and detection accuracy of the nanocarbon tracer were higher than the other two. The detection sensitivity, specificity, and positive and negative prediction rates of nanocarbon for SLNB were also higher than those of the other two tracers. When comparing the performance of tracers in different injection sites, it was found that the detection of three tracers injected in the SA was better than the injection in the PT. Conclusion. For women with early-stage breast cancer, nanocarbon can be used as the preferred tracer for SLNB to determine the status of the patient’s ALNs, and the areola area can be used as the best injection site.

AimThe aim of this study was to assess the sentinel lymph node (SLN) detection rate and accuracy of 99mTc-labeled sodium phytate and stannous chloride (99mTc-PHY) injection versus 99mTc-labeled sulfur colloid (99mTc-SC) injection in sentinel lymph node biopsy (SLNB) in patients with early stage breast cancer.MethodsA total of 146 consecutive female patients with early stage breast cancer were recruited in this open-labeled, randomized, controlled study. SLNB was conducted on all patients, and 99mTc-PHY or 99mTc-SC was used as the radioactive agent (RA). Axillary lymph node dissections were performed in all patients post SLN dissections.ResultsThe detection rate of 99mTc-PHY group was higher compared with that of 99mTc-SC group (p=0.023), but no difference in the detection rate by dye alone (p=0.190) or by RAs alone (p=0.615) was found between the two groups, and the number of identified SLNs (p=0.100), number of identified SLNs by dye alone (p=0.161), and number of identified SLNs by RA alone (p=0.242) were similar between the two groups. In addition, the sensitivity, specificity, false-negative rate, false-positive rate, and accuracy rate of SLNB showed no difference between 99mTc-PHY and 99mTc-SC groups (sensitivity: p=0.645; specificity: p=0.511; false-negative rate: p=0.645; false-positive rate: p=0.511; accuracy rate: p=0.464).ConclusionOur study revealed that 99mTc-PHY was qualified to be a convincing radiopharmaceutical in SLNB.

<b><i>Introduction:</i></b> In recent years, the regulatory activities of long noncoding RNAs have received increasing attention as an important research focus. This study aimed to characterize the expression and detailed roles of TTC39A antisense RNA 1 (TTC39A-AS1) in breast cancer (BC), in addition to concentrating on its downstream mechanisms. <b><i>Methods:</i></b> Quantitative RT-PCR was performed to determine the expression levels of TTC39A-AS1, microRNA-483-3p (miR-483-3p), and metastasis-associated gene 2 (MTA2). Further, the detailed functions of TTC39A-AS1 in BC cells were confirmed using the Cell Counting Kit 8 assay, flow cytometric analysis, and Transwell cell migration and invasion assays. The targeting relationship between TTC39A-AS1, miR-483-3p, and MTA2 in BC was predicted via bioinformatics analysis and further confirmed by performing the luciferase reporter assay and RNA immunoprecipitation. <b><i>Results:</i></b> TTC39A-AS1 was present in high levels in BC; this result was confirmed in our sample cohort and The Cancer Genome Atlas database. Patients with BC with a high level of TTC39A-AS1 had a shorter overall survival than those with a low level of TTC39A-AS1. Functionally, the absence of TTC39A-AS1 accelerated cell apo­ptosis but retained cell proliferation, migration, and invasion. Mechanistically, TTC39A-AS1 functioned as a competing endogenous RNA in BC by sponging miR-483-3p and thereby indirectly increasing MTA2 expression. Finally, rescue experiments revealed that the tumor-inhibiting actions of TTC39A-AS1 knockdown on the malignant characteristics of BC cells could be reversed by inhibiting miR-483-3p or upregulating MTA2. <b><i>Conclusion:</i></b> The newly identified TTC39A-AS1/miR-483-3p/MTA2 pathway was revealed to be a critical regulator in the tumorigenicity of BC, possibly offering a novel therapeutic direction for the anticancer treatment of BC.