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Purpose: Surgical meshes are often used in retro-pectoral implant-based breast reconstruction (IBBR) to improve lower pole expansion. However, using of surgical meshes is associated with increased complications and costs. To solve this problem, we have adopted a modified fascia-based IBBR technique using fasciae of pectoral major, serratus anterior, and external oblique muscles to form a sling covering the lower pole of prosthesis since 2014. Methods: Data of 788 retro-pectoral IBBR cases, including 250 fascia-based IBBR cases (fascial group) and 538 traditional IBBR cases (control group), treated between 2014 and 2019 were retrospectively analyzed. The surgical outcomes of the fascial and control group were compared. The primary endpoint was the rate of post-operative complications requiring interventions. The secondary endpoint was the rate of explantation. The exploratory endpoint was the time from surgery to complication and explantation. Results: The fascial group had significantly lower rates of developing major post-operative complications (1.2 vs. 6.1%, p = 0.002) and losing prostheses (1.2 vs. 4.3%, p = 0.025), as compared with the control group. The median time from surgery to complication and explantation were 61 (range, 35–115) days and 92 (range, 77–134) days for the fascial group and 35 (range, 6–239) days and 63 (range, 23–483) days for the control group, respectively. Conclusion: Fascia-based IBBR technique had low rates of major post-operative complications and explantation. Fascia-based IBBR technique could be considered as an alternative reconstruction method in properly selected patients. [ABSTRACT FROM AUTHOR]

Toll-like receptor 3 (TLR3) is a viral sensor that induces apoptosis in response to double-stranded RNA (dsRNA). Common genetic changes in the TLR3 gene may influence breast cancer susceptibility and development. However, all of the polymorphisms in the previous study were only markers of the TLR3 gene, not causative polymorphisms. In this study, we performed a case-control study focusing on the relationship between rs5743305 (−926T>A), a single nucleotide polymorphism (SNP) in the promoter region of TLR3, and breast cancer. We found that the genetic variant rs5743305 increased the risk of breast cancer under the dominant and codominant models (dominant model: AT+AA vs TT.: OR = 1.3023, 95%CI: 1.0778–1.5736, P =.0062; codominant model: AA vs. TT: OR = 1.3919, 95%CI: 1.0177–1.9036, P =.0384; AT vs. TT: OR = 1.2799, 95%CI: 1.0475–1.5639, P =.0158) but not under the recessive model (TT vs. AT+AA, OR = 1.2387, 95%CI: 0.9197–1.6682, P =.1588). The same trends were found in the age-adjusted logistic regression study and stage 2 study. Furthermore, the electrophoretic mobility shift assay (EMSA) and luciferase reporter assay showed that rs5743305 decreased the transcriptional activity of TLR3. There was consistently reduced TLR3 mRNA and protein expression in human breast cancer samples from patients with TLR3 − 926A. Therefore, TLR3 rs5743305 increases the risk of breast cancer by decreasing the transcriptional activity of TLR3. This study may provide a better understanding of the genetic architecture underlying disease susceptibility and may advance the potential for preclinical prediction in future genetic testing. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the additional value of DKI in discriminating suspicious breast lesions on DCE-MRI, as compared with conventional DWI; and to explore connection between DKI-parameters and prognostic factors of breast cancers.Methods: The institutional review board approved this retrospective study and written informed consent was waived. Totally, 300 women (mean age, 43.2 ± 10.4 years) with suspicious breast lesions on DCE-MRI were enrolled from November 2014 to September 2019. With pathology as reference, performance of ADC, Kapp and Dapp in discriminating suspicious breast lesions were analyzed by receiver operating characteristic (ROC) analysis with area under ROC curve (AUC). The specificities of parameters were compared by Chi-square test. The ADC, Kapp and Dapp of breast cancers with different receptor status were compared using Student's t or Mann-Whitney U or Kruskal-Wallis test.Results: There were 344 suspicious breast lesions (220 malignant, 124 benign) in 300 women. No significant differences were found for AUCs of ADC and DKI-parameters in discriminating suspicious breast lesions (0.882 vs. 0.888, p = 0.480). The specificities were significantly higher with ADC and Dapp than that with DCE-MRI (p = 0.003 and 0.005). The ADC, Kapp and Dapp were correlated with HER2 expression and lymph node status, and ADC and Kapp differed between ER-positive and negative tumors (all p < 0.05). Except Kapp, DKI/DWI-parameters showed relation with Ki-67 expression. None of the DKI/DWI-parameters showed relation with lesion grade (all p > 0.05).Conclusion: The more complicated and time-consuming DKI is not superior to conventional DWI in differentiating suspicious breast lesions and reflecting prognostic information of breast cancer. [ABSTRACT FROM AUTHOR]

Background: Breast cancer is the most common cancer among women worldwide, and approximately 70% of breast cancers are hormone receptor-positive and express estrogen receptor-α (ERα) or/and progesterone receptor. ERα has been identified to promote the growth of primary breast cancer, however, it can also antagonize signaling pathways that lead to epithelial-mesenchymal transition (EMT), including transforming growth factor-β (TGF-β) signaling. miRNA alteration or dysfunction is involved in cancer development and progression. Although miR-1271 has identified as a tumor suppressor in various cancers, the role of miR-1271 in breast cancer is still limited. Methods: The effect of miR-1271 on breast cancer progression was investigated both in vitro and in vivo. The EMT-related protein expression levels and localization were analyzed by western blotting and immunofluorescence, respectively. Chromatin immunoprecipitation and dual-luciferase reporter assays were used to validate the regulation of ERα-miR-1271-SNAI2 feedback loop. Results: miR-1271 suppresses breast cancer progression and EMT phenotype both in vitro and in vivo by targeting SNAI2. Estrogen reverses TGF-β-induced EMT in a miR-1271 dependent manner. Furthermore, ERα transactivates the miR-1271 expression and is also transcriptionally repressed by SNAI2. Conclusions: Our data uncover the ERα-miR-1271-SNAI2 feedback loop and provide a mechanism to explain the TGF-β network in breast cancer progression. [ABSTRACT FROM AUTHOR]

Breast cancer is the most common cancer among women worldwide. Chemoresistance remains to be a considerable obstacle in breast cancer therapy and it is often involves dysregulation of a variety of microRNAs (miRNAs). miR-485-5p functions as a tumor suppressor in several types of human cancers. However, its role in breast cancer chemosensitivity have not been determined. In the present study, we demonstrated that overexpression of miR-485-5p suppresses breast cancer progression and enhances chemosensitivity both in vitro and in vivo . Further study demonstrated that miR-485-5p directly targeted the 3′-untranslated region of survivin and overexpression of survivin overcomes the miR-485-5p induced effects on breast cancer. In conclusion, our study identified that miR-485-5p suppresses cancer progression and enhances the chemosensitivity by targeting survivin. Targeting survivin by miR-485-5p may provide a potential approach to reverse chemosensitivity in breast cancer cells. [ABSTRACT FROM AUTHOR]

Highlights: [•] FOXD3 is down-regulated in breast cancer tissues. [•] FOXD3 inhibits breast cancer cell proliferation and invasion. [•] FoxD3 deficiency induces epithelial–mesenchymal transition. [ABSTRACT FROM AUTHOR]

Toll-like receptor 3 (TLR3) is a receptor recognizing double-stranded RNA (dsRNA) from viruses as well as from lytic mammalian cells. In the present study, we performed a two-stage association study (n = 3,551) and found that the minor alleles of two SNPs (the T-allele of rs5743312 and the T-allele of rs3775296) conferred increased risks of breast cancer incidence. The adjusted odds ratios (ORs) were 2.281 (P = 7.01 × 10−5) and 2.086 (P = 8.69 × 10−5), respectively. Specifically, the susceptibility variants within TLR3 were significantly associated with larger tumor size (adjusted P-values: 0.004 for rs5743312 and 0.004 for rs3775296). Furthermore, we investigated the biological function of the TLR3 protein in breast cancer cell lines. Notably, the stable expression of TLR3 directly inhibited cell proliferation both in vitro and in vivo. We also verified that TLR3 conferred less invasive phenotypes on breast cancer cells by regulating the mRNA expression of a panel of genes. TLR3-mediated inhibition of proliferation was caused by downregulation of the EGFR/PI3K/AKT pathway. In summary, our findings strongly suggest that common genetic changes in the TLR3 gene may influence breast cancer susceptibility and development, and TLR3 plays a negative regulatory role in the initiation and progression of human breast cancer cells, at least in part by downregulating the EGFR/PI3K/AKT pathway. [ABSTRACT FROM AUTHOR]