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ObjectiveOur aim was to develop dual-modal CNN models based on combining conventional ultrasound (US) images and shear-wave elastography (SWE) of peritumoral region to improve prediction of breast cancer.MethodWe retrospectively collected US images and SWE data of 1271 ACR- BIRADS 4 breast lesions from 1116 female patients (mean age ± standard deviation, 45.40 ± 9.65 years). The lesions were divided into three subgroups based on the maximum diameter (MD): ≤15 mm; >15 mm and ≤25 mm; >25 mm. We recorded lesion stiffness (SWV1) and 5-point average stiffness of the peritumoral tissue (SWV5). The CNN models were built based on the segmentation of different widths of peritumoral tissue (0.5 mm, 1.0 mm, 1.5 mm, 2.0 mm) and internal SWE image of the lesions. All single-parameter CNN models, dual-modal CNN models, and quantitative SWE parameters in the training cohort (971 lesions) and the validation cohort (300 lesions) were assessed by receiver operating characteristic (ROC) curve.ResultsThe US + 1.0 mm SWE model achieved the highest area under the ROC curve (AUC) in the subgroup of lesions with MD ≤15 mm in both the training (0.94) and the validation cohorts (0.91). In the subgroups with MD between15 and 25 mm and above 25 mm, the US + 2.0 mm SWE model achieved the highest AUCs in both the training cohort (0.96 and 0.95, respectively) and the validation cohort (0.93 and 0.91, respectively).ConclusionThe dual-modal CNN models based on the combination of US and peritumoral region SWE images allow accurate prediction of breast cancer.

We investigated the expression and biological function of retinoic acid inducible gene I (RIG-I) in esophageal squamous cell carcinoma (ESCC). Materials and methods: An immunohistochemical analysis was performed on 86 pairs of tumor tissue and adjacent normal tissue samples of patients with ESCC. We generated RIG-I-overexpressing ESCC cell lines KYSE70 and KYSE450, and RIG-I- knockdown cell lines KYSE150 and KYSE510. Cell viability, migration and invasion, radioresistance, DNA damage, and cell cycle were evaluated using CCK-8, wound-healing and transwell assay, colony formation, immunofluorescence, and flow cytometry and Western blotting, respectively. RNA sequencing was performed to determine the differential gene expression between controls and RIG-I knockdown. Tumor growth and radioresistance were assessed in nude mice using xenograft models. RIG-I expression was higher in ESCC tissues compared with that in matched non-tumor tissues. RIG-I overexpressing cells had a higher proliferation rate than RIG-I knockdown cells. Moreover, the knockdown of RIG-I slowed migration and invasion rates, whereas the overexpression of RIG-I accelerated migration and invasion rates. RIG-I overexpression induced radioresistance and G2/M phase arrest and reduced DNA damage after exposure to ionizing radiations compared with controls; however, it silenced the RIG-I enhanced radiosensitivity and DNA damage, and reduced the G2/M phase arrest. RNA sequencing revealed that the downstream genes DUSP6 and RIG-I had the same biological function; silencing DUSP6 can reduce the radioresistance caused by the overexpression of RIG-I. RIG-I knockdown depleted tumor growth in vivo, and radiation exposure effectively delayed the growth of xenograft tumors compared with the control group. RIG-I enhances the progression and radioresistance of ESCC; therefore, it may be a new potential target for ESCC-targeted therapy.

Purpose: Gastric cancer (GC) is the second most lethal cancer globally and is associated with poor prognosis. Fatty acid-binding proteins (FABPs) can regulate biological properties of carcinoma cells. FABP5 is overexpressed in many types of cancers; however, the role and mechanisms of action of FABP5 in GC remain unclear. In this study, we aimed to evaluate the clinical and biological functions of FABP5 in GC. Materials and Methods: We assessed FABP5 expression using immunohistochemical analysis in 79 patients with GC and evaluated its biological functions following in vitro and in vivo ectopic expression. FABP5 targets relevant to GC progression were determined using RNA sequencing (RNA-seq). Results: Elevated FABP5 expression was closely associated with poor outcomes, and ectopic expression of FABP5 promoted proliferation, invasion, migration, and carcinogenicity of GC cells, thus suggesting its potential tumor-promoting role in GC. Additionally, RNA-seq analysis indicated that FABP5 activates immune-related pathways, including cytokine)cytokine receptor interaction pathways, interleukin-17 signaling, and tumor necrosis factor signaling, suggesting an important rationale for the possible development of therapies that combine FABP5-targeted drugs with immunotherapeutics. Conclusions: These findings highlight the biological mechanisms and clinical implications of FABP5 in GC and suggest its potential as an adverse prognostic factor and/or therapeutic target. [ABSTRACT FROM AUTHOR]

The incidence rate of esophageal squamous cell carcinoma (ESCC) has risen significantly in recent years. RNA binding protein (RBP) has been attracting increased attention in the treatment of ESCC. Therefore, the primary aim of this study was to explore the roles of the RBP Hu antigen R (HuR) in ESCC. The mRNA levels were detected via reverse transcription-quantitative PCR, while the expression levels of protein were evaluated using western blotting. Cell proliferation was estimated by cell counting kit-8 assay and colony formation assay. Flow cytometry was applied to measure cell apoptosis. Luciferase assay and RIP assay were applied to verify whether interferon-β (IFN-β) was targeted by HuR. The results unambiguously demonstrated that HuR was upregulated in ESCC. Overexpression of HuR alleviated chemosensitivity to cisplatin in ESCC cells, as evidenced by increased cell proliferation and decreased apoptosis. Moreover, IFN-β was found to be a target of HuR and downregulated in ESCC cells. And overexpression of IFN-β abrogated the effects of HuR on cisplatin-sensitivity of ESCC cells. Taken together, these findings suggested that HuR may alleviate the chemosensitivity of ESCC cells to cisplatin via binding to IFN-β. Therefore, the HuR/IFN-β axis may be a novel biomarker for improving the chemosensitivity of ESCC. [ABSTRACT FROM AUTHOR]