Value of sonoelastography for diagnosis of breast non-mass lesions and comparison with BI-RADS: A systematic review and meta-analysis.

BACKGROUND: Not all the breast lesions were mass-like, some were non-mass-like at ultrasonography. In these lesions, conventional ultrasonography had a high sensitivity but a low specificity. Sonoelastography can evaluate tissue stiffness to differentiate malignant masses from benign ones. Then what about the non-mass lesions? The aim of this study was to evaluate the current accuracy of sonoelastography in the breast non-mass lesions and compare the results with those of the American College of Radiology breast Imaging-Reporting and Data System (BI-RADS). METHODS: An independent literature search of English medical databases, including PubMed, Web of Science, Embase & MEDLINE (Embase.com) and Cochrane Library, was performed by 2 researchers. The accuracy of sonoelastography was calculated and compared with those of BI-RADS. RESULTS: Fourteen relevant studies including 1058 breast non-mass lesions were included. Sonoelastography showed a pooled sensitivity of 0.74 (95% CI: 0.70-0.78), specificity of 0.89 (95% CI: 0.85-0.91), diagnostic odds ratio (DOR) of 25.22 (95% CI: 17.71-35.92), and an area under the curve of 0.9042. Eight articles included both sonoelastography and BI-RADS. The pooled sensitivity, specificity, DOR and AUC were 0.69 versus 0.91 (P < .01), 0.90 versus 0.68 (P < .01), 19.65 versus 29.34 (P > .05), and 0.8685 versus 0.9327 (P > .05), respectively. CONCLUSIONS: Sonoelastography has a higher specificity and a lower sensitivity for differential diagnosis between malignant and benign breast non-mass lesions compared with BI-RADS, although there were no differences in AUC between them.

Gut Microbiota and Colorectal Cancer.

BACKGROUND: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide whose incidence has increased rapidly in recent years. There is growing evidence that the complex gut microbiota community plays an important role in the development of intestinal tumorigenesis. SUMMARY: This review aimed to explore the correlation between gut microbiota and CRC as well as to identify the pathogens and their metabolites that affect CRC and the potential models of gut microbiota action. It promotes our understanding of the correlation between gut microbiota and CRC. KEY MESSAGE: Our knowledge of the risk factors associated with gut microbiota for CRC development, as well as of the mechanism how intestinal bacteria act on colorectal tumorigenesis, has improved, leading to a better understanding of the correlation between gut microbiota and CRC. PRACTICAL IMPLICATIONS: The intestinal microbiota community has a close relationship with CRC by influencing the mechanism of the body and by regulating the physiological function of the colorectum and even the entire digestive system. Gut microbiota have been linked to CRC based upon their toxic and genotoxic metabolites production by fermentation of dietary ingredients. These metabolites could bind specific intestinal cell surface receptors and subsequently affect intracellular signal transduction. The mechanisms by which gut microbiota affect CRC development include the 'Alpha-bug' model, the 'driver-passenger' model and the 'intestinal microbiota adaptions' model. This review promotes our understanding of the correlation between gut microbiota and CRC.