A review of quantitative diffusion-weighted MR imaging for breast cancer: Towards noninvasive biomarker.

Quantitative diffusion-weighted imaging (DWI) is an important adjunct to conventional breast MRI and shows promise as a noninvasive biomarker of breast cancer in multiple clinical scenarios, from the discrimination of benign and malignant lesions, prediction, and evaluation of treatment response to a prognostic assessment of breast cancer. Various quantitative parameters are derived from different DWI models based on special prior knowledge and assumptions, have different meanings, and are easy to confuse. In this review, we describe the quantitative parameters derived from conventional and advanced DWI models commonly used in breast cancer and summarize the promising clinical applications of these quantitative parameters. Although promising, it is still challenging for these quantitative parameters to become clinically useful noninvasive biomarkers in breast cancer, as multiple factors may result in variations in quantitative parameter measurements. Finally, we briefly describe some considerations regarding the factors that cause variations.

Apigenin inhibits TGF-ß1-induced proliferation and migration of airway smooth muscle cells.

It is well known that the proliferation and migration of ASM cells (ASMCs) plays an important role in the pathogenesis of airway remodeling in asthma. Previous studies reported that apigenin can inhibit airway remodeling in a mouse asthma model. However, its effects on the proliferation and migration of ASMCs in asthma remain unknown. Therefore, the aim of our present study was to investigate the effects of apigenin on ASMC proliferation and migration, and explore the possible molecular mechanism. We found that apigenin inhibited transforming growth factor-ß1 (TGF-ß1)-induced ASMC proliferation. The cell cycle was blocked at G1/S-interphase by apigenin. It also suppressed TGF-ß1-induced ASMCs migration. Furthermore, apigenin inhibited TGF-ß1-induced Smad 2 and Smad 3 phosphorylation in ASMCs. Taken together, these results suggested that apigenin inhibited the proliferation and migration of TGF-ß1-stimulated ASMCs by inhibiting Smad signaling pathway. These data might provide useful information for treating asthma and show that apigenin has potential for attenuating airway remodeling.