Search

Lung cancer, which is a leading cause of cancer-related deaths worldwide, frequently metastasizes to the bones, significantly diminishing patients’ quality of life and complicating treatment strategies. This study aims to develop an advanced 3D Mask R-CNN model, enhanced with the ConvNeXt-V2 backbone, for the automatic segmentation of bone tumors and identification of lung cancer metastasis to support personalized treatment planning. Data were collected from two hospitals: Center A (106 patients) and Center B (265 patients). The data from Center B were used for training, while Center A’s dataset served as an independent external validation set. High-resolution CT scans with 1 mm slice thickness and no inter-slice gaps were utilized, and the regions of interest (ROIs) were manually segmented and validated by two experienced radiologists. The 3D Mask R-CNN model achieved a Dice Similarity Coefficient (DSC) of 0.856, a sensitivity of 0.921, and a specificity of 0.961 on the training set. On the test set, it achieved a DSC of 0.849, a sensitivity of 0.911, and a specificity of 0.931. For the classification task, the model attained an AUC of 0.865, an accuracy of 0.866, a sensitivity of 0.875, and a specificity of 0.835 on the training set, while achieving an AUC of 0.842, an accuracy of 0.836, a sensitivity of 0.847, and a specificity of 0.819 on the test set. These results highlight the model’s potential in improving the accuracy of bone tumor segmentation and lung cancer metastasis detection, paving the way for enhanced diagnostic workflows and personalized treatment strategies in clinical oncology.

Fluorofenidone (AKF-PD) is a novel pyridone agent. The purpose of this study is to investigate the inhibitory effects of AKF-PD on liver fibrosis in rats and the involved molecular mechanism related to hepatic stellate cells (HSCs). Rats treated with dimethylnitrosamine or CCl4 were randomly divided into normal, model, AKF-PD treatment, and pirfenidone (PFD) treatment groups. The isolated primary rat HSCs were treated with AKF-PD and PFD respectively. Cell proliferation and cell cycle distribution were analyzed by bromodeoxyuridine and flow cytometry, respectively. The expression of collagen I and a-smooth muscle actin (a-SMA) were determined by Western blot, immunohistochemical staining, and real-time RT-PCR. The expression of cyclin D1, cyclin E, and p27kip1 and phosphorylation of MEK, ERK, Akt, and 70-kDa ribosomal S6 kinase (p70S6K) were detected by Western blot. AKF-PD significantly inhibited PDGF-BB-induced HSC proliferation and activation by attenuating the expression of collagen I and a-SMA, causing G0/G1 phase cell cycle arrest, reducing expression of cyclin D1 and cyclin E, and promoting expression of p27kip1. AKF-PD also downregulated PDGF-BB-induced MEK, ERK, Akt, and p70S6K phosphorylation in HSCs. In rat liver fibrosis, AKF-PD alleviated hepatic fibrosis by decreasing necroinflammatory score and semiquantitative score, and reducing expression of collagen I and a-SMA. AKF-PD attenuated the progression of hepatic fibrosis by suppressing HSCs proliferation and activation via the ERK/MAPK and PI3K/Akt signaling pathways. AKF-PD may be used as a potential novel therapeutic agent against liver fibrosis. [ABSTRACT FROM AUTHOR]