Primary liver cancer is the sixth most commonly diagnosed cancer and was the third leading cause of cancer deaths worldwide in 2020. It includes hepatocellular carcinoma (HCC) (representing 75%-85% of cases), intrahepatic cholangiocarcinoma (representing 10%-15% of cases), and other rare types. The survival rate of patients with HCC has risen with improved surgical technology and perioperative management in recent years; however, high tumor recurrence rates continue to limit long-term survival, even after radical surgical resection (exceeding 50% recurrence). For resectable recurrent liver cancer, surgical removal [either salvage liver transplantation (SLT) or repeat hepatic resection] remains the most effective therapy that is potentially curative for recurrent HCC. Thus, here, we introduce surgical treatment for recurrent HCC. Areas Covered: A literature search was performed for recurrent HCC using Medline and PubMed up to August 2022. Expert commentary: In general, long-term survival after the re-resection of recurrent liver cancer is usually beneficial. SLT has equivalent outcomes to primary liver transplantation for unresectable recurrent illness in a selected group of patients; however, SLT is constrained by the supply of liver grafts. SLT seems to be inferior to repeat liver resection when considering operative and postoperative results but has the major advantage of disease-free survival. When considering the similar overall survival rate and the current situation of donor shortages, repeat liver resection remains an important option for recurrent HCC.

Background: Single-drug albumin-bound paclitaxel is one of the standard second-line treatments for advanced gastric cancer. Some clinical studies suggest that albumin-bound paclitaxel combined with S-1 can be used in the first-line treatment of gastric cancer. Both the two regimens have been commonly used in the past few years. Which is more effective? What's the safety? Methods: From 2016 to 2021, a total of 70 untreated patients with advanced gastric cancer were included in our study. They all received at least two cycles of chemotherapy. Among them, 37 cases received standard S-1 and oxaliplatin (SOX) regimen, and 33 cases received albumin-bound paclitaxel combined with S-1 (aTS) regimen. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR), and adverse events (AEs) were analyzed. The OS and PFS curves were estimated using the Kaplan-Meier method.Results: The PFS of the aTS group was higher than that of the SOX group (9.27 vs. 7.03 months; P=0.046), but there was no significant difference in the OS between the two groups (19.2 vs. 12.5 months; P=0.131). The ORR of the aTS group was higher than that of the SOX group, and the side effects were tolerable.Conclusions: Both regimens can be applied to advanced gastric cancer patients. Albumin-bound paclitaxel showed a higher ORR and could effectively prolong PFS.

Introduction: Hypertrophic scar (HS), a fibroproliferative disorder of the skin with some tumor-like properties, is closely related to dysregulated inflammation. PD-1/PD-L1 inhibitor is a promising medication for cancer therapy as its potent functions on adaptive immune response; whether it could be a candidate for HS therapy has aroused our interest. This study aimed to explore the effect and the mechanism of BMS-202, a PD-1/PD-L1 inhibitor, in HS. Methods: Ten HS and adjacent normal skin tissues collected from HS patients were used to detect α-SMA, collagen I, and PD-L1 expression by Quantitative reverse transcription-polymerase chain reaction and western blot (WB) analysis. Fibroblasts derived from HS tissues (HFBs) were exposed to diverse concentrations of BMS-202, of which proliferation, migration, apoptosis, and collagen synthesis were evaluated by Cell Counting Kit-8, wound healing, terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End labeling, and [ 3 H]-proline incorporation assays, respectively. The effect of BMS-202 on α-SMA and collagen I expression, and transforming growth factor beta 1 (TGFβ1)/Smad signaling in HFBs was also determined by WB and enzyme-linked immunosorbent assay.Results: The expression level of PD-L1 was significantly elevated in both HS tissues and HFBs, which was positively correlated with α-SMA and collagen I expressions. BMS-202 exerted a significant suppression effect on the cell proliferation, migration, collagen synthesis, and α-SMA and collagen I expression of HFBs in a concentration-dependent way; but did not affect apoptosis. Finally, BMS-202 could reduce the phosphorylation of ERK1/2, Smad2, and Smad3, and the TGFβ1 expression once its concentration reached 2.5 nM. Conclusion:BMS-202 effectively suppressed proliferation, migration, and extracellular matrix deposition of HFBs, potentially through the regulation of the ERK and TGFβ1/Smad signaling pathways.

To establish and validate an optimal predictive model based on multiparametric MRI for staging liver fibrosis (LF) in rabbits with magnetic resonance elastography (MRE), spin-lattice relaxation time in the rotating frame (T1ρ imaging), SWI, intravoxel incoherent motion (IVIM), and DCE-MRI. Methods:The LF group included 120 rabbits induced by subcutaneous injections of carbon tetrachloride (CCl 4 ); 30 normal rabbits served as the control group.Multiparametric MRI was performed, including MRE, T1ρ, SWI, IVIM, and DCE-MRI. The quantitative parameters were analyzed in two groups, with histopathological results serving as the reference standard. The diagnostic performance of multiparametric MRI and the predictive model established by multivariable logistic regression analysis were evaluated by receiver operating characteristic (ROC) curve analysis. Results:In total, 32, 67, and 51 rabbits were histologically diagnosed as no fibrosis (stage F0), early-stage LF (F1-F2), and advanced-stage LF (F3-F4), respectively. The LF stages presented a strong correlation with liver stiffness (LS) on MRE (r = 0.90), signal-intensity ratio (SIR) on SWI (r = −0.84), and K trans on DCE-MRI (r = 0.71; p < 0.05 for all). The LS and SIR parameters had higher AUC values for distinguishing early-stage LF from both no fibrosis (0.94 and 0.93, respectively) and advanced-stage LF (0.95 and 0.87, respectively). The predictive model showed a slightly higher AUC value of 0.97 (0.90-0.99) than LS and SIR in distinguishing early-stage LF from no fibrosis (p > 0.05), a significantly higher AUC value of 0.98 (0.93-0.99) than the SIR in distinguishing early-stage from advanced-stage LF (p < 0.05). Conclusion: SWI, DCE-MRI, and MRE in particular showed improved performance for LF diagnosis and stage. The predictive model based on multiparametric