原发性肝癌超声造影特征及其与病理相关性的研究(英文)

Objective:The aim of this study was to evaluate the value of contrast-enhanced ultrasound(CEUS) for blood perfusion of primary liver cancer(PHC) and investigate the correlation between microvascular architecture of PHC and pathological differentiation.Methods:Two hundred and seventy-eight patients with 329 PHC lesions were examined by CEUS and analysised the contrast enhancement pattern and correlation with pathology.Results:1.CEUS patterns of PHC:71.7%(236/329) showed "swift enhancement in the arterial phase and swift expurgation in the portal phase",13.4%(44/329) for as "swift enhancement and slow expurgation",7.3%(24/329) as "swift enhancement and simultaneity expurgation",4.3%(14/329) for the "slow enhancement and swift expurgation",2.1%(7/329) as "slow enhancement and expurgation",1.2%(4/329) as "not fast forward".2.90.3%(297/329) of PHC lesions were hypervascular liver cancer and 9.7%(32/329) were hypovascular.Hepatocellular carcinoma(HCC) were hypervascular lesions and intrahepatic cholangiocarcinoma(ICC) were hypovascular lesions.3.PHC size had a significant difference on the contrast media purfusion pattern(P < 0.05),but not on the contrast media expurgation pattern.4.The accuracy of PHC by CEUS were 97.3% and compared to pathology,9 lesions of PHC were misdiagnosed.Conclusion:CEUS can show the different blood perfusion characteristics of PHC with closely related to pathological differentiation,which be valuable to diagnose liver cancer.

Low-dose decitabine enhances the effect of PD-1 blockade in colorectal cancer with microsatellite stability by re-modulating the tumor microenvironment

PD-1 blockade has demonstrated impressive clinical outcomes in colorectal cancers that have high microsatellite instability.However,the therapeutic efficacy for patients with tumors with low microsatellite instability or stable microsatellites needs further improvement.Here,we have demonstrated that low-dose decitabine could increase the expression of immune-related genes such as major histocompatibility complex genes and cytokine-related genes as well as the number of lymphocytes at the tumor site in CT26 colorectal cancer-bearing mice.A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone.The anti-tumor effect of the PD-1 blockade was enhanced by low-dose decitabine.The results of RNA sequencing and whole-genome bisulfite sequencing of decitabine-treated CT26 cells and tumor samples with microsatellite stability from the patient tumor-derived xenograft model have shown that many immune-related genes,including antigen-processing and antigen-presenting genes,were upregulated,whereas the promoter demethylation was downregulated after decitabine exposure.Therefore,decitabine-based tumor microenvironment re-modulation could improve the effect of the PD-1 blockade.The application of decitabine in PD-1 blockade-based immunotherapy may elicit more potent immune responses,which can provide clinical benefits to the colorectal cancer patients with low microsatellite instability or stable microsatellites.

Correction to: Low-dose decitabine enhances the effect of PD1 blockade in colorectal cancer with microsatellite stability by re-modulating the tumor microenvironment

In the published version of this paper,we repeatedly copied the image of the DAC-7 day as the DAC-14 day.The corrected Fig.6 is provided below.The figure legend was revised in order to avoid confusion and is shown below for reference.Although we regret our mistake during figure assembly and would like to apologize for any inconvenience it may have caused,we did not manipulate our data in any way.This unintentional error also has no bearing on the work's scientific conclusions.