Background and AimsCurrently, acute-on-chronic liver failure (ACLF) has been defined differently by Asia–Pacific Association for the Study of the Liver (APASL) and Chinese Medical Association (CMA) in the East, as well as EASL-Chronic Liver Failure (EASL-CLIF) Consortium in the West. This study aimed to compare current different diagnostic criteria for ACLF and to determine predictors of the progression into post-enrollment EASL-CLIF ACLF from ACLF at enrollment defined by APASL alone or by both APASL and CMA but not by EASL-CLIF Consortium.MethodsWe retrospectively analyzed clinical data from 394 eligible cirrhotic patients fulfilling at least APASL criteria for ACLF at enrollment. Patient survival was estimated by Kaplan-Meier analysis and subsequently compared by log-rank test. Independent predictors of disease progression were determined using univariate analysis and multivariate Cox regression analysis.ResultsThe 90-day mortality rate was 13.1% in patients with ACLF at enrollment defined by APASL alone, 25.3% in patients with ACLF at enrollment defined by both APASL and CMA but not EASL-CLIF Consortium, and 59.3% in patients with ACLF at enrollment defined by EASL-CLIF Consortium in addition to APASL. Baseline Chronic Liver Failure-Sequential Organ Failure Assessment (CLIF-SOFA) score, and the maximum rising rates of CLIF-SOFA score, Model for End-Stage Liver Disease-Sodium (MELD-Na) score and total bilirubin were independent predictors of progression into post-enrollment EASL-CLIF ACLF from ACLF at enrollment defined by APASL alone or by both APASL and CMA but not by EASL-CLIF Consortium.ConclusionDifferent diagnostic criteria for ACLF caused different patient prognosis. So, it is imperative to formulate a unifying diagnostic criteria for ACLF worldwide, thus attaining early identification and treatment, and eventual improvement in survival of ACLF patients. Baseline CLIF-SOFA score, and the maximum rising rates of CLIF-SOFA score, MELD-Na score and total bilirubin may early predict post-enrollment development of EASL-CLIF ACLF.

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Hypoxia-inducible factor 1-alpha (HIF-1a) has been shown to contribute to resistance to chemotherapy in breast cancer. The purpose of this study was to investigate whether HIF-1a is predictive for pathological response and the prognostic value of HIF-1a in local advanced breast undergoing neoadjuvant chemotherapy.Two hundred twenty patients with none-metastatic locally advanced invasive breast cancer (stages II–III) that subsequently received neoadjuvant chemotherapy were included in an observational study to assess the HIF-1a protein expression by immunohistochemistry. Associations between HIF-1a expression and pathological complete response (pCR) were analyzed using univariate and multivariate analysis. Independent prognostic factors for RFS were identified by multivariate Cox's proportional hazard analysis. A P value < .05 was considered to be statistically significant.The median age was 46 years, Luminal A, Luminal B, HER2-positive, and triple-negative accounted for 3.6%, 57.7%, 7.0% and 16.0%, respectively. A total of 41 patients (18.6%) achieved a pCR after neoadjuvant chemotherapy in the present study. HIF-1α negative patients had a significantly higher pCR rate than HIF-1α positive patients (P = .027). Multivariate analysis demonstrated that HIF-1α negative expression is an independent favorable predictor of pCR. Multivariate Cox regression analysis demonstrated that the HIF-1a expression before NCT showed an independent prognostic value for RFS (HR = 4.168, 95% CI: 1.012–17.170, P = .048).HIF-1a expression correlates with pCR in breast cancer undergoing neoadjuvant chemotherapy. Absent expression of HIF-1a was associated with a better pathological response and could indicate a favorable prognosis in non-pCR breast cancer patients.

Gastric cancer is the fifth most common cancer and the third most common cause of cancer death all over the world. E-cadherin encoded by human CDH1 gene plays important roles in tumorigenesis as well as in tumor progression, invasion and metastasis. Full-length E-cadhrin tethered on the cell membrane mainly mediates adherens junctions between cells and is involved in maintaining the normal structure of epithelial tissues. After proteolysis, the extracellular fragment of the full-length E-cadhein is released into the extracellular environment and the blood, which is called soluble E-cadherin (sE-cadherin). sE-cadherin promots invasion and metastasis as a paracrine/autocrine signaling molecule in the progression of various types of cancer including gastric cancer. This review mainly summarizes the dysregulation of E-cadherin and the regulatory roles in the progression, invasion, metastasis, and drug-resistance, as well as its clinical applications in diagnosis, prognosis, and therapeutics of gastric cancer.