[Application Value of Abbreviated Comprehensive Geriatric Assessment in Elderly Female Breast Cancer Patients].

Objective To evaluate the application value of abbreviated comprehensive geriatric assessment(aCGA)in elderly female breast cancer patients. Methods Eight aspects of the traditional CGA were simplified to form the aCGA assessment table,based on which the patients were classified into three grades of A,B and C according to the total scores.This study enrolled the elderly female patients with breast cancer aged 70 years and above who were treated in PUMC Hospital from June 2018 to January 2020.Eastern Cooperative Oncology Group(ECOG)scoring and aCGA grading were performed respectively,and the results of the two methods were compared. Results Of the 162 patients,111(68.5%)were classified by the aGGA method as grade A,43(26.5%)as grade B,and 8(5.0%)as grade C;131(80.9%)cases have concurrent diseases,and the most common complications were hypertension(n=89),cardiovascular diseases(n=47)and diabetes mellitus(n=39).The ECOG score was 0-1 in 133(82.0%)cases,2 in 24(14.8%)cases and 3 in 5(3.2%)cases.The ECOG score showed 133(82.0%)cases with good status and 29 cases with poor status.However,according to the aCGA classification,111 cases were in good health status and 51 cases were in poor health status;the difference in the result between the two groups was statistically significant(χ 2=14.24,P<0.001).Conclusion Compared with ECOG score,aCGA grading can more comprehensively evaluate the health status of elderly female breast cancer patients and can be applied to the patients aged 70 and above.

IFIT1 modulates the proliferation, migration and invasion of pancreatic cancer cells via Wnt/ß-catenin signaling.

OBJECTIVES: Previously, Interferon-induced Protein with Tetratricopeptide Repeats 1 (IFIT1) has been shown to promote cancer development. Here, we aimed to explore the role of IFIT1 in the development and progression of pancreatic cancer, including the underlying mechanisms. METHODS: We explored IFIT1 expression in pancreatic cancer samples using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Cell Counting Kit-8 (CCK8), colony formation, scratch wound-healing and Transwell assays were performed to assess the proliferation, migration and invasion abilities of pancreatic cancer cells. Gene Set Enrichment Analysis (GSEA) and Western blotting were performed to assess the regulatory effect of IFIT1 on the Wnt/ß-catenin pathway. RESULTS: We found that upregulation of IFIT1 expression is common in pancreatic cancer and is negatively associated with overall patient survival. Knockdown of IFIT1 expression led to decreased proliferation, migration and invasion of pancreatic cancer cells. We also found that IFIT1 could regulate Wnt/ß-catenin signaling, and that a Wnt/ß-catenin agonist could reverse this effect. In addition, we found that IFIT1 can promote epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. CONCLUSIONS: Our data indicate that IFIT1 increases pancreatic cancer cell proliferation, migration and invasion by activating the Wnt/ß-catenin pathway. In addition, we found that EMT could be regulated by IFIT1. IFIT1 may serve as a potential therapeutic target for pancreatic cancer.

Prognostic value and immune infiltration of ARMC10 in pancreatic adenocarcinoma via integrated bioinformatics analyses.

Background: Armadillo repeat-containing 10 (ARMC10) is involved in the progression of multiple types of tumors. Pancreatic adenocarcinoma (PAAD) is a lethal disease with poor survival and prognosis. Methods: We acquired the data of ARMC10 in PAAD patients from the cancer genome atlas (TCGA) and gene expression omnibus (GEO) datasets and compared the expression level with normal pancreatic tissues. We evaluated the relevance between ARMC10 expression and clinicopathological factors, immune infiltration degree and prognosis in PAAD. Results: High expression of ARMC10 was relevant to T stage, M stage, pathologic stage, histologic grade, residual tumor, primary therapy outcome (P < 0.05) and related to lower Overall-Survival (OS), Disease-Specific Survival (DSS), and Progression-Free Interval (PFI). Gene set enrichment analysis showed that ARMC10 was related to methylation in neural precursor cells (NPC), G alpha (i) signaling events, APC targets, energy metabolism, potassium channels and IL10 synthesis. The expression level of ARMC10 was positively related to the abundance of T helper cells and negatively to that of plasmacytoid dendritic cells (pDCs). Knocking down of ARMC10 could lead to lower proliferation, invasion, migration ability and colony formation rate of PAAD cells in vitro. Conclusions: Our research firstly discovered ARMC10 as a novel prognostic biomarker for PAAD patients and played a crucial role in immune regulation in PAAD.

IFIT1 modulates the proliferation, migration and invasion of pancreatic cancer cells via Wnt/ß-catenin signaling.

OBJECTIVES: Previously, Interferon-induced Protein with Tetratricopeptide Repeats 1 (IFIT1) has been shown to promote cancer development. Here, we aimed to explore the role of IFIT1 in the development and progression of pancreatic cancer, including the underlying mechanisms. METHODS: We explored IFIT1 expression in pancreatic cancer samples using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Cell Counting Kit-8 (CCK8), colony formation, scratch wound-healing and Transwell assays were performed to assess the proliferation, migration and invasion abilities of pancreatic cancer cells. Gene Set Enrichment Analysis (GSEA) and Western blotting were performed to assess the regulatory effect of IFIT1 on the Wnt/ß-catenin pathway. RESULTS: We found that upregulation of IFIT1 expression is common in pancreatic cancer and is negatively associated with overall patient survival. Knockdown of IFIT1 expression led to decreased proliferation, migration and invasion of pancreatic cancer cells. We also found that IFIT1 could regulate Wnt/ß-catenin signaling, and that a Wnt/ß-catenin agonist could reverse this effect. In addition, we found that IFIT1 can promote epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. CONCLUSIONS: Our data indicate that IFIT1 increases pancreatic cancer cell proliferation, migration and invasion by activating the Wnt/ß-catenin pathway. In addition, we found that EMT could be regulated by IFIT1. IFIT1 may serve as a potential therapeutic target for pancreatic cancer.

Identification METTL18 as a Potential Prognosis Biomarker and Associated With Immune Infiltrates in Hepatocellular Carcinoma.

Methyltransferase-like 18 (METTL18), a METTL family member, is abundant in hepatocellular carcinoma (HCC). Studies have indicated the METTL family could regulate the progress of diverse malignancies while the role of METTL18 in HCC remains unclear. Data of HCC patients were acquired from the cancer genome atlas (TCGA) and gene expression omnibus (GEO). The expression level of METTL18 in HCC patients was compared with normal liver tissues by Wilcoxon test. Then, the logistic analysis was used to estimate the correlation between METTL18 and clinicopathological factors. Besides, Gene Ontology (GO), Gene Set Enrichment Analysis (GSEA), and single-sample Gene Set Enrichment Analysis (ssGSEA) were used to explore relevant functions and quantify the degree of immune infiltration for METTL18. Univariate and Multivariate Cox analyses and Kaplan-Meier analysis were used to estimate the association between METTL18 and prognosis. Besides, by cox multivariate analysis, a nomogram was conducted to forecast the influence of METTL18 on survival rates. METTL18-high was associated with Histologic grade, T stage, Pathologic stage, BMI, Adjacent hepatic tissue inflammation, AFP, Vascular invasion, and TP53 status (P < 0.05). HCC patients with METTL18-high had a poor Overall-Survival [OS; hazard ratio (HR): 1.87, P < 0.001), Disease-Specific Survival (DSS, HR: 1.76, P = 0.015), and Progression-Free Interval (PFI, HR: 1.51, P = 0.006). Multivariate analysis demonstrated that METTL18 was an independent factor for OS (HR: 2.093, P < 0.001), DSS (HR: 2.404, P = 0.015), and PFI (HR: 1.133, P = 0.006). Based on multivariate analysis, the calibration plots and C-indexes of nomograms showed an efficacious predictive effect for HCC patients. GSEA demonstrated that METTL18-high could activate G2M checkpoint, E2F targets, KRAS signaling pathway, and Mitotic Spindle. There was a positive association between the METTL18 and abundance of innate immunocytes (T helper 2 cells) and a negative relation to the abundance of adaptive immunocytes (Dendritic cells, Cytotoxic cells etc.). Finally, we uncovered knockdown of METTL18 significantly suppressed the proliferation, invasion, and migration of HCC cells in vitro. This research indicates that METTL18 could be a novel biomarker to evaluate HCC patients' prognosis and an important regulator of immune responses in HCC.

Prognostic significance of MMP-7 expression in colorectal cancer: a meta-analysis.

OBJECTIVE: Matrix metalloproteinase-7 (MMP-7) is a member of the family of matrix metalloproteinases (MMPs); it is associated with invasive tumor growth and distant metastasis in colorectal cancer (CRC). However, the prognostic value of MMP-7 in CRC remains controversial. Thus, we conducted a meta-analysis to investigate the prognostic value of MMP-7 expression in CRC. METHODS: We systematically searched for studies evaluating the relationship between MMP-7 expression and the outcome of CRC patients in PubMed, the Cochrane library, Embase, Google Scholar, and Wanfang databases updated to August 2014. Studies were assessed for quality using REMARK (REporting recommendations for tumor MARKer prognostic studies). Hazard ratios (HRs) with 95% confidence intervals (95%CIs) were pooled to estimate the hazard for overall survival (OS) and disease-free survival (DFS), and odds ratios (ORs) with 95%CIs were pooled to estimate the impact of MMP-7 on the 5-year survival rate. RESULTS: In total, 2985 patients from 17 studies were included in this meta-analysis. Our results showed that MMP-7 over-expression predicted poor OS (HR=3.57, 95%CI 2.21-5.75, P=0.000, random-effect model), poor DFS (HR=2.49, 95%CI 1.73-3.57, P=0.000, fixed-effect model), and decreased 5-year survival rate (OR=0.26, 95%CI 0.19-0.37, P=0.000, fixed-effect model). Therefore, MMP-7 is an indicator of poor survival and high recurrence rate in CRC patients. CONCLUSION: MMP-7 can serve as a prognostic indicator and a potential novel target for treatment in CRC patients. More well-designed prospective studies with better methodology for MMP-7 assessment are required to clarify the prognostic significance of MMP-7 expression in CRC patients.