RESUMEN
BACKGROUND: Nil by mouth is considered the standard of care during the first days following esophagectomy. However, with the routine implementation of enhanced recovery after surgery, early oral intake is more likely to be the preferred mode of nutrition following esophagectomy. The present study aims to evaluate the safety and effectiveness of early oral intake following esophagectomy for esophageal cancer. METHODS: Comprehensive literature searches were conducted using PubMed, Web of Science, Embase, and Cochrane Library. Weighted mean differences (WMD) and odds ratios (OR) with 95% confidence intervals (CI) were calculated as the effect sizes for continuous and dichotomous variables, respectively. RESULTS: Fourteen studies with a total of 1947 patients were included. Length of hospital stay (WMD = - 3.94, CI: - 4.98 to - 2.90; P < 0.001), the time to first flatus (WMD = - 1.13, CI: - 1.25 to - 1.01; P < 0.001) and defecation (WMD = - 1.26, CI: - 1.82 to - 0.71; P < 0.001) favored the early oral intake group. There was no statistically significant difference in mortality (OR = 1.23, CI: 0.45 to 3.36; P = 0.69). Early oral intake also did not increase the risk of pneumonia and overall postoperative complications. CONCLUSIONS: Current evidence indicates early oral intake following esophagectomy seems to be safe and effective. It may be the preferred mode of nutrition following esophagectomy. However, more high-quality studies are still needed to further validate this conclusion.
Asunto(s)
Neoplasias Esofágicas , Esofagectomía , Nutrición Enteral , Neoplasias Esofágicas/cirugía , Esofagectomía/efectos adversos , Humanos , Tiempo de Internación , Complicaciones Posoperatorias/epidemiologíaRESUMEN
BACKGROUND: Esophagectomy and definitive chemoradiotherapy are commonly used in the treatment of stage I esophageal cancer (EC). The present study aims to compare the efficacy and safety of esophagectomy and definitive chemoradiotherapy as the initial treatment for clinical stage I EC. METHODS: This study was registered with the International Prospective Register of Systematic Reviews (CRD42020197203). Relevant studies were identified through PubMed, Web of Science, EMBASE, and Cochrane Library from database inception to June 30, 2020. Hazard ratio (HR) with 95% confidence intervals (CI) was employed to compare overall survival (OS) and progression-free survival (PFS). Odds ratio (OR) with 95% CI was employed to compare treatment-related death, complications, and tumor recurrence. RESULTS: A total of 13 non-randomized controlled studies involving 3,346 patients were included. Compared with definitive chemoradiotherapy, esophagectomy showed an improved OS (HR 0.69, 95% CI 0.55-0.86; P < 0.001), PFS (HR 0.47, 95% CI 0.33-0.67; P < 0.001), and a lower risk of tumor recurrence (OR 0.43, 95% CI 0.30-0.61; P < 0.001). There was no significant difference in the incidence of complications (OR 1.11, 95% CI 0.75-1.65; P = 0.60) and treatment-related death (OR 1.15, 95% CI 0.31-4.30; P = 0.84) between the two treatments. CONCLUSIONS: Current evidence shows esophagectomy has superior survival benefits as the initial treatment for clinical stage I EC. It is still the preferred choice for patients with clinical stage I EC. However, future high-quality randomized controlled trials are needed to validate this conclusion.
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Neoplasias Esofágicas , Esofagectomía , Quimioradioterapia , Neoplasias Esofágicas/patología , Humanos , Recurrencia Local de Neoplasia/cirugíaRESUMEN
The purpose of this study is to investigate the significance of alpha-enolase (ENO1) expression in squamous cell carcinoma of the lung (LUSC), its prognostic value, and prospective molecular mechanism. Using multiplatforms data, including in-house immunohistochemistry, in-house real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), in-house microarray, and public high-throughput data, the expression significance and prognostic role of ENO1 in LUSC tissues were analyzed comprehensively. With the combination of all eligible cases, compared with 941 non-LUSC lung tissues, ENO1 was significantly overexpressed in 1163 cases of LUSC (standardized mean difference (SMD) = 1.23, 95% confidence interval (CI) = 0.76-1.70, P < 0.001). ENO1 also displayed a great ability to differentiate LUSC tissues from non-LUSC lung tissues (AUC = 0.8705) with the comprehensive sensitivity being 0.88 [0.83-0.92], and comprehensive specificity being 0.89 [0.84-0.94]). Moreover, in 1860 cases of LUSC with survival information, patients with higher expression of ENO1 had poorer prognosis (hazard ratio (HR) = 1.20, 95% CI = 1.01-1.43, P = 0.043). ENO1 and its related genes mainly participated in the pathways of cell division and proliferation. In conclusion, the upregulation of ENO1 could affect the carcinogenesis and unfavorable outcome of LUSC.
RESUMEN
Cyclin-dependent kinase 1 (CDK1) plays a significant role in certain malignancies. However, it remains unclear whether CDK1 plays a role in esophageal squamous cell carcinoma (ESCC). The aim of this study was to analyze the expression and clinical value of CDK1 in ESCC. CDK1 protein in 151 ESCC tissues and 138 normal esophageal tissues was detected by immunohistochemistry. RNA-seq of eight pairs of ESCC and adjacent esophageal specimens was performed to evaluate the levels of CDK1 mRNA. Microarray and external RNA-seq data from 664 cases of ESCC and 1733 cases of control tissues were used to verify the difference in CDK1 expression between the two groups. A comprehensive analysis of all data was performed to evaluate the difference in CDK1 between ESCC tissues and control tissues. Further, functional enrichment analyses were performed based on differentially expressed genes (DEGs) of ESCC and co-expressed genes (CEGs) of CDK1. In addition, a lncRNA-miRNA-CDK1 network was constructed. The expression of CDK1 protein was obviously increased in ESCC tissues (3.540 ± 2.923 vs. 1.040 ± 1.632, P < 0.001). RNA-seq indicated that the mRNA level of CDK1 was also highly expressed in ESCC tissues (5.261 ± 0.703 vs. 2.229 ± 1.161, P < 0.0001). Comprehensive analysis revealed consistent up-regulation of CDK1 (SMD = 1.41; 95% CI 1.00-1.83). Further, functional enrichment analyses revealed that the functions of these genes were mainly concentrated in the cell cycle. A triple regulatory network of PVT1-hsa-miR-145-5p/hsa-miR-30c-5p-CDK1 was constructed using in silico analysis. In summary, overexpression of CDK1 is closely related to ESCC tumorigenesis.
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Proteína Quinasa CDC2/genética , Carcinoma de Células Escamosas de Esófago/genética , Biomarcadores de Tumor/genética , Proteína Quinasa CDC2/metabolismo , Proliferación Celular/genética , China , Biología Computacional/métodos , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/metabolismo , Carcinoma de Células Escamosas de Esófago/metabolismo , Expresión Génica/genética , Perfilación de la Expresión Génica/métodos , Regulación Neoplásica de la Expresión Génica/genética , Redes Reguladoras de Genes/genética , Humanos , MicroARNs/genética , Mapas de Interacción de Proteínas/genética , ARN Largo no Codificante/genética , ARN Mensajero/genética , RNA-Seq , Transcriptoma/genéticaRESUMEN
This study aimed to investigate the clinicopathological significance and prospective molecular mechanism of RUNX family transcription factor 2 (RUNX2) in lung squamous cell carcinoma (LUSC). The authors used immunohistochemistry (IHC), RNA-seq, and microarray data from multi-platforms to conduct a comprehensive analysis of the clinicopathological significance and molecular mechanism of RUNX2 in the occurrence and development of LUSC. RUNX2 expression was significantly higher in 16 LUSC tissues than in paired non-cancerous tissues detected by IHC (P < 0.05). RNA-seq data from the combination of TCGA and genotype-tissue expression (GTEx) revealed significantly higher expression of RUNX2 in 502 LUSC samples than in 476 non-cancer samples. The expression of RUNX2 protein was also significantly higher in pathologic T3-T4 than in T1-T2 samples (P = 0.031). The pooled standardised mean difference (SMD) for RUNX2 was 0.87 (95% CI, 0.58-1.16), including 29 microarrays from GEO and one from ArrayExpress. The co-expression network of RUNX2 revealed complicated connections between RUNX2 and 45 co-expressed genes, which were significantly clustered in pathways including ECM-receptor interaction, focal adhesion, protein digestion and absorption, human papillomavirus infection and PI3K-Akt signalling pathway. Overexpression of RUNX2 plays an essential role in the clinical progression of LUSC.
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Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patología , Subunidad alfa 1 del Factor de Unión al Sitio Principal/genética , Regulación Neoplásica de la Expresión Génica , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patología , Humanos , Análisis de Secuencia por Matrices de OligonucleótidosRESUMEN
RUNX family transcription factor 2 (RUNX2) overexpression has been found in various human malignancies. However, the expression levels of RUNX2 mRNA and protein in lung adenocarcinoma (LUAD) were not investigated. This study aims to thoroughly analysis the expression level and potential mechanisms of RUNX2 mRNA in LUAD. We applied in-house immunohistochemistry, high-throughput RNA-sequencing, and gene microarrays to comprehensively investigate the expression level of RUNX2 in LUAD. A pool standard mean difference (SMD) and summary receiver operating characteristic curves (SROC) were calculated to assess the integrated expression value of RUNX2 in LUAD. The hazard ratios (HRs) were integrated to evaluate the overall prognostic effect of RUNX2 on the LUAD patients. The differentially expressed genes (DEGs) of LUAD, the potential target genes of RUNX2, and its co-expressed genes were overlapped to obtain a set of specific genes for GO and KEGG enrichment analyses. RUNX2 overexpression in LUAD was validated using a large number of cases (2 418 LUAD and 1 574 non-tumor lung samples). The pooled SMD was 0.85 (95 % CI: 0.64-1.05) and the area under the curve (AUC) of the SROC was 0.86 (95 %CI: 0.83-0.89). The integrated HR was 1.20 [1.04-1.38], indicating that increased expression of RUNX2 was an independent risk factor for the poor survival of the LUAD patients. RUNX2 and its transcriptionally regulates potential target genes may promote cell proliferation and drug resistance of LUAD by modulating the cell cycle and MAPK signaling pathways. RUNX2 can provide new research directions for targeted drug therapy and drug resistance for LUAD treatment.
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Adenocarcinoma del Pulmón/metabolismo , Subunidad alfa 1 del Factor de Unión al Sitio Principal/metabolismo , Regulación Neoplásica de la Expresión Génica/fisiología , Neoplasias Pulmonares/metabolismo , Adenocarcinoma del Pulmón/diagnóstico , Adenocarcinoma del Pulmón/patología , Proliferación Celular/fisiología , Subunidad alfa 1 del Factor de Unión al Sitio Principal/genética , Resistencia a Antineoplásicos/fisiología , Humanos , Inmunohistoquímica , Pulmón/patología , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/patología , Sistema de Señalización de MAP Quinasas/fisiología , Pronóstico , ARN Mensajero/análisis , Transcripción Genética/fisiología , Regulación hacia ArribaRESUMEN
Esophageal squamous cell carcinoma (ESCC) is the major histological type of esophageal cancers worldwide. Transcription factor PTTG1 was seen highly expressed in a variety of tumors and was related to the degree of tumor differentiation, invasion, and metastasis. However, the clinical significance of PTTG1 had yet to be verified, and the mechanism of abnormal PTTG1 expression in ESCC was not clear. In this study, the comprehensive analysis and evaluation of PTTG1 expression in ESCC were completed by synthesizing in-house immunohistochemistry (IHC), clinical sample tissue RNA-seq (in-house RNA-seq), public high-throughput data, and literature data. We also explored the possible signaling pathways and target genes of PTTG1 in ESCC by combining the target genes of PTTG1 (displayed by ChIP-seq), differentially expressed genes (DEGs) of ESCC, and PTTG1-related genes, revealing the potential molecular mechanism of PTTG1 in ESCC. In the present study, PTTG1 protein and mRNA expression levels in ESCC tissues were all significantly higher than in non-cancerous tissues. The pool standard mean difference (SMD) of the overall PTTG1 expression was 1.17 (95% CI: 0.72-1.62, P < 0.01), and the area under curve (AUC) of the summary receiver operating characteristic (SROC) was 0.86 (95% CI: 0.83-0.89). By combining the target genes displayed by ChIP-seq of PTTG1, DEGs of ESCC, and PTTG1-related genes, it was observed that PTTG1 may interact with these genes through chemokines and cytokine signaling pathways. By constructing a protein-protein interaction (PPI) network and combining ChIP-seq data, we obtained four PTTG1 potential target genes, SPTAN1, SLC25A17, IKBKB, and ERH. The gene expression of PTTG1 had a strong positive correlation with SLC25A17 and ERH, which suggested that PTTG1 might positively regulate the expression of these two genes. In summary, the high expression of PTTG1 may play an important role in the formation of ESCC. These roles may be completed by PTTG1 regulating the downstream target genes SLC25A17 and ERH.