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1% vs 89.3% for 1 year, P=0.041; 68.7% vs 61.2% for 3 years, P=0.035). In addition, the patients in ERAS group had lower incidences of postoperative hemorrhage, bile leak, and postoperative deep vein thrombosis/pulmonary embolism (DVT/PE), decreased 30-day readmission rate and total readmission rate, and shorter LOS.

ERAS program could be safely applied to patients who underwent hepatectomy thereby improving their recovery and prolonging OS and DFS.

ERAS program could be safely applied to patients who underwent hepatectomy thereby improving their recovery and prolonging OS and DFS.

Growing evidences imply that multiple long non-coding RNAs (lncRNAs) play a significant role in the treatment of cancer. Therefore, it is of great significance to discover new biomarkers or therapeutic targets of gastric cancer (GC). However, the potential molecular mechanism of lncPROX1-AS1 in GC remains unknown. The objective of current study is to investigate the effect of PROX1-AS1 in GC.

Thus, we detect that PROX1-AS1 is over-expressed in tissues and cell lines of GC using qRT-PCR analysis. CCK-8, colony formation, flow cytometry, wounding healing and transwell analyses were performed to explore the effect of PROX1-AS1 on GC malignant behaviors.

It is further disclosed that silencing of PROX1-AS1 represses cell proliferation, migration, and invasion, whereas promotes cell apoptosis in GC. Bioinformatics analysis suggests that miR-877-5p is negatively regulated by PROX1-AS1 and ectopic of miR-877-5p alleviates the malignant behaviors of GC. Subsequently, miR-877-5p suppresses the activity of PD-L1-3' UTR. At last, rescue assays demonstrated that the GC progression is suppressed by sh-PROX1-AS1 and facilitated on account of miR-877-5p inhibitors and then is retrieved by sh-PD-L1.

Our findings reveal that PROX1-AS1 exerts its role via miR-877-5p/PD-L1 axis in the GC progression, suggesting that PROX1-AS1 may represent a new therapeutic target for the diagnosis and treatment of GC patients.

Our findings reveal that PROX1-AS1 exerts its role via miR-877-5p/PD-L1 axis in the GC progression, suggesting that PROX1-AS1 may represent a new therapeutic target for the diagnosis and treatment of GC patients.

Intestinal microbiota play a critical role in the development of colorectal cancer. However, little is known about the structure and characteristics of gut microbial in colorectal cancer, especially in locally advanced rectal cancer after neoadjuvant chemoradiation therapy.

Here, we performed this study to evaluate microbial characteristics between pathologic complete response (pCR) (n=12) and non-pathological complete response (Non-pCR) (n=45) tumor tissues from patients with locally advanced rectal cancer after neoadjuvant chemoradiation therapy. In this study, 16S rRNA gene sequencing was used to detect the microbial diversity including Alpha diversity and Beta diversity. Moreover, we used PICRUSt from the Kyoto Encyclopedia of Genes and Genomes (KEGG) database to predict the microbial metabolism functions.

There was significant statistical difference in PFS between pCR and Non-pCR group (

< 0.05). However, there was no significant difference in OS between pCR and Non-pCR group. The microbial co locally advanced rectal cancer patients after neoadjuvant chemoradiation therapy. Our results present new alterations in the microbiome in locally advanced rectal cancer after neoadjuvant chemoradiation therapy, suggesting that it will provide a new perspective for the precise treatment of neoadjuvant rectal cancer by targeting specific microbial species in the future.[This retracts the article DOI 10.2147/CMAR.S268222.].

Based on a multi-centered and a large sample size, this study aims to analyze the relationship between preoperative and postoperative serum CEA and recurrence of rectal cancer without preoperative therapy.

This retrospective cohort study enrolled stage I to III rectal cancer patients without preoperative therapy (N = 1,022) who received radical resection of rectal cancer from 2 hospitals in China. Based on the preoperative and postoperative serum carcinoembryonic antigen, the patients were subdivided into 3 groups ie, normal preoperative CEA (≤5.0 ng/mL, N = 627), elevated preoperative (>5.0 ng/mL) but normalized postoperative CEA (normalized postoperative CEA, N = 255), as well as elevated preoperative and postoperative CEA (elevated postoperative CEA, N = 67). The generalized additive model was used to assess the relationship between carcinoembryonic antigen and the risk of recurrence. Further, the Cox regression model was used to evaluate the relationship between carcinoembryonic antigen and 3-year tients. Therefore, it is necessary to combine preoperative and postoperative CEA to predict the prognosis of patients with rectal cancer, rather than using it alone.

We found that preoperative and postoperative serum CEA of rectal cancer patients were related to the 3-year recurrence-free survival rate. Moreover, the risk of recurrence in the normalized postoperative CEA group of patients was insignificantly different from that of the normalized preoperative CEA patients. Therefore, it is necessary to combine preoperative and postoperative CEA to predict the prognosis of patients with rectal cancer, rather than using it alone.

Lung cancer has been recognized as the most fatal malignant tumor with the highest morbidity and mortality in recent years.

In this study, we found that LMNB1, which is an important component protein of the nuclear skeleton, was significantly upregulated in lung adenocarcinoma (LUAD) and correlated with the pathological stage as well as lymphatic metastasis.

In vitro loss-of-function study utilizing

knockdown LUAD cell lines demonstrated that depletion of

inhibited development of LUAD through regulating cell proliferation, cell apoptosis, cell cycle and cell motility. Decreased tumorigenesis of

knockdown LUAD cells was proved in mice xenograft models. Tepotinib Moreover, the mechanism by which

promotes LUAD was explored through the expression evaluation of apoptosis-related proteins and cancer-related signaling pathways.

In conclusion, our study identified

as a tumor promotor and a potential therapeutic target in LUAD.

In conclusion, our study identified LMNB1 as a tumor promotor and a potential therapeutic target in LUAD.

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