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Will be the Conjunctiva any Target with regard to Superior Treatments Medical Goods?
This study aims to elucidate the biological functions of CDCA2 (cell division cycle associated 2) in hepatocellular carcinoma (HCC) progression and the potential mechanism.

CDCA2 levels in HCC tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between CDCA2 and clinical characteristics in HCC patients was analyzed. Curcumin analog C1 mw Cox proportional-hazards model was applied for assessing the potential factors influencing overall survival in HCC. Three CDCA2 siRNAs were generated and the most effective one was used in the following experiments. After knockdown of CDCA2 in HCC-LM3 cells, clonality and viability were examined. Meanwhile, cell cycle progression was detected by flow cytometry. Relative levels of CDCA2, p21, p27, CDK2, CCND1, CCNE1 and CCNB1 in HCC-LM3 cells were determined by qRT-PCR. The activation of the protein kinase B (Akt) signaling was examined by Western blot. Subsequently, we constructed HCC xenograft model in nude mice. Tumor volume and tumor weight of xenografted HCC were recorded.

CDCA2 was upregulated in HCC tissues than that of para-tumor ones, especially HCC tissues with larger than 5 cm in tumor size or vascular invasion. CDCA2 level was related to tumor size, vascular invasion and tumor differentiation in HCC. Knockdown of CDCA2 inhibited clonality and viability in HCC-LM3 cells, and arrested cell cycle progression in G1 phase via downregulating CCND1. The phosphatidilinositol 3-kinase (PI3K)/Akt was activated by CDCA2 during the progression of HCC. Tumor volume and tumor weight of xenografted HCC decreased in nude mice with in vivo knockdown of CDCA2.

CDCA2 triggers proliferative potential in HCC by targeting CCND1 via activating the PI3K/Akt signaling.
CDCA2 triggers proliferative potential in HCC by targeting CCND1 via activating the PI3K/Akt signaling.
We aimed to investigate the effect of celecoxib on rats with liver cancer through the extracellular signal-regulated kinase (ERK)/c-Jun N-terminal kinase (JNK)/p38 pathway.

Sprague-Dawley rats (n=36) were divided into 3 groups (n=12 per group) randomly. In model group, the liver cancer model was established, and normal saline was intraperitoneally injected. In celecoxib group, the liver cancer model was also established, and celecoxib was intraperitoneally injected. After intervention for 30 d, the samples were taken. The body weight of rats was measured before modeling and before sampling. The morphology of liver tissues was observed via hematoxylin-eosin (HE) staining, the expressions of related proteins and messenger ribonucleic acids (mRNAs) were determined via Western blotting and quantitative polymerase chain reaction (qPCR), respectively, and the protein expressions of cysteinyl aspartate specific proteinase 3 (Caspase3) and Cyclin D1 in liver tissues were detected.

Before modeling, there was no difference in t.
Before modeling, there was no difference in t.
To explore the efficacy and safety of sorafenib combined with transcatheter hepatic arterial chemoembolization (TACE) in the treatment of intermediate-advanced hepatocellular carcinoma (HCC).

A total of 132 intermediate-advanced HCC patients were divided into two groups, namely, control group (n=66, TACE) and Sorafenib group (n=66, TACE combined with sorafenib). Then, the clinical efficacy and incidence rate of adverse reactions were compared s. Besides, the levels of tumor markers and liver function indicators were detected before and after treatment. Additionally, the survival of patients was followed up and recorded.

The overall response rate (ORR) and clinical benefit rate (CBR) were significantly higher in Sorafenib group than those in control group. Both Sorafenib group and control group exhibited significantly lowered levels of serum AFP, CEA, CA125 and CA19-9 after treatment compared with those before treatment. In addition, such levels were prominently lower in Sorafenib group than those in conis able to significantly reduce the levels of serum tumor markers and prolong the survival of patients, and results in tolerable adverse reactions.
The purpose of this study was to clarify the expression pattern of Nek2B in hepatocellular carcinoma (HCC) and its influence on malignant phenotypes of HCC through regulating SFRP1 and the Wnt/β-catenin pathway.

Nek2B levels in 64 paired HCC tissues and adjacent normal ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The correlation between Nek2B level and clinical parameters of HCC patients was analyzed. Regulatory effects of Nek2B and SFRP1 on clonality, proliferation and apoptosis of MHCC97H and Hep3B cells were determined through functional experiments. Western blot was conducted to detect protein levels of SFRP1, β-catenin, c-myc, cyclinD1 and MMP7 in HCC cells with overexpression or knockdown of Nek2B. At last, rescue experiments were performed to clarify the role of Nek2B/SFRP1 regulatory loop in aggravating the progression of HCC.

Nek2B was upregulated in HCC tissues and cells. HCC patients expressing a high level of Nek2B were in more advanced tumor stage and had worse prognosis. Overexpression of Nek2B in MHCC97H cells enhanced clonality, 5-Ethynyl-2'- deoxyuridine (EdU)-positive ratio and suppressed apoptosis. Besides, knockdown of Nek2B in Hep3B cells yielded the opposite results. SFRP1 was downregulated in HCC, and low level of SFRP1 predicted worse prognosis of HCC. Overexpression of Nek2B downregulated SFRP1, but upregulated β-catenin, c-myc, cyclinD1 and MMP7 in HCC cells. Importantly, Nek2B/SFRP1 regulatory loop was identified to aggravate the progression of HCC.

Nek2B is upregulated in HCC, and closely linked to tumor stage and poor prognosis in HCC patients. Through interaction with SFRP1, Nek2B aggravates the progression of HCC by activating the Wnt/β-catenin pathway.
Nek2B is upregulated in HCC, and closely linked to tumor stage and poor prognosis in HCC patients. Through interaction with SFRP1, Nek2B aggravates the progression of HCC by activating the Wnt/β-catenin pathway.
We aimed to assess whether skeletal muscle loss during EGFR thyrosine kinase inhibitor therapy of advance non-small cell lung cancer patients is an independent prognostic factor for progression-free survival (PFS) and overal survival (OS).

A total of 45 patients who had computed tomography images were retrospectively evaluated at the diagnosis and during the treatment period before progression occurs.

During treatment 19 patients (42.2%) had skeletal muscle loss. Objective response rates in muscle loss group and muscle stable group were 36.8% and 73.0%, respectively (p<0.01). Median follow-up time was 18.9 months (14.8-32.1). Median PFS was 14.7 months (95% CI 12.1-17.3) in muscle stable group and 7.6 months (95% CI 6.7-8.5) in muscle loss group (p<0.01). Median OS was 18.3 months (95% CI 16.5-20.2) in muscle loss group while it was 30.1 months (95% CI 22.1-38.2) in muscle stable group (p<0.01). In multivariate analysis for both PFS and OS, skeletal muscle loss was an independent prognostic factor.
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