Locally advanced cervical cancer (LACC) is an early-stage cervical cancer characterized by a local tumor diameter of ≥4 cm. Patients with LACC have a relatively poor prognosis. Although preoperative radiochemotherapy (PRCT) might offer a valuable opportunity for subsequent radical surgery, surgeons should also consider the nonresponsive rate, the adverse effects of PRCT, and the surgical complications before designing a treatment plan. Therefore, biomarkers for predicting PRCT sensitivity and prognosis in patients with LACC are of high importance. We investigated the prognostic significance of vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1α (HIF-1α) in patients with LACC. A total of 43 patients with LACC who underwent PRCT (one course each of intravenous chemotherapy and after-loading intracavitary brachytherapy followed by a radical hysterectomy) during the period 2009–2014 were included in this study. VEGF and HIF-1α expression levels were evaluated by immunohistochemistry in LACC lesions before and after PRCT. In addition, we analyzed the association of these proteins with the clinical response and pathological findings of pelvic lymph node metastasis (PLNM) after the subsequent surgery. The total clinical response rate was 81.39% after PRCT, including five complete responses and 30 partial responses. VEGF and HIF-1α expression before PRCT was significantly higher than after PRCT (VEGF: 85.71% vs 66.67%; HIF-1α: 83.33% vs 59.52%, P<0.05). In addition, the same trend was found in patients with PLNM compared to those without PLNM (VEGF: 100% vs 77.78%; HIF-1α: 100% vs 74.07%, P<0.05). The areas under the receiver operating characteristic curves were 0.896 and 0.835 when using pre-PRCT VEGF and HIF-1α expression levels, respectively, to diagnose PLNM in patients with LACC. Serial detection of VEGF and HIF-1α demonstrated a sensitivity of 66.67% and specificity of 88.89%. These findings suggest that VEGF and HIF-1α expressions are potential biomarkers for PRCT and have great clinical significance for the prediction of PRCT response and prognosis in patients with LACC.
Green credit policy is designed to address the global climate risk. However, few studies have investigated empirically whether green credit policy indeed reduces corporate carbon emission intensity. Based on firm‐level data in China and a difference‐in‐differences model, this study explores how corporate carbon emission intensity evolves following the green credit policy. We find that, on the whole, the green credit can effectively reduce corporate carbon emission intensity, while the dynamic negative effect tends to alleviate after 2017. Specifically, green credit reduces corporate carbon emission intensity mainly through lowering investment carbon intensity and enhancing environmental supervision. However, the signaling mechanism of green credit does not significantly alleviate corporate carbon emission intensity. The green credit has a stronger reduction effect on corporate carbon emission intensity with third‐party certification, non‐state‐owned ownership, and high financing constraint. We thereby suggest that innovations should be made to the standards and processes of green credit to ensure sustainability and stability. Quantitative and standardized corporate environmental information disclosure is essential for the low‐carbon effect on green finance innovation.
Introduction
Since Vichow proposed the hypothesis that chronic inflammation was closely related to tumor in 1863, experimental, clinical and epidemiological studies have shown that inflammation plays an important role in tumor progression, immune response, tumor therapy and prognosis. In this study, 38B9 cells were injected into BALB/c mice to establish lymphoma-burdened mice model. The expression of IL-10, TNF- and IL-6 were observed in plasma and tissues to study the effects of tumor inflammatory factors on tumor environment.
Methods
Ten 9-week-old BALB/c mice were randomly divided into the control group and the tumor-burdened group. Each mouse in tumor-burdened group was injected with 2×106/200μl 38B9 cells, while the control group was injected with 200μl PBS buffer solution. The establishment of B-cell lymphoma tumor-burdened mice model was confirmed by magnetic resonance information (MRI). The peripheral blood samples were collected before injection, after tumorigenesis and when sacrificed. The tumor tissues were also collected. The level of IL-6, IL-10, TNF-α in the plasm were detected by enzyme-linked immuno sorbent assay (ELISA) and the relative value of mRNA in tissues were measured by quantitative real-time polymerase chain reaction (qRT-PCR).
Results
1.Compared with the control group, the levels of IL-6 and TNF-α in the tumor-burdened group were increased after injected 14 days (P <0.05). However, the level of IL-10 showed no significant difference (P >0.05). After injected 19 days, the levels of IL-6, IL-10 and TNF-α of tumor-burdened group were decreased (P<0.05).
2. The expression of IL-10 mRNA in tumor tissues was lower than the control group (P <0.05), while the expression of IL-6 mRNA in borderline tissues was higher than the control group (P<0.05). Compared with tumor tissue, the expression of IL-10 mRNA was increased in borderline tissue (P <0.05). The level of IL-6 and TNF-α showed no significant difference (P>0.05).
Conclusions
1. The level of IL-6, IL-10 and TNF-α in the tumor tissues and plasma were significantly higher after tumorigenesis.
2. The increased expression of inflammatory factors is related to tumor-induced inflammatory microenvironment.
Disclosures
No relevant conflicts of interest to declare.
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