Huopuxialing Decoction: A Promising Candidate for Precancerous Lesions of Gastric Cancer Treatment Based on Bioinformatics and Experimental Verification.

BACKGROUND: The Precancerous Lesion of Gastric Cancer (PLGC) is an early stage in the development of gastric cancer. The clinical application of HPXLD has been found to be effective in treating PLGC, but the mechanism of how HPXLD acts on PLGC is still unclear. OBJECTIVE: The objectives of this study were to reveal the molecular mechanism of how HPXLD can be used to treat PLGC and investigate this mechanism through bioinformatics and experimental validation. METHODS: PLGC-associated target genes were identified through bioinformatics analysis. A rat model of PLGC was induced using N-methyl-N'-nitro-N-nitrosoquanidine (MNNG) in combination with ranitidine, hot saline, ethanol, and intermittent fasting, with interventions by HPXLD. The pathological alterations in gastric mucosa were assessed through Hematoxylin-eosin staining (HE). Immunohistochemistry (IHC) and Western blot analyses were employed to evaluate the changes in expression levels of inflammation-related proteins. RESULTS: After conducting bioinformatics analysis, it was found that there were 23 HPXLDPLGC crossover genes, which were significantly enriched in the IL-17 signaling pathway, TNF signaling pathway, and NF-kappa B signaling pathway. The results of HE showed that HPXLD was effective in improving gastric mucosal histopathological changes. Additionally, the IHC results demonstrated that HPXLD was able to downregulate the expression of IL-6, COX-2, MCP- 1, and MMP-9. Furthermore, Western blot analysis revealed that HPXLD was able to downregulate the expressions of IL-6, IL-17RA, ACT1, NF-κB, and TNF-α. CONCLUSION: HPXLD has been shown to improve PLGC by reducing the expression of inflammation- related proteins. This suggests that HPXLD may potentially be a treatment option for PLGC.

Identification of INHBA as a potential biomarker for gastric cancer through a comprehensive analysis.

Inhibin subunit beta A (INHBA) is a member of the transforming growth factor-beta (TGF-ß) superfamily that plays a fundamental role in various cancers. However, a systematic analysis of the exact role of INHBA in patients with gastric cancer (GC) has not yet been conducted. We evaluated the expression levels of INHBA and the correlation between INHBA and GC prognosis in GC. The relationship between INHBA expression, immune infiltration levels, and type markers of immune cells in GC was also explored. In addition, we studied INHBA mutations, promoter methylation, and functional enrichment analysis. Besides, high expression levels of INHBA in GC were significantly related to unfavorable prognosis. INHBA was negatively correlated with B cell infiltration, but positively correlated with macrophage and most anticancer immunity steps. INHBA expression was positively correlated with the type markers of CD8+ T cells, neutrophils, macrophages, and dendritic cells. INHBA has a weak significant methylation level change between tumor and normal tissues and mainly enriched in cancer-related signaling pathways. The present study implies that INHBA may serve as a potential biomarker for predicting the prognosis of patients with GC. INHBA is a promising predictor of immunotherapy response, with higher levels of INHBA indicating greater sensitivity.

Clinical course and management of insidious adrenal crisis manifested initially as hyperpyrexia secondary to pembrolizumab: Case reports and literature review.

Immune checkpoint inhibitors (ICIs) are novel drugs with a dramatic survival benefit in patients with advanced malignancies. With the widespread use, several immune-related adverse events (irAEs) have emerged, which may be life-threatening. Herein we report two patients with adrenal crisis who received anti-programmed cell death protein 1 (PD-1) (pembrolizumab) therapy. Several reports of secondary adrenal insufficiency caused by pembrolizumab exist, including during treatment or late onset. Severe adrenal insufficiency according to the Common Terminology Criteria for Adverse Events (CTCAE) has rarely been described in the literature, since it initially manifests as high-grade fever. The two male patients developed adrenal crisis that was first characterized by hyperpyrexia accompanied by abdominal symptoms. These initial manifestations confused the clinicians who misdiagnosed them as infection. Timely identification, hydrocortisone pulse therapy, and fluid resuscitation improved the patients' condition. Compliance with the standardized treatment approach and course can prevent or relieve the crisis as soon as possible. Assessment of relevant laboratory test results and patient education, including when to use stress-dose hydrocortisone and guidance on route of administration, can reduce the incidence of adrenal crisis. We report these two cases and have evaluated the literature on previously reported cases to improve our understanding of this condition and offer a more scientific approach to diagnosis and treatment options.

Effects of early palliative care on patients with incurable cancer: A meta-analysis and systematic review.

OBJECTIVE: This meta-analysis aims to compare the effects of early palliative care on patients with incurable cancer with those of standard oncologic care or on-demand palliative care. METHODS: Pubmed, Embase, Web of Science, Cochrane Library, ClinicalTrials.gov and World Health Organization International Clinical Trials Registry Platform (ICTRP) were searched for relevant randomised controlled trials. We also screened reference lists of included studies for additional qualified studies. We used Cochrane Collaboration Risk of Bias Tool to evaluate quality of included studies. DerSimonian and Laird's random effects meta-analysis was used to synthesise the effects. RESULTS: Sixteen in 1376 studies were included. The pooled data suggested that patients receiving early palliative care had better quality of life (SMD = 0.737, 95% CI: 0.240-1.234), fewer symptoms (SMD = 0.304, 95% CI: 0.097-0.510), better mood (SMD = -0.443, 95% CI: -0.605 to -0.282), better survival (hazard ratio [HR] of death: HR = 1.521, 95% CI: 1.521-1.923; 1-year overall survival probability: HR = 1.238, 95% CI: 1.031-1.486) and higher probability of dying at home (HR = 1.153, 95% CI: 1.027-1.295) than patients in the control group. And there is no difference between resource use. CONCLUSION: Early palliative care improves lives of patients with incurable cancer, but the evidence level is low because of high heterogeneity of quality of life and small numbers of included studies for other results.

Cystathionine ß-synthase expression correlates with tumor development and poor prognosis in patients with adenocarcinoma of the gastroesophageal junction.

OBJECTIVES: To reveal the expression level of cystathionine ß-synthase (CBS) in adenocarcinoma of esophagogastric junction (AEG) and discuss the relationship between CBS expression level and tumor microvascular density (MVD), clinical features and prognosis. METHODS: Paraffin samples from 214 patients with AEG were selected to make pathological microchips. Immunohistochemistry was performed based on the microchips to detect the expression level of CBS and microvascular density (MVD) in cancer tissues and adjacent control tissues. Relationships between expression level of CBS and MVD, clinical characteristics and prognosis were analyzed. RESULTS: In total, 214 AEG cases were classified into three groups: CBS negative staining (n=26), low staining (n=44), and high staining (n=144). Quantitative alterations in CBS and CD31 expression were explored using immunohistochemistry. The 5-year recurrence rate of enrolled patients was followed up and found that CBS expression was significantly increased in tumor tissue compared with adjacent non-tumor tissue (P<0.0001). There were significant differences in microvascular density between the groups with negative and high CBS staining (P<0.0001), and between the groups with low and high CBS staining (P<0.0001). Univariate analysis revealed significant differences in tumor stage (P<0.0001), T stage (P=0.008), N stage (P=0.028), differentiation degree (P=0.037), and 5-year survival (P=0.0034) among the three groups. Multivariate logic regression analysis showed that increased CBS scores were associated with an increased probability of 5-year recurrence (P=0.018). Finally, different CBS expression levels were associated with disease-free survival in AEG patients. CONCLUSIONS: CBS expression level is closely related to microvascular density and tumor stage in AEG. High level of CBS not only accelerates tumor angiogenesis but also affects patient's survival and prognosis.

Research on the mechanisms of taraxerol for the treatment of gastric cancer effect based on network pharmacology.

BACKGROUND: Modern pharmacological studies have shown that traditional Chinese medicine (TCM) Taraxacum mongolicum possesses anti-cancer activity. Taraxerol (TRX) is a pentacyclic triterpene isolated from T. mongolicum, which is widely used in clinical treatment, and its anti-cancer effects have been extensively studied. However, the effects and molecular mechanism of TRX in gastric cancer (GC) have not been fully explicated. METHODS: We used public databases to derive information on potential targets of TRX and proteins related to GC. Also, STRING and R3.6.2 software were used to analyze the protein-protein interaction (PPI). The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were done to explain the potential mechanism underlying the regulatory role of TRX in GC. The role of TRX in GC was verified by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, apoptosis analysis, Transwell assay, and wound healing assay, and the key signaling pathways were verified. RESULTS: We identified 135 potential targets for the treatment of GC via network pharmacological analysis. GO and KEGG enrichment analysis showed that steroid hormone receptor activity and the PI3K/AKT signaling pathway were the biological processes and pathways with the highest degree of enrichment. Additionally, cellular experiments revealed that TRX inhibited the proliferation, migration, and invasion of GC cells as well as induced G1 phase arrest and apoptosis in GC cells. CONCLUSION: Here, we used multi-target and multi-pathway network pharmacological analysis to verify the anti-cancer activity of TRX in GC. Also, in vitro experimental data were used to derive the potential molecular mechanism.

Regulatory Mechanism and Experimental Verification of Patchouli Alcohol on Gastric Cancer Cell Based on Network Pharmacology.

BACKGROUND: Pogostemon cablin is a traditional Chinese medicine (TCM) that is frequently used to treat various gastrointestinal diseases. Patchouli alcohol (PA), a compound extracted from the Pogostemon cablin, has been shown to have anti-tumor efficacy in human colorectal cancer. However, the mechanism of PA's anticancer effect on gastric cancer (GC) remains unknown. METHODS: We used the public database to obtain the potential targets of PA and genes related to GC. Bioinformatic analyses, such as the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and protein-protein interactions (PPI), were used for analyzing the potential signal pathways and targets. Cell experiments were also conducted to further explain the impact and molecular mechanism of PA on GC, as well as to confirm the findings of network pharmacology. RESULTS: Using network pharmacological analysis, 161 possible targets were identified for the treatment of GC. Network analysis and functional enrichment analysis show that PA produced a marked effect in the treatment of GC through multi-targets and multi-pathways, especially the MAPK and PI3K/AKT signal pathways. In addition, PA showed the inhibition of GC cell proliferation, migration and invasion in cell experiments. According to our findings, PA could also cause G0/G1 phase arrest and apoptosis in GC cells. CONCLUSION: Using network pharmacology, we aim to uncover the possible molecular mechanism of PA on GC treatment in this research. Cell experiments were also conducted to confirm the therapeutic effect of PA on GC.

TMT-based proteomics analysis of the effects of Qianjinweijing Tang on lung cancer.

Qianjinweijing Tang (QJWJ) is a classic traditional Chinese formula that is often used in the treatment of treat lung cancer (LC). However, the underlying cellular mechanisms of the anticancer effects of QJWJ remain unclear. Cell viability was determined by MTS assay and levels of apoptosis measured by flow cytometry. Animal experiments were conducted to determine the effects of QJWJ on tumor growth in vivo. We used a proteomics approach to study the effects of QJWJ on LC cells and applied bioinformatics analysis to identify differentially expressed proteins that were validated by western blotting. QJWJ inhibited the proliferation of LC cells and induced apoptosis. The tumor growth delay effects of QJWJ were confirmed in vivo. We identified 104 differentially expressed proteins following QJWJ treatments of which 45 proteins were upregulated and 59 were downregulated. The levels of differentially expressed proteins were validated by western blotting. Our study indicated that QJWJ has anticancer effects in vivo and in vitro and that these effects are mediated by modulating the expression of tumor-related proteins.

Relationship between thymidine kinase 1 before radiotherapy and prognosis in breast cancer patients with diabetes.

In a retrospective study design, we explored the relationship between serum thymidine kinase 1 (TK1) concentration before radiotherapy and clinical parameters and evaluated the prognostic value of serum TK1 concentration before radiotherapy in breast cancer patients with type 2 diabetes mellitus. The present study finally consisted of 428 breast cancer patients with a mean age of 53.0 years. Compared with low TK1 group, the high TK1 group tended to have larger tumor size (P=0.011) and had more lymph node number (P=0.021). Significant differences were also observed in clinical stages I, II and III (P=0.000). There was no significant difference between TK1 and other clinical parameters. For disease-free survival (DFS), the univariate analysis indicated that the high TK1 increased the risk of poor prognosis (HR = 2.38, 95% CI: 1.64-4.23, P=0.000). The Kaplan-Meier curve indicated the high TK1 group was poorer than that in the low TK1 group (P=0.002). For the overall survival (OS), similar results were found that the high TK1 was related to poor OS (HR = 1.89, 95% CI: 1.34-3.67, P=0.000). The multivariate Cox regression indicated that the TK1 was still associated with DFS (HR = 1.83, 95% CI: 1.22-3.17, P=0.001) and OS (HR = 1.63, 95% CI: 1.19-2.08, P=0.006). The high pretreatment serum TK1 levels in breast cancer patients were associated with poor OS and DFS. TK1 could be a potential predictive factor in differential diagnosis of poor prognosis from all patients.

The role of procalcitonin in differential diagnosis between acute radiation pneumonitis and bacterial pneumonia in lung cancer patients receiving thoracic radiotherapy.

Acute Radiation Pneumonitis (ARP) is one of the most common dose-limiting toxicities of thoracic radiotherapy. The accurate diagnosis of ARP remains a challenge because of the lack of a rapid biomarker capable of differentiating ARP from bacterial pneumo (BP). The aim of this study was to investigate the potential usefulness of procalcitonin (PCT) in the differential diagnosis of ARP and BP. Lung cancer patients who had undergone thoracic radiotherapy within 6 months and were admitted to hospital for ARP or BP were retrospectively analyzed. The serum levels of PCT, C-reactive protein (CRP) and white blood cells (WBC) were compared between the two groups. Receiver operating characteristic (ROC) curve was used to assess the diagnostic value of PCT, CRP and WBC in the differential diagnosis of ARP and BP and determine the best cut-off values. One hundred eighteen patients were included. Among them, seventy-seven patients were diagnosed with ARP, and 41 patients were diagnosed with BP. The PCT concentrations for patients diagnosed with ARP group were significantly lower than those in the BP group (P < 0.001). There were no differences in CRP and WBC between the two groups. The areas under the ROC curves (AUC) for PCT, CRP and WBC were 0.745, 0.589 and 0.578, respectively. The best cutoff values of PCT, CRP and WBC were 0.47 µg/L, 54.5 mg/L and 9.9 × 109/L, respectively. Low serum PCT levels are associated with ARP. PCT is a useful biomarker to distinguish ARP from BP.

Antitumor Effect of Periplocin in TRAIL-Resistant gastric cancer cells via upregulation of death receptor through activating ERK1/2-EGR1 pathway.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor family, induces apoptosis in a variety of cancer cells. However, gastric cancer (GC) cells are insensitive to TRAIL usually. In the previous study, we showed that Periplocin could induce apoptosis in GC cells via the activation of ERK1/2-EGR1 pathway. In the present study, we have shown that the combination of Periplocin and TRAIL had a greater inhibitory effect on gastric cancer cell viability in vitro and in vivo than Periplocin or TRAIL alone. Through upregulating the expression of DR4 and DR5 at transcriptional and protein levels, Periplocin enhanced the sensitivity of gastric cancer cells to TRAIL. Furthermore, enhanced activity of ERK1/2-EGR1 pathway was responsible for upregulating of DR4 and DR5 uponPeriplocin treatment, subsequently reducing the expression of Mcl-1 and Bcl2 and activating Bid and caspase-3/8. Collectively, these data implied that Periplocin might act as a sensitizer of TRAIL and could be a potential strategy for the treatment of GC.

p-Hydroxylcinnamaldehyde slows the progression of 4NQO-induced oesophageal tumourigenesis via the RhoA-MAPK signaling pathway.

p-Hydroxylcinnamaldehyde isolated from the Cochinchina momordica seed (CMSP) has been identified to inhibit growth and metastasis in oesophageal squamous cell carcinoma (ESCC) by inducing differentiation. The aim of the present study was to evaluate the effect and underlying mechanism of CMSP on 4-nitroquinoline 1-oxide (4NQO)-induced oesophageal tumourigenesis. In the present study, a mouse model of oesophageal preneoplastic lesions was established by providing 4NQO-containing drinking water to C57BL/6 mice. The effect of CMSP on tumourigenesis induced by the chemical mutagen and the effect of CMSP on immune function were investigated. The results showed that the incidence and pathological stage of atypical hyperplasia in oesophageal tissues were significantly reduced in CMSP-treated mice compared with untreated mice. Immunohistochemistry and pull-down assay results revealed that the expression levels of p-ERK1/2, p-SAPK/JNK, and GTP-RhoA were significantly decreased in the oesophageal tissue of CMSP-treated mice. In addition, the proportions of CD4+ T cells, CD8+ T cells, and NK cells were increased, while the proportion of CD4+ CD25+ regulatory T cells (Tregs) was decreased, in the peripheral blood of CMSP-treated mice. These results indicated that CMSP could hamper 4NQO-induced oesophageal tumourigenesis by regulating the RhoA-ERK/JNK signaling pathway and promoting immune system function, thus providing a new potential strategy for treating preneoplastic lesions of the oesophagus.

Optimizing miRNA-module diagnostic biomarkers of gastric carcinoma via integrated network analysis.

Several microRNAs (miRNAs) have been suggested as novel biomarkers for diagnosing gastric cancer (GC) at an early stage, but the single-marker strategy may ignore the co-regulatory relationships and lead to low diagnostic specificity. Thus, multi-target modular diagnostic biomarkers are urgently needed. In this study, a Zsummary and NetSVM-based method was used to identify GC-related hub miRNAs and activated modules from clinical miRNA co-expression networks. The NetSVM-based sub-network consisting of the top 20 hub miRNAs reached a high sensitivity and specificity of 0.94 and 0.82. The Zsummary algorithm identified an activated module (miR-486, miR-451, miR-185, and miR-600) which might serve as diagnostic biomarker of GC. Three members of this module were previously suggested as biomarkers of GC and its 24 target genes were significantly enriched in pathways directly related to cancer. The weighted diagnostic ROC AUC of this module was 0.838, and an optimized module unit (miR-451 and miR-185) obtained a higher value of 0.904, both of which were higher than that of individual miRNAs. These hub miRNAs and module have the potential to become robust biomarkers for early diagnosis of GC with further validations. Moreover, such modular analysis may offer valuable insights into multi-target approaches to cancer diagnosis and treatment.

Effect of overexpression of hypoxia-inducible factor-1α induced by hyperoxia in vivo in LNCaP tumors on tumor growth rate.

OBJECTIVE: To study effect of overexpression of hypoxia-inducible factor-1α induced by hyperoxia in vivo in LNCaP tumors on tumor growth rate. METHODS: The prostate cancer LNCaP cells were inoculated in the abdomen of mice. All the mice were randomly placed in the gas chamber with different oxygen content. The groups were divided as follows: twelve mice in hypoxia group, sixteen mice in normoxia group, ten mice in hyperoxia group. After 28 d of treatment, the mice were weighed, the blood samples were taken from the left ventricle, and the tumor was isolated and weighed. Tumor growth, angiogenesis and vascularization, HIF-1α expression and intracellular signal transduction molecules expression in each group of xenografts were detected and analyzed by using Western blotting and immunofluorescence and determination of hemoglobin. RESULTS: Comparison of the growth of xenografts in each group showed that, the xenografts growth of hypoxia group was more quickly than that of normoxia group. The difference was statistically significant (P = 0.004). The difference in xenografts growth between hyperoxia group compared and normoxia group was not statistically significant (P > 0.05). The expressions of HIF-1α, VEGF and VEGF-R of xenografts in hyperoxia group were significantly higher than those of normoxia group (P < 0.05). The expression of HIF-1α of xenografts in hypoxia group and normoxia group were similar. The blood growth rate of xenografts in hypoxia group (170%) was significantly higher than that of normoxia group (40%) (P < 0.05). The expression of Nrf2 of xenografts in hyperoxia group was significantly higher than that of normoxia group (P < 0.05). CONCLUSIONS: When hyperoxia induces the overexpression of HIF-1α in LNCaP tumor, it will not affect tumor growth. It provides a new ideas and theoretical basis for the clinical treatment of prostate cancer.

Expression and clinical significance of the microRNA-200 family in gastric cancer.

Gastric cancer is one of the most common malignant tumors and one of the leading causes of cancer-related mortality. Recent studies have revealed that there is a difference in microRNA (miR/miRNA) profiles between cancerous and normal tissues. To find a potentially useful prognostic predictor and a promising therapeutic tool for gastric cancer, the present study investigated the expression and clinical significance of the miR-200 family in gastric cancer. The miR-200 family has five members: hsa-miR-200a, hsa-miR-200b, hsa-miR-200c, hsa-miR-141 and hsa-miR-429. In 46 clinical samples of gastric cancer and paired non-cancerous tissues, the present study observed that the expression levels of the miR-200 family in the cancer tissues were significantly lower than those in the non-cancerous tissues (P<0.001). Lower levels of the five family members were associated with histological grade and the presence of an intravascular cancer embolus (P<0.05). The results revealed that the miR-200 family is downregulated in gastric cancer, and that there are significant differences in the expression of the miR-200 family between normal and cancer tissues. The miR-200 family may therefore become a potentially useful prognostic predictor of the aggressiveness of gastric cancer and a possible therapeutic tool in affected patients.

Ginsenoside Rg3 enhances the inhibitory effects of chemotherapy on esophageal squamous cell carcinoma in mice.

The present study was conducted in order to investigate the inhibitory effects of ginsenoside Rg3 combined with chemotherapy on Eca-109 esophageal squamous cell carcinoma (ESCC) in mice. Tumor xenograft models were established in the right forelimb of 20 BALB/c nude mice by subcutaneous injection. The tumor-bearing mice were randomly assigned to 4 treatment groups (n=5 per group) as follows: the control group (saline), the ginsenoside Rg3 alone group (6 mg/kg/day, once a day for 3 weeks), the chemotherapy alone group (paclitaxel 10 mg/kg/day + cisplatin 5 mg/kg/day on days 1, 7, 14 and 21) and the chemotherapy + Rg3 group (combined treatment). The length and width of the tumor were directly measured with calipers at different time points and the tumor volume (cm3) was calculated using the formula 0.52 × length × width2 every other day. The mice were sacrificed by cervical dislocation following completion of therapy, the tumors were removed and weighed and the expression levels of Ki-67 were determined by immunohistochemistry. The results indicated that the coadministration of ginsenoside Rg3 significantly enhanced the inhibitory effects of chemotherapy on tumor growth. In addition, the expression levels of Ki-67 in the chemotherapy + Rg3 group were significantly lower compared to those in the other 3 groups. The chemotherapy + Rg3 group also exhibited the lowest microvascular density among all four groups. These findings suggested that ginsenoside Rg3 may improve the antitumor efficacy of chemotherapy in Eca-109 ESCC in mice.

MicroRNA-200c regulates the sensitivity of chemotherapy of gastric cancer SGC7901/DDP cells by directly targeting RhoE.

Gastric cancer remains a worldwide burden as the second leading cause of cancer-related death. Drug resistance of chemotherapy looms as a major clinical obstacle to successful treatment. Recent evidence indicated that miRNA-200c can restore the sensitivity of NSCLC cells to cisplatin and cetuximab. The expression of miRNA-200c and RhoE were investigated in gastric cancer tissues and cells (SGC7901 and SGC7901/DDP) by qRT-PCR. A luciferase reporter assay was done to understand the potential correlation between miRNA-200c and RhoE. Pre-miR-200c was transfected in SGC7901/DDP cells to confirm whether miRNA-200c could regulate RhoE expression. RhoE was knocked down to explore the role of RhoE on sensitivity of chemotherapy in gastric cancer by MTT. Western blot analysis was performed to further explore the mechanism of RhoE in regulating drug resistance. The results showed that miRNA-200c was significantly lower in cancerous tissues than those in the paired normal tissues, whereas the expression of RhoE was just the opposite. The significant difference of miRNA-200c and RhoE were observed between SGC7901 cells and SGC7901/DDP cells. miRNA-200c has target sites in the 3'-UTR of RhoE mRNA by luciferase reporter assay. Transfection of pre-miR-200c reduces RhoE expression. Meanwhile, the knockdown of RhoE enhanced the sensitivity of SGC7901/DDP cells and changed expression of some genes. These suggested that miRNA-200c regulated the sensitivity of chemotherapy to cisplatin (DDP) in gastric cancer by possibly targeting RhoE.

The inhibitory effects of Endostar combined with chemotherapy on human esophageal squamous cell carcinoma xenograft in mice.

The purpose of this study was to investigate the efficacy of Endostar combined with chemotherapy on human esophageal squamous cell carcinoma Eca-109 in mice. The tumor xenograft models were established and randomly assigned to 4 groups: control group, Endostar group (1.5 mg/kg day, once daily for 3 weeks), chemotherapy group (Paclitaxel 10 mg/kg day, Cisplatin 5 mg/kg day, for 1, 7, 14, 21 days), and chemotherapy + Endostar group (combination). The length and width of tumor were measured and the tumor volumes (cm(3)) were calculated every other day. Three weeks later, the mice were executed, and the tumor tissues were collected to weigh and analyse the histopathology and proliferation for tumor xenograft. The results demonstrated that the tumor volumes and weight in chemotherapy + Endostar group were significantly lower than that in other three groups. Meanwhile, the cell proliferation of tumor xenograft in combined treatment group was significantly lower than that in other three groups. It was concluded that Endostar combined with chemotherapy could obviously enhance the inhibitory effect on esophageal squamous cell carcinoma Eca-109 in mice.