Objective To investigate the influence of different pressures and duration of CO2 pneumoperitoneum on the adhesive and invasive ability of gastric cancer cells based on the expressions of adhesive and invasive molecules. Methods With an artificial CO2 pneumoperitoneum model in vitro, human gastric cancer cell lines including MKN-45, SGC-7901, and MKN-28 were exposed to CO2 in different environments: 0 mm Hg （1 mm Hg=0.133 kPa）, 9 mm Hg （2 h, 4 h）, and 15 mm Hg （2 h, 4 h）. The expressions of mRNA of E-cadherin, intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-2 (MMP-2), and vascular endothelial growth factor-A (VEGF-A) in the different environments were measured by RT-PCR. The expressions of protein of E-cadherin and ICAM-1 in the environments of 0 mm Hg and 15 mm Hg （4 h） were measured by FCM. Results With the increase of duration or pressure, RT-PCR showed that there was a downward trend in the expression of E-cadherin mRNA as well as there were upward trends in the expressions of ICAM-1, MMP-2, and VEGF-A mRNA; FCM showed that there was a downward trend in the expression of E-cadherin protein while the expression of ICAM-1 protein showed the opposite change. But there were no obvious differences under different environment (P＞0.05). Conclusions Under low pressure (≤15 mm Hg) and short time (≤4 h) of CO2 pneumoperitoneum, the adhesive and invasive ability of gastric cancer cells could not be affected, which means that under this environment, CO2 pneumoperitoneum will not increase the possibility of neoplasm metastasis.
Tenascin-C (TNC) is an extracellular matrix glycoprotein, which is usually highly expressed in embryonic tissues and tumor tissues, but is not expressed or just lowly expressed in mature tissues. TNC is involved in various complex signaling pathways during tumor metastasis, especially through modulating FAK, RhoA, Wnt and Notch pathways by interacting with syndecan-4, integrinα5β1, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF). As a result, TNC affects epithelial mesenchymal transition, tumor cell adhesion, proliferation and angiogenesis, which eventually enhances the invasion and metastasis ability of many tumors. Further studies have demonstrated that TNC could be used as prognosis or metastasis marker of patients with malignant tumor.
Objective To determine the efficacy of radioisotopes to control metastasic pain in patients with tumor bone metastases and complications due to bone metastases (hypercalcaemia, bone fracture and spinal cord compression). The effectiveness of radioisotopes in relation to patient survival and adverse effects were also assessed. Methods MEDLINE (1966 to April 2005),EMBASE (1966 to April 2005), The Cochrane Library (Issue 1, 2005) and CBMdisc (1979 to April 2005) were searched for randomized controlled trials (RCTs). Data were extracted by two reviewers using a designed extraction form. The quality of included RCTs was critically assessed. RevMan 4.2 software was used for data analysis. Results Four RCTs were included. The results of meta-analysis showed that small dose of radioisotopes couldn’t control metastatic pain in short term(2 months) with relative risk (RR) 1.13, 95%confidence interval (CI) 0.34 to 3.76, but large dose can significantly control metastatic pain in medium term(6 month) with RR 1.90, 95％CI 1.23 to 2.92; no evidence was available to assess long term(≥12 months) effects. No study provided data on quality of life, mortality, bone metastatic complications (hypercalcaemia, bone fracture) and analgesic use etc. Leukocytopenia and thrombocytopenia were secondary effects associated with the administration of radioisotopes. The incidences of leukocytopenia and thrombocytopenia were significantly greater in patients treated by radioisotopes with RR 8.28, 95％CI 2.24 to 30.67, and RR 3.70, 95％CI 1.59 to 9.04, respectively. Conclusions There is some evidence indicating that large dose of radioisotopes can relieve metastatic bone pain over one to six months, but adverse effects, particularly leukocytopenia and thrombocytopenia, have also been experienced.
Objective To investigate the expressions of CXCR4 and β-catenin in pancreatic cancer, explore the relationship between them, and explore the possible biomarkers about invasion and metastasis of pancreatic cancer. Methods Forty-eight samples of pancreatic cancer and 20 samples of normal pancreas tissues were selected. The expressions of CXCR4 and β-catenin were examined by the immunohistological technique. Spearman, Chi-square， and rank test were used to analyze the relation between the protein expressions and clinical characteristics. Survival analysis was evaluated by Kaplan-Meier product limit method and Log-rank test. Variables were evaluated by Cox proportional hazards analysis. The size of test was 0.05. Results The positive expression rates of CXCR4 and β-catenin in pancreatic cancer tissues were 85.4% (41/48) and 75.0% (36/48), respectively. Co-expression rate of CXCR4 and β-catenin was 70.8% (34/48). There were significant differences between various CXCR4 staining and lymph node metastasis and TNM stage (P=0.012, 0.005, respectively). β-catenin positive expression was associated with lymph node metastasis (P=0.047). However, abnormal β-catenin positive expression could not determine the clinical survival. Kaplan-Meier estimated curves suggested that clinical prognosis was poor for patients with CXCR4 expression. Multivariate analysis showed that CXCR4, late TNM stage, and lymph node metastasis were independent prognostic factors for pancreatic cancer. Conclusions Both CXCR4 and β-catenin abnormally express in pancreatic cancer. CXCR4 may be an important marker for pancreatic cancer progression.
ObjectiveTo explore the clinical features, primary lesions and prognosis of optic nerve metastases.MethodsSeven patients (11 eyes) with optic nerve metastatic tumor diagnosed by the examinations of ophthalmology, laboratory and pathology in Chinese PLA General Hospital from April 2015 to September 2017 were included in this study. All patients underwent BCVA, flash VEP, OCT, orbital MRI, serum tumor marker, cerebral spinal fluid detection and PET-CT. Histopathological examination of primary or near superficial metastases was performed. The follow-up period was ranged from 16 to 44 months, with the mean of 23.0±10.9 months. The clinical characteristics, primary tumor, imaging features, treatment and clinical prognosis in the patients were analyzed.ResultsAmong 7 patients, there were 5 males and 2 females, with the mean age of 53.90±14.99 years; 3 patients with unilateral optic nerve involvement, 4 patients with bilateral optic nerve involvement; 5 patients (71.4%) first diagnosed in ophthalmology. Five patients (45.5%) were misdiagnosed as optic neuritis, optic disc edema in 6 eyes (54.5%). All of them appear loss of visual acuity, including 8 eyes (72.7%) with BCVA＜0.1, 2 eyes (18.2%) with BCVA 0.1-0.5, 1 eye (9.1%) with BCVA＞0.5. MRI results show that 1 patient with intraorbital segment, 1 patient with internal segment of optic canal, 4 patients with intracranial segment, 1 patient with intracranial segment and optic chiasma involved simultaneously, 4 patients involving surrounding tissue. There were 4 patients (57.1 %) with lung cancer, 2 patients (28.6%) with kidney cancer, 1 patient (14.3%) with gastric cance; 6 patients (85.7%) with metastasis from other sites, 2 patients with brain metastasis (1 patient with meningitis carcinomatosa). There were 2 patients (28.6%) with previous primary cancer surgery. After diagnosis, 1 patient received chemotherapy, 1 patient received radiotherapy, 5 patients gave up treatment. At the end of follow-up, 1 patient (1 eye) of chemotherapy with BCVA increased by 2 line; 1 patient (2 eyes) of radiotherapy with no change in BCVA; of the 5 patients who gave up treatment, 1 patient died of disease, 1 patient lost follow-up, and 3 patients (4 eyes) had no change in BCVA.ConclusionsWith atypically clinical manifestations, the optic nerve metastases easily misdiagnosed as optic neuritis, and with poor therapeutic effect. Primary lesions are mostly found in lung cancer.