Clinical Effects of Treatment for Lung Cancer with Double Points Cryoablation through Percutaneous Puncture Guided by Computed Tomography

OBJECTIVE To investigate the clinical effects of the application of double points cryoablation through percutaneous puncture for advanced lung cancer patients.METHODS Forty-one patients diagnosed with stage III-IV pulmonary carcinoma were selected for the study. The patients were found to have from 1 to 3 foci of carcinoma, and in each case the disease was limited to one lung. The study patients were divided randomly into 3 groups. There were 16 cases receiving routine chemotherapy and radiotherapy in group I, 13 cases treated with cryoablation at a single point in group II, and 12 cases treated with cryoablation at 2 points simultaneously in group III. The patients in the 2 cryoablation groups also received the same treatment as the patients did in group I. The clinical effects were evaluated within 6 months after treatment, and the survival rate was followed-up for 3 years.RESULTS The clinical effects were improved significantly after treatment in group II and in group III compared with those in group I (P < 0.05), including an enhanced regressive rate of 21%, postponed tumor progression of 50.58% and a clinical benefit rate of 92%. The effective rate of regression in group III was higher than that in group II, 43.59% (P < 0.05), and the 3-year survival rate was 37.25%. Significant differences in side effects were not found between the 2 cryoablation groups. CONCLUSION Cryosurgery ablation at 2 points, simultaneously, and directed at 1 foci might improve the effects of treatment and the prognosis of lung cancer patients, when used in combination with routine treatment

Inhibitors of glioma growth that reveal the tumour to the immune system

Treated glioblastoma patients survive from 6 to 14 months. In the first part of this review, we describe glioma origins, cancer stem cells and the genomic alterations that generate dysregulated cell division, with enhanced proliferation and diverse response to radiation and chemotherapy. We review the pathways that mediate tumour cell proliferation, neo-angiogenesis, tumor cell invasion, as well as necrotic and apoptotic cell death. Then, we examine the ability of gliomas to evade and suppress the host immune system, exhibited at the levels of antigen recognition and immune activation, limiting the effective signaling between glioma and host immune cells.The second part of the review presents current therapies and their drawbacks. This is followed by a summary of the work of our laboratory during the past 20 years, on oligosaccharide and glycosphingolipid inhibitors of astroblast and astrocytoma division. Neurostatins, the O-acetylated forms of gangliosides GD1b and GT1b naturally present in mammalian brain, are cytostatic for normal astroblasts, but cytotoxic for rat C6 glioma cells and human astrocytoma grades III and IV, with ID50 values ranging from 200 to 450 nM. The inhibitors do not affect neurons or fibroblasts up to concentrations of 4 ?M or higher.At least four different neurostatin-activated, cell-mediated antitumoral processes, lead to tumor destruction: (i) inhibition of tumor neovascularization; (ii) activation of microglia; (iii) activation of natural killer (NK) cells; (iv) activation of cytotoxic lymphocytes (CTL). The enhanced antigenicity of neurostatin-treated glioma cells, could be related to their increased expression of connexin 43. Because neurostatins and their analogues show specific activity and no toxicity for normal cells, a clinical trial would be the logical next step