Introduction: Stereotactic ablative radiosurgery (SRS) or stereotactic ablative body radiotherapy (SABR) is the standard treatment for patients with inoperable early stage non-small cell lung cancer (NSCLC), the body gamma knife SRS (ɤ-SRS) is a special SABR technology developed in China. This study prospectively assessed the clinical outcome, toxicity and cost following body ɤ-SRS for early stage NSCLC.Methods: From 2007 to 2010, a total of 29 patients with early stage NSCLC were prospectively enrolled in this study. The prescription dose for Planning Target Volume (PTV), Clinical Target Volume (CTV), and Gross Target Volume (GTV) were 50, 60, and 70 gray (Gy) in 10 fractions. Isodose curves of 50, 60, and 70% covered at least 100% of PTV, 90% of CTV, and 80% of GTV, respectively. The body ɤ-SRS was delivered 5 days per week and completed in 2 weeks.Results: Median follow-up time was 62.0 (range 11.1-140.3) months. 1-, 3-, 5-year OS rates were 93.1%, 72.0%, 60.3%; PFS rates were 86.2, 64.2 and 48.8%; and LR, RR, and DM rates were 10.9%, 21.4%, 29.0%. The median cost of the body ɤ-SRS during treatment was 4,838 (range 4,615–4,923) dollars and the median cost through 5 years was 36,960 (range 9920-56,824) dollars.Conclusion: With existing clinical data, the body ɤ-SRS is an effective treatment option for patients with medically inoperable early stage NSCLC or patients who do not prefer operation, as they may benefit from the minimized toxicity. Due to excellent cost effectiveness, the availability of the body ɤ-SRS will expand, especially in developing nations, and underdeveloped countries.
MicroRNAs (miRNAs) have been reported to be associated with the modulation of tumor development, including alterations associated with the development of human laryngeal squamous cell carcinoma (LSCC). The present study was designed to investigate whether miRNA‑195 was associated with the pathophysiologic process of human LSCC and to identify its potential roles and underlying molecular mechanisms. To determine whether miRNA‑195 serves a role in LSCC, reverse transcription‑quantitative polymerase chain reaction was used to detect miRNA‑195 expression in LSCC tissues. The tumor‑suppressive effect of miRNA‑195 was determined by in vitro assays. Gain‑of‑function studies using miRNA‑195 mimics were performed to investigate cell viability, migration and invasion, and apoptosis in the AMC‑HN‑8 cell line. Western blotting was performed to reveal the molecular mechanisms of miRNA‑195 and its downstream signaling pathways in the LSCC AMC‑HN‑8 cell line. The present study demonstrated that miRNA‑195 is downregulated in primary LSCC tumors. Upregulating miRNA‑195 in vitro suppressed cell viability, migration and invasion in AMC‑HN‑8 cells. Overexpression of miRNA‑195 alone in AMC‑HN‑8 cells was sufficient to induce cell apoptosis, as identified by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Compared with the high expression of miRNA‑195 in AMC‑HN‑8 cells, the expression levels of vascular endothelial growth factor receptor‑II protein and downstream signaling pathway proteins, which were associated with cell viability, migration, invasion and apoptosis, were markedly decreased compared with control or miRNA‑195 negative control treatment group. Together, these data suggest the therapeutic potential of miRNA‑195 in modulating cell growth, migration and apoptosis during the pathophysiological progression of LSCC and that miRNA‑195 may serve as a potential therapeutic target in human LSCC.
ObjectiveThe aim of this study was to investigate the efficacy and safety of combined applications of local consolidative radiation therapy (LCRT) and first-line tyrosine kinase inhibitors (TKIs) for the treatment of primary tumors and oligometastatic sites in oligometastatic NSCLC harboring Epidermal Growth Factor Receptor (EGFR) activating mutations.Patients and MethodsElderly patients with oligometastatic NSCLC (≤5 metastases) harboring EGFR activating mutations at the time of diagnosis were identified. They were treated with first-line TKIs alone or in combination with LCRT. Progression‐free survival (PFS) and overall survival (OS) were estimated through the Kaplan–Meier method.ResultsA total of 122 elderly patients were enrolled between February 2010 and January 2018. Among them, 41.0% (n = 50) received TKIs combined with LCRT (TKIs + LCRT group), whereas 59.0% (n = 72) received TKIs monotherapy (TKIs alone group). Patients were followed up for a median length of 34 months (ranging from 7.0 to 64 months). The median PFS in TKIs + LCRT group was 17 months (95%CI: 15.37–18.63), which was significantly longer than that of the TKIs-alone group (12 months; 95%CI: 11.05–12.95) (p <0.001). Median OS in TKIs + LCRT group was 38 months (95%CI: 35.61–40.39), while that of the TKIs-alone group was 29 months (95%CI: 26.86–31.14) (p <0.001). Multivariate analyses revealed that LCRT, one to two metastases, and good ECOG PS were independent predictors for better PFS (p <0.001, p = 0.004, and p = 0.027). Moreover, LCRT, good ECOG PS, and T1-2 stage were independent predictors for better OS (p <0.001, p = 0.007 and p = 0.007). Most of the patients suffered from grade 1 to 2 toxicities, and treatment-related deaths were not recorded.ConclusionFirst-line TKIs combined with LCRT may improve survival outcomes for elderly patients with oligometastatic NSCLC harboring EGFR activating mutations. This approach was not associated with much toxicity, therefore, it can be used for the treatment of elderly patients with oligometastatic disease.
Cancer, also known as malignant tumour or neoplasm, is a leading cause of death worldwide. One distinct feature from normal cells is that cancerous cells often overexpress protein on the cell membrane—for instance, the overexpression of human epidermal growth factor receptor 2. The expression of a specific protein on the cancerous cell surface acts as a marker that differentiates the normal cell and facilitates the recognition of cancerous cells. An emerging anticancer treatment, Antibody–Drug Conjugates (ADCs), utilises this unique feature to kill cancerous cells. ADCs consist of an antibody linked with a cytotoxic payload, mainly targeting the antigen found on cancerous cells. This design can increase the specificity in delivering the cytotoxin to the drug target, thus increasing the drug efficacy and reducing the side effect of cancer treatment due to off-target toxicities. There are tremendous quantities of clinical trials conducted to evaluate the safety and effectiveness of this magic drug in treating different types of cancers. However, only 12 ADCs have been approved by the FDA until now. This review provides the principles of ADCs and highlights the ADCs that FDA has approved. In addition, some of the ADCs that undergo clinical trials are discussed in this review. The application of computational techniques in addressing ADCs’ challenges and neoantigen-targeted cancer vaccines is also highlighted. Although ADCs have been seen as promising magic drugs in cancer treatment, the problems such as toxicity, the stability of the linker, the specificity of an antibody with antigen, and so on, remain a challenge in developing ADCs.
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