13 research outputs found
Strategies for monitoring and combating resistance to combination kinase inhibitors for cancer therapy
Level IIb lymph node metastasis in transglottic laryngeal squamous cell carcinoma
The treatment of laryngeal squamous cell carcinoma (SCC) is based on proper design of therapeutic strategies aimed to control cervical lymph node metastasis. Cervical nodal metastasis is one of the most important prognostic factors in carcinoma of the larynx. [1] The incidence of clinically detectable lymph node metastasis in laryngeal carcinoma is high, and the levels II, III, and IV are the most commonly involved lymphatic groups in carcinoma of the larynx. Abstract Objective: To evaluate the clinical and pathologic parameters associated with level IIb metastasis in transglottic laryngeal carcinoma. Methods: A total of 238 laryngeal squamous cell carcinoma patients admitted to our tertiary center and surgically treated between January 2006 and January 2014. Of these 238 patients, 134 patients with transglottic laryngeal SCC were enrolled in the study. The type of neck dissection, the location of histopathologically proven metastatic lymph nodes, clinical N and T stages were reviewed. Palpable lymph nodes were accepted clinically cN(+) and the opposite as cN(-). Results: Of the 134 patients, 116 were diagnosed as cN(-), and 18 were as cN(+). Level IIb metastasis was diagnosed in 12 patients in the cN(+) group, and in two patients in the cN(-) group. Histopathological level IIb metastasis was shown in 14 of 134 patients, representing 16 of 268 neck dissection specimens. Level IIb metastasis was shown in the ipsilateral specimens in 12 patients and contralateral specimens in two patients. Forty-one of 134 patients presented cartilage invasion, and nine of them were diagnosed with level IIb metastasis. Conclusion: Thyroid cartilage invasion, the presence of level IIa invasion and advanced stage disease are the risk factors for level IIb metastasis. Therefore, level IIb should not be neglected during neck dissection in transglotticlaryngeal carcinoma
Accelerating resistance breeding in wheat by integrating marker-assisted selection and doubled haploid technology
Prediction of acid mine drainage generation potential of various lithologies using static tests: Etili coal mine (NW Turkey) as a case study
Histamine H3R receptor activation in the dorsal striatum triggers stereotypies in a mouse model of tic disorders
A search for the common ground between Tic; Obsessive-compulsive and Autism Spectrum Disorders: part I, Tic disorders
Evolocumab and clinical outcomes in patients with cardiovascular disease
BACKGROUND Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%). CONCLUSIONS In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets