Schuller HM

Schuller HM. 567). In multivariate analysis, beta-blocker intake was associated with a significantly better DMFS [hazard ratio (HR), 0.67; = 0.01], DFS (HR, 0.74; = 0.02), and OS (HR, 0.78; = 0.02) with adjustment for age, Karnofsky performance score, stage, histology type, concurrent chemotherapy, radiation dose, gross tumor volume, hypertension, chronic obstructive pulmonary disease and the use of aspirin. There was no association of beta-blocker use with LRPFS (HR = 0.91, = 0.63). Conclusion Beta-blocker use is usually associated with improved DMFS, DFS, and OS in this large cohort of NSCLC patients. Future prospective trials can validate these retrospective findings and determine whether the length and timing of beta-blocker use influence survival outcomes. value of 0.05 was considered to indicate statistical significance; all assessments were two-sided. All patients were included in UVA and MVA. Statistical analyses were carried out using Stata/SE v10.1 (Stata Corp LP, College Station, TX). results The final study population consisted of 722 patients, 155 of whom experienced taken beta-blockers during definitive RT and 567 who had not. Patient and tumor characteristics are outlined in Table ?Table1.1. The median age of the patients was 65 years (range 34C95 years), and most patients in both the groups experienced stage III disease. Patients taking beta-blockers were more likely to be older ( 0.01), have poorer performance status (Karnofsky Performance Status scores 80) (= 0.04), have hypertension ( 0.01), and likely to take aspirin ( 0.01). Patients taking beta-blockers also experienced less-advanced (lower-stage) disease (= 0.04), but were less likely to have received concurrent chemotherapy (= 0.02) and were given higher RT doses ( 0.01). Other prognostic factors were not significantly different between the groups. The median follow-up time for surviving Rabbit Polyclonal to Catenin-gamma patients was 44 months (range 1C155 months). Table 1. Patient and tumor characteristics = 155)= 567)value= 43 [6%]), induction chemotherapy followed by concurrent chemotherapy and radiation (= 252 [35%]), concurrent chemotherapy and radiation without induction treatment (= 351 [49%]), or radiation alone (= 76 [10%]). Of the 155 patients taking beta-blockers during RT for NSCLC, 105 (68%) experienced a diagnosis of hypertension, and the other 50 (32%) experienced non-hypertensive disorders, most often coronary heart disease. The drugs used are shown in Table ?Table2.2. The two most commonly prescribed drugs (given in 85% of cases) were metoprolol and atenolol. Table 2. Beta-blockers used to treat preexisting hypertension (R)-(-)-Mandelic acid or coronary heart disease in patients with lung malignancy 0.01, Physique ?Physique2A),2A), DFS ( 0.01, Physique ?Physique2B),2B), and OS (= 0.01, Physique ?Physique2C).2C). The findings from UVA using Cox proportional hazards models of the influence of clinical characteristics on the survival outcome (Table ?(Table3)3) indicate that the use of beta-blockers was associated with better DMFS, DFS, and OS, but not LRPFS. Of other variables examined, more youthful age and advanced disease (T3, 4/N2, 3) were linked with reduced DMFS and DFS, and the poor performance status and advanced disease were linked with decreased OS. Notably, the use of concurrent chemotherapy was associated with improved OS ( 0.01). (R)-(-)-Mandelic acid Table 3. Univariable Cox proportional hazards model for all those patients = 0.01), DFS (HR 0.74, 95% CI 0.58C0.95, = 0.02), and OS (HR 0.78, 95% CI 0.63C0.97, = 0.02) ,but not with LRPFS (HR = 0.91, 95% CI, 0.64C1.31, = 0.63) (Table ?(Table4).4). When examining other clinical factors, only advanced stage, poorer overall performance status, larger GTV, and the lack of concurrent chemotherapy remained associated with reduced survival outcomes. Table 4. Multivariable Cox proportional hazards model for all those patients study has shown that this beta-blocker propranolol can reverse the proliferation of NSCLC cells caused by nicotine through cooperative regulation of nicotinic (R)-(-)-Mandelic acid and beta-adrenergic receptors [23]. Other such studies indicated that beta-adrenergic signaling can regulate several of the cellular.