Disease relevance of Survival Analysis

• A survival analysis of the length of time to the first recurrent febrile seizure did not show a significant difference between the treatment groups (P = 0.064 by the log-rank test), but after adjustment for covariates, diazepam was found to have a benefit (P = 0.027 by Cox regression analysis) [1].
• Univariate survival analyses of patients with anaplastic astrocytoma identified PTEN (P =.002) and p53 (P =.012) mutations as statistically significantly associated with reduced and prolonged survival, respectively [2].
• Multivariate Cox survival analysis identified the age of the patient, p73 expression status, co-existing cirrhosis, and Edmondson grade as independent prognostic factors [3].
• In addition, survival analysis clearly showed that the onset age of HCC was also accelerated among chronic hepatitis B patients who were carrying IL10-ht2 [4].
• Multivariate survival analyses by the proportional hazards technique demonstrated that neopterin provided statistically independent predictive information in addition to either presence versus absence of distant metastases or Dukes' stage [5].

Psychiatry related information on Survival Analysis

• Effectiveness of venlafaxine, extended release formulation, in the short-term and long-term treatment of generalized anxiety disorder: results of a survival analysis [6].
• The results of a survival analysis showed that patients with a diagnosis of schizophreniform disorder responded to haloperidol significantly more rapidly than did patients with a diagnosis of schizophrenia [7].
• The use of survival analysis techniques in evaluating the effect of long-term tacrine (Cognex) treatment on nursing home placement and mortality in patients with Alzheimer's disease [8].

High impact information on Survival Analysis

• We applied a survival analysis adjusted for the quality of life to data from a randomized trial conducted by the AIDS Clinical Trials Group. The trial compared treatment with 500 mg of zidovudine per day, 1500 mg of zidovudine per day, and placebo (Protocol 019) in 1338 asymptomatic HIV-infected patients [9].
• Using a combination of high-resolution magnetic resonance imaging and histopathological and survival analyses, we show that tumor progression was significantly impaired in Egr1-/- mice [10].
• In survival analysis, time to biochemical progression (P<.001), Gleason score (P<.001), and PSA doubling time (P<.001) were predictive of the probability and time to the development of metastatic disease [11].
• MAIN OUTCOME MEASURE: Cumulative incidence of PUBs for rofecoxib vs NSAIDs, based on survival analysis of time to first PUB diagnosis, using PUBs that met pre-specified criteria judged by a blinded, external adjudication committee [12].
• MAIN OUTCOME MEASURES--Relative risks (RRs), estimated with Cox proportional hazards (survival) analysis, for 25-year CHD mortality for cholesterol quartiles and per 0.50-mmol/L (20-mg/dL) cholesterol increase [13].

Chemical compound and disease context of Survival Analysis

• Paclitaxel and carboplatin in combination in the treatment of advanced non-small-cell lung cancer: a phase II toxicity, response, and survival analysis [14].
• By Kaplan-Meier survival analysis, the only significant predictor of progression to ESRD was serum creatinine >2.5 mg/dl at biopsy (P = 0. 008) [15].
• Multivariate survival analysis demonstrated acute renal failure, length of mechanical ventilation, age, and methicillin resistance to be independently associated with mortality (P<.05) [16].
• By survival analysis, it was found that marriage breakup adversely affected duodenal ulcer course, that age 50 years and under, female sex, and aspirin use tended to do so, and that smoking, alcohol ingestion, and paracetamol use did not [17].
• RESULTS: Postprandial plasma glucose concentrations were decreased in the lispro group compared with the regular-insulin group for all three meal types (P < 0.05), and hypoglycemia developed more frequently and rapidly in the lispro group, compared with the regular-insulin group by survival analysis [18].

Biological context of Survival Analysis

• A multivariate survival analysis (Cox's regression model) using clinical, biochemical and histological data obtained at diagnosis disclosed seven factors that predicted prognosis: serum bilirubin; serum gamma-globulin concentration; hepatic stigmata; prothrombin time; sex; age, and alkaline phosphatase [19].
• Kaplan-Meier survival analysis and log-rank statistics revealed a significant (P < 0.05) difference in cumulative islet graft survival depending on the presence of islet cell and/or GAD65 antibodies [20].
• Although EZH2 expression was significant in univariate survival analysis, only tumor cell proliferation and lymph node status were significant in the final multivariate model [21].
• RESULTS: Survival analysis demonstrated that patients with high STAT1 activation have substantially longer overall and relapse-free survival, irrespective of whether STAT1 activation was determined by its DNA binding activity (P = 0.003 and 0.010, respectively) or by its tyrosine phosphorylation (P = 0.046 and 0.011, respectively) [22].
• Kaplan-Meier survival analysis and Cox models adjusted for age, race, body mass index, smoking status, blood pressure, diabetes mellitus, cardiovascular disease, categories of estimated glomerular filtration rate, serum concentrations of albumin and cholesterol, and proteinuria were examined [23].

Anatomical context of Survival Analysis

• The present report of 1484 patients with LMCD in the Coronary Artery Surgery Study (CASS) Registry extends the originally published 5-year surgical and medical group survival analysis to more than 16 years of follow-up and permits analysis of LMCD patient subgroups [24].
• PEA3 mRNA expression in stromal cells emerged as an independent predictor of poor outcome in multivariate survival analysis, in which all molecules previously studied in this patient cohort were included (P = 0.015) [25].
• Multivariate survival analysis showed that both TPO.Ab and thyroid volume were independently associated with prognosis in breast carcinoma and that RRs for disease-free survival were of a similar order of magnitude to well-established prognostic indices such as axillary nodal status or tumor size [26].
• Kaplan-Meier survival analyses showed that a slower progression of disease, i.e. higher proportion of subjects with CD4+ T cell counts > 500/microl (p = 0.0006) and a trend toward a slower progression to AIDS (p = 0.077), was associated with the CCR5/delta ccr5 genotype [27].
• Clinico-prognostic implications of increased levels of soluble CD54 in the serum of B-cell chronic lymphocytic leukemia patients. Results of a multivariate survival analysis [28].

Associations of Survival Analysis with chemical compounds

• Survival analysis with log-normal regression showed that the duration of intubation was shorter with steroid therapy (p less than 0.003) and increasing age (p less than 0.02), but was not influenced by endotracheal tube size or abnormality on chest radiograph [29].
• Survival analysis disclosed essentially three categories of treatment response: one for noncompliant subjects (0% to 7% abstinent), one for compliant subjects not attaining therapeutic serum lithium levels (31% to 44% abstinent), and one for compliant subjects with therapeutic serum levels (67% abstinent) [30].
• RESULTS: In an intention-to-treat survival analysis, the likelihood of treatment failure was significantly lower in the cyclophosphamide (P = 0.04) and combination therapy (P = 0.002) groups than in the methylprednisolone group [31].
• Survival analysis demonstrated a highly significant prophylactic effect for active imipramine hydrochloride maintained at an average dose of 200 mg and a modest prophylactic effect for monthly interpersonal psychotherapy [32].
• Using survival analysis during the entire 2 years, we did not find a significant difference between fluphenazine and placebo in the likelihood that a prodrome would continue to an exacerbation [33].

Gene context of Survival Analysis

• Besides the traditional clinical prognostic variables, E-cad and alpha-, beta-, and gamma-catenin expression were of positive prognostic value in univariate survival analyses [34].
• Importantly, Kaplan-Meier survival analysis and log-rank test revealed a significant inverse correlation between high nuclear EGFR and overall survival (P = 0.009) [35].
• Survival analysis revealed a significant association of stromal SPARC with poor prognosis (P = 0.006), a finding that was also confirmed in multivariate models [36].
• Overall survival analysis of breast carcinoma patients indicated a statistically significant correlation between SEL1L down-modulation and poor prognosis [37].
• In Kaplan-Meyer survival analysis, there was a tendency toward a more favorable prognosis in patients with CYP2A6-positive tumors in comparison with patients with CYP2A6-negative tumors [38].

Analytical, diagnostic and therapeutic context of Survival Analysis

• In Kaplan-Meier survival analysis, increased cytoplasmic expression of HuR was a significant prognostic indicator for progression-free survival (P = 0.03) as well as overall survival (P = 0.007) [39].
• Furthermore, Cox survival analysis results indicated that patients with a higher Pin1 expression had a significantly higher probability of recurrence than their counterparts with low Pin1 expression, as defined by a serum prostate-specific antigen level of > or =0.4 ng/ml on two consecutive occasions after radical prostatectomy [40].
• A survival analysis of the patient series with homogeneous conditions derived from a short study period suggests the need for additional strategies including right hepatectomy for Bismuth type I or II tumors [41].
• Their EGFR and EGFRvIII status was determined by immunohistochemistry and survival analyses were done [42].
• Two survival analyses were performed: (1) a retrospective study, including 400 patients with COPD none of whom had received nutritional therapy; (2) a post hoc analysis of a prospective study, including 203 patients with COPD who had participated in a randomized placebo-controlled trial [43].

References