RESUMO
Quantitative assessments of tumor burden and modeling of longitudinal growth could improve phase II oncology trials. To identify obstacles to wider use of quantitative measures we obtained recorded linear tumor measurements from three published lung cancer trials. Model-based parameters of tumor burden change were estimated and compared with similarly sized samples from separate trials. Time-to-tumor growth (TTG) was computed from measurements recorded on case report forms and a second radiologist blinded to the form data. Response Evaluation Criteria in Solid Tumors (RECIST)-based progression-free survival (PFS) measures were perfectly concordant between the original forms data and the blinded radiologist re-evaluation (intraclass correlation coefficient = 1), but these routine interrater differences in the identification and measurement of target lesions were associated with an average 18-week delay (range, -20 to 55 weeks) in TTG (intraclass correlation coefficient = 0.32). To exploit computational metrics for improving statistical power in small clinical trials will require increased precision of tumor burden assessments.
Assuntos
Determinação de Ponto Final , Modelos Biológicos , Neoplasias/diagnóstico por imagem , Neoplasias/patologia , Critérios de Avaliação de Resposta em Tumores Sólidos , Tomografia Computadorizada por Raios X , Proliferação de Células , Ensaios Clínicos como Assunto , Intervalo Livre de Doença , Humanos , Cinética , Controle de Qualidade , Carga TumoralRESUMO
Objective To investigate the molecular mechanism of As 2 O3 in suppressing metastasis of esophagus carcinoma cells.Methods The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay, adhesion and invasion assay were performed to observe the inhibitory effect of As 2 O3 on proliferation and metastasis of esophagus carcinoma cells .The expressions of matrix metalloproteinases ( MMP)2, MMP9, E-cadherin, and protein tyrosine phosphatase receptor-type O ( PTPRO) were analyzed with Western blot .Results Exposure to As 2 O3 significantly presented suppressive functions on growth and metastasis of esophagus carcinoma cells in a dose-dependent manner ( P <0.01 ) .Additionally , MMP2 and MMP9 expressions were increased after treatment with casticin ( P <0.01 ) , whereas E-cadherin and PTPRO expressions were down-regulated ( P <0.01 ) .Conclusions As2 O3 had a significant function to inhibit proliferation and metastasis of esophagus carcinoma cells .
