ABSTRACT
El cambio de estadio clínico del carcinoma pulmonar no microcítico al comparar los períodos pre y posoperatorio puede repercutir negativamente a la hora de definir las estrategias terapéuticas. El objetivo del presente estudio fue evaluar la magnitud de dichos cambios y su efecto sobre el paciente. Se realizó un estudio retrospectivo con una base de datos prospectiva de 259 pacientes tratados entre enero de 2002 y diciembre de 2007. Se excluyeron enfermos con tratamiento neoadyuvante, intervenciones por recidiva o paliativas y neoplasias de células pequeñas. Las variables estudiadas fueron los factores tumor (T), nódulos (N) y metástasis (M), posición y localización del tumor y pulmón afectado. El coeficiente de concordancia permitió evaluar la magnitud del cambio y la prueba de ji al cuadrado, la asociación entre dos variables. Valores de p < 0,05 se consideraron significativos. . El factor T cambió en 91 pacientes (35,1 por ciento), con más frecuencia en lesiones de lóbulos superiores (p = 0,04). La posición no se asoció al cambio (p = 0,110). El factor N se modificó en 50 casos (19,3 por ciento). Se asociaron al cambio: localización lobular (p = 0,001), pulmón afectado (p = 0,002) y factor T (p = 0,013). El cambio del factor M ocurrió en 11 pacientes (4,2 por ciento) y no se asoció a la posición (p = 0,120), localización (p = 0,225) o factor T (p = 0,339). El coeficiente de concordancia fue bajo (k = 0,381; p < 0,001), debido a que el cambio ocurrió en el 49,03 por ciento de los pacientes. CONCLUSIONES. El cambio de estadio clínico fue de magnitud apreciable y, por tanto, tiene el potencial de inducir a la práctica de tratamientos inadecuados, tanto médicos como quirúrgicos(AU)
INTRODUCTION. Change of clinical stage of non-microcyst pulmonary cancer in comparing the pre-postoperative and postoperative periods may to have negative repercussions on the definition of therapeutical strategies. The aim of present paper was to assess the magnitude of such changes and its effect on the patient. METHODS. A retrospective study was conducted with a prospective database of 259 patients treated from January, 2002 to December, 2007. Patients with neoadjuvant therapy, palliative interventions or relapse and small cells neoplasms were excluded. The study variables were: tumor factors (T), nodules (N) and metastasis (M), tumor position and location and involved lung. Agreement coefficient allowed assessing the change magnitude and the Chi² test, the association between the two variables. RESULTS. T factor changed in 91 patients (35,1 percent) more frequent in superior lobules lesions (p = 0,04). Position wasn't associated with the change (p = 0,110). N factor was modified in 50 cases (19,3 percent). Associated with change were: lobular location (p = 0,001), involved lung (p = 0,002) and T factor (p = 0,013). The change in T factor happened in 11 patients (4,2 percent) and wasn't associated with the position (p = 0,120), location (p = 0,225) or T factor (p = 0,339). Agreement coefficient was low (k = 0,381; p < 0,001), because of the change occurred in the 49,03 percent of patients. CONCLUSIONS. The change in clinical stage was of a significant magnitude and thus, has the potential to induce to inappropriate medical and surgical treatments practice(AU)
Subject(s)
Humans , Carcinoma, Non-Small-Cell Lung/etiology , Lung Neoplasms/epidemiology , Neoplasm Staging , Retrospective StudiesABSTRACT
The inactivation of tumour suppressor genes by aberrant methylation of promoter regions has been described as a frequent event in neoplasia development, including lung cancer. The p16 gene is a tumour suppressor gene involved in the regulation of cell cycle progression that has been reported to be inactivated by promoter methylation in lung carcinomas at variable frequencies around the world in a smoking habit dependent manner. The purpose of this study was to investigate the methylation status of the promoter region of the p16 gene in 74 non-small cell lung carcinomas from Chile. The frequency of p16 gene inactivation by promoter methylation was determined as 79.7 percent (59/74). When we considered histological type, we observed that p16 promoter methylation was significantly higher in squamous cell carcinomas (30/33, 91 percent) compared with adenocarcinomas (21/30, 70 percent) (p=0.029). In addition, no association between p16 promoter methylation and gender, age or smoking habit was found (p=0.202, 0.202 and 0.147 respectively). Our results suggest that p16 promoter hypermethylation is a very frequent event in non-small cell lung carcinomas from Chile and could be smoking habit-independent.
Subject(s)
Aged , Female , Humans , Male , Carcinoma, Non-Small-Cell Lung/genetics , DNA Methylation/drug effects , Lung Neoplasms/genetics , Promoter Regions, Genetic , Smoking/adverse effects , Chile , Carcinoma, Non-Small-Cell Lung/etiology , Lung Neoplasms/etiology , Polymerase Chain ReactionABSTRACT
BACKGROUND: The association between TP53/TP73 gene polymorphisms and tobacco smoking was evaluated with regard to risk of non-small cell lung cancer (NSCLC). METHODS: A case-control study with 192 histologically confirmed NSCLC cases and 241 non-cancer controls was conducted. Subjects were genotyped for TP53 Arg72Pro and TP73 G4C14 to A4T14 polymorphisms by PCR-based methods. Risk and interactions were assessed as odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The analyses according to TP53 genotypes for the risk of tobacco smoking illustrated that risk with heavy smoking was much higher for subjects with the TP53 ProPro genotype (OR: 16.4, 95% CI 1.77-151.7) as compared with those with TP53 ArgArg/ArgPro (3.36, 1.69-6.68). Similar analyses for TP73 genotypes did not show any differences for NSCLC risk. CONCLUSION: A risk relation of heavy smoking for the NSCLC is suggested with the TP53 but not the TP73 polymorphism.