Previously, it had been shown that T-lymphocytes are the predominant inflammatory cells found in the alveolar wall of smokers and their numbers correlated with the extent of emphysema. However, the phenotype of these cells was not defined. The aim of this study was to describe the different T-cell phenotypes and investigate the possible presence of apoptosis in the lung parenchyma of smokers.Samples from lungs were obtained at surgery from 15 patients who smoked and six who had never smoked. Samples were frozen and prepared for histological and immunocytochemical examination. Slides were stained for CD3+, CD4+, CD8+, γδ T-cells, CD56 natural killers ((NK) cells), and elastase (neutrophils). Anti-CD95 monoclonal antibodies andin situend-labelling techniques were used to detect Fas expression and apoptosis. Positive staining cells were expressed as cells·mm alveolar wall−1, percentage of total cells, and Fas/APO and apoptosis index. Emphysema was identified macroscopically, microscopically and reported as present or absent. All subjects had pulmonary function tests before surgery.Neutrophils were the predominant cell in the lung parenchyma of nonsmokers and smokers without emphysema. In smokers with emphysema, the CD3+ and CD8+ were the predominant cells (p<0.05) in the alveolar wall. γδ cells were increased in all smokers and no increased numbers of NK cells was found. The T-cell numbers·mm alveolar wall−1showed a bilinear relationship with the amount smoked increasing at an inflection point of 30 packs yr−1(R2=0.345; p<0.01). Apoptosis in smokers showed a bilinear relationship with the amount smoked increasing sharply in smokers with emphysema (R2=0.3613; p<0.009).It is concluded that the pathogenesis of emphysema might be mediated by T-lymphocytes, mainly CD8+ cytolytic T-cells, and that apoptosis might be one of the mechanisms of lung destruction leading to the development of emphysema. If this is the case, it could be speculated that T-cell inflammation is a response to antigenic stimuli originating in the lung and induced by cigarette smoking.

Lung cancer is the most common cancer, with dismal outcome. Treatment approaches, including cisplatin-based chemotherapy and surgery, are currently based on the clinical classification of the tumor, without genetic assessment for predicting differential chemosensitivity. BRCA1 plays a central role in DNA repair, and decreased BRCA1 mRNA expression in the human breast cancer HCC1937 cell line caused cisplatin hypersensitivity, but the relation between BRCA1 and survival in lung cancer patients has never been examined. We used real-time quantitative polymerase chain reaction to determine BRCA1 mRNA levels in 55 surgically resected tumors of non-small-cell lung cancer patients who had received neoadjuvant gemcitabine/cisplatin chemotherapy, and divided the gene expression values into quartiles. When results were correlated with outcome, two cut-offs were observed; patients with levels <0.61 had better outcome, and those >2.45 had poorer outcome. Median survival was not reached for the 15 patients in the bottom quartile, whereas for the 28 in the two middle quartiles, it was 37.8 months (95% CI, 10.6-65), and for the 12 patients in the top quartile, it was 12.7 months (95% CI, 0.28-28.8) (P=0.01). Moreover, when patients were stratified by pathologic stage, those in the bottom quartile had a decreased risk of death (HR=0.206; 95% CI, 0.05-0.83; P=0.026) compared with those in the top quartile, and those in the two middle quartiles also had a decreased risk of death (HR=0.294; 95% CI, 0.10-0.83; P=0.020) compared with those in the top quartile. BRCA1 expression is potentially an important tool for use in cancer management and should be assessed for predicting differential chemosensitivity and tailoring chemotherapy in lung cancer.

No abstract

Patients with RRM1 levels in the bottom quartile benefited significantly from gemcitabine/cisplatin neoadjuvant chemotherapy, leading us to conclude that RRM1 mRNA levels should be additionally validated to proceed with tailored chemotherapy.

Lymphangioleiomyomatosis (LAM) is a rare disease characterized by pulmonary cysts at computed tomography (CT) and proliferation of abnormal smooth muscle cells at lung biopsy. Almost all patients are female, and all have pulmonary cysts at high-resolution CT. Although the presence of cysts may be suggested at conventional CT or chest radiography, high-resolution CT is superior for cyst detection and is essential for diagnosis. The cysts are typically round; in most cases, the cyst wall is barely seen at thin-section CT. They are typically diffusely distributed throughout the central and peripheral lung parenchyma. The lung bases are affected in all patients. Some patients also have increased lung attenuation or a reticular pattern. Expiratory CT shows no air trapping between the cysts, and most of the cysts decrease in size. Pneumothorax, pleural effusion, and chylothorax are complications of LAM. Certain abdominal findings may provide additional corroborative evidence of the diagnosis. Renal angiomyolipomas, the most frequent abdominal lesions, usually manifest as asymptomatic, small, bilateral tumors of fat attenuation in the renal cortex. Lymphangiomas are cystic retroperitoneal masses that occur in up to 20% of patients. Other CT findings are hypo- or hyperattenuating lymph nodes, a dilated thoracic duct, and ascites.