[Relationship between primary lung cancer and tobacco consumption. Results of the KBP-2010-CPHG study by the French College of General Hospital Respiratory Physicians]. / Relation entre cancer bronchique primitif et consommation tabagique. Résultats de l'étude KBP-2010-CPHG du Collège des pneumologues des hôpitaux généraux.

INTRODUCTION: The Collège des Pneumologues des Hôpitaux Généraux has performed a prospective multicentre epidemiological study which aims to describe the baseline characteristics of all new cases of primary lung cancer histologically or cytologically diagnosed in 2010 and followed-up in the respiratory department of general hospitals. The present publication compares the characteristics of these presentations according to their smoking history. METHODS: Seven thousand and fifty-one adult patients were included from 104 respiratory departments. A standardized form was completed at diagnosis and a steering committee checked the completeness of inclusion. RESULTS: Only 10.9% of patients were never-smokers and 89.1% ever-smokers (i.e., current or former smokers). Respectively, 3.7%, 10.7% and 85.6% of ever-smokers consumed/had consumed 1-10, 11-20, and >20 pack-years. Mean smoking duration was 37.5 years. Former smokers had stopped smoking on average 14.8 years previously. Only 20.7% of never-smokers reported that they had been exposed to tobacco smoke passively. At diagnosis, statistically significant differences were found between never- and ever-smokers (P<0.0001) for sex (women: 60.8% vs 18.8%), age (mean: 70.7 years vs 64.9 years), stage (IV: 70.8% vs 58.7%), histology (adenocarcinoma: 68.5% vs 42.6%), EGFR mutation exploration (51.4% vs 28.0%) and positivity (37.0% vs 4.6%). Differences between never- and ever-smokers rose with increasing tobacco consumption. CONCLUSIONS: This study confirms that differences exist between never- and ever-smoker patients presenting with primary lung cancer and shows the impact of the level of tobacco consumption, in particular on histology.

[Pituitary metastasis revealing a lung cancer]. / Métastase hypophysaire symptomatique révélant un cancer bronchique.

INTRODUCTION: Pituitary metastases are rare and difficult to diagnose. Their optimal approach and management remains to be defined. CASE REPORT: We report the case of a 56-year-old patient suffering from squamous cell lung carcinoma who developed pituitary metastasis with secondary hypopituitarism, the symptoms of which were initially attributed to depression. CONCLUSION: Pituitary metastases can be difficult to diagnose, which may lead to delays in care, which can be fatal.

Early detection of lung cancer: role of biomarkers.

Early detection of lung cancer requires none or few invasive techniques. Distal lung cancer (40% of the cases in most European countries) can be sensitively detected by spiral computed tomography. Theoretically, in 60% of cases, the proximal lesions (main to segmental bronchi, accessible by bronchoscopy) should be able to be detected by sputum cytology. Unfortunately, this very specific technique has a low sensitivity and is time consuming. Fluorescent bronchoscopy increases the detection rate of early or micro-invasive lesions and may be proposed in highly selected populations, but not as a screening test. Biomarkers in blood and sputum have not yet been clinically validated. However, the amount of data generated from studies first on resected tumours, then on early bronchial lesions and more recently on blood and sputum offer a wide field for investigation. Lung carcinogenesis is a multistep process characterised by the accumulation of successive molecular genetic and epigenetic abnormalities, resulting in selection of clonal cells with uncontrolled growth capacities throughout the whole respiratory tract (field cancerisation). Molecular lesions far precede morphological transformation of preneoplastic bronchial lesions (dysplasia) or alveolar lesions (atypical alveolar hyperplasia). Genetic and epigenetic abnormalities in the genes involved in cell cycle, senescence, apoptosis, repair, differentiation and cell migration control may be detected on bronchial biopsies, on respiratory cells from the sputum and even in the circulating deoxyribonucleic acid (DNA). The key genes involved include those in the P53-retinoblastoma (Rb) pathways. The balance between cyclin-dependent kinases and their inhibitors regulates the level of Rb phosphorylation and its function at G1-S transition; P53 plays at least two functions (cell cycle and apoptosis control). The balance of bax-bcl2 is important in the control of apoptosis as well as loss of fragile histidine triad expression. O(6)-methylguanine-DNA methyltransferase seems to be important in DNA repair control, the RARbeta receptor in differentiation, and cadherin H and E and different metalloproteases genes in cell migration. The demonstration of hyperexpression or silencing of these genes needs different validated techniques: immunohistochemistry on biopsies or cytological preparations, molecular biology techniques for mutations, loss of heterozygosity and aberrant methylation abnormalities. Automation and miniaturisation of these techniques will allow early detection and may be widely applied once clinically validated.