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L'essentiel de la littérature réçente en Pneumologie

Dans cette rubrique on vous propose une revue de la littérature à travers une sélection d'abstracts d'articles originaux.
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Prognostic Model to Predict Outcomes in Non-Small Cell Lung Cancer Patients with Erlotinib as Salvage Treatment. Imprimer Envoyer
Mardi, 30 Novembre 2010 07:06
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Prognostic Model to Predict Outcomes in Non-Small Cell Lung Cancer Patients with Erlotinib as Salvage Treatment.

Oncology. 2010 Nov 12;79(1-2):78-84

Authors: Kim ST, Lee J, Sun JM, Park YH, Ahn JS, Park K, Ahn MJ

Purpose: To devise a prognostic model based on clinical parameters for non-small cell lung cancer (NSCLC) patients treated with erlotinib as a salvage therapy. Patients and Methods: Between July 2006 and September 2008, two hundred fifty-seven metastatic/relapsed NSCLC patients who had been treated with erlotinib as a salvage therapy were analyzed retrospectively. Results: For the 257 patients, the median overall survival (OS) and progression-free survival (PFS) with erlotinib treatment were 12.4 and 2.8 months. Multivariate analysis showed that an ECOG performance status of 2 or more, an elevated serum LDH level, and the absence of skin rash were independent adverse prognostic factors for OS and that the presence of intra-abdominal metastasis, 2 or more prior chemotherapy regimens, and the absence of skin rash were prognostic factors for PFS. Patients were categorized into the following 4 prognosis groups on the basis of each adverse prognostic factor: good, intermediate, poor, and very poor prognosis. The median OS times for the good, intermediate, poor, and very poor prognosis groups were 22.0, 9.3, 5.4, and 2.7 months (p < 0.001) and the median PFS times were 6.5, 3.0, 1.2, and 0.9 months (p < 0.001). Conclusion: This prognostic model based on clinical parameters would be useful to identify patients who might be most likely to benefit from erlotinib therapy in clinical practice.

PMID: 21071994 [PubMed - as supplied by publisher]

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THE BRONCHODILATION RESPONSE TO DEEP INSPIRATIONS IN ASTHMA IS DEPENDENT ON AIRWAY DISTENSIBILITY AND AIR TRAPPING. Imprimer Envoyer
Mardi, 30 Novembre 2010 07:06
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THE BRONCHODILATION RESPONSE TO DEEP INSPIRATIONS IN ASTHMA IS DEPENDENT ON AIRWAY DISTENSIBILITY AND AIR TRAPPING.

J Appl Physiol. 2010 Nov 11;

Authors: Pyrgos G, Scichilone N, Togias A, Brown RH

In healthy individuals, deep inspirations (DIs) have a potent bronchodilatory ability against methacholine (Mch)-induced bronchoconstriction. This is variably attenuated in asthma. We hypothesized that inability to bronchodilate with DIs is related to reduced airway distensibility. We examined the relationship between DI-induced bronchodilation and airway distensibility in 15 asthmatics with a wide range of baseline lung function (FEV(1) range: 60-99% predicted). After abstaining from DIs for 20 minutes, subjects received a single dose Mch challenge followed by DIs. The effectiveness of DIs was assessed by their ability to improve FEV(1). The same individuals had two sets of high-resolution computerized tomography (HRCT) scans, one at FRC and one at TLC. In each subject, the areas of 21 to 41 airways (0.8-6.8 mm in diameter at FRC) were matched and measured and airway distensibility (the increase in airway diameter from FRC to TLC) was calculated. The bronchodilatory ability of DIs was significantly lower in individuals with FEV(1) <75%, compared to those with ≥ 75% predicted (15±11% vs. 46±9%, p=0.04), and strongly correlated with airway distensibility (r= 0.57, p=0.03), but also with RV/TLC (r= -0.63, p=0.01). In multiple regression, only RV/TLC was a significant determinant of DI-induced bronchodilation. These relationships were lost when the airways were examined after maximal bronchodilation with albuterol. Our data indicate that the loss of the bronchodilatory effect of deep inspiration in asthma is related to the ability to distend the airways with lung inflation, which is, in turn, related to the extent of air trapping and ASM tone. These relationships only exist in the presence of airway tone indicating that structural changes in the conducting airways visualized by HRCT do not play a pivotal role.

PMID: 21071596 [PubMed - as supplied by publisher]

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Oncomutations as biomarkers of cancer risk. Imprimer Envoyer
Mardi, 30 Novembre 2010 07:02
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Oncomutations as biomarkers of cancer risk.

Environ Mol Mutagen. 2010 Oct-Dec;51(8-9):836-50

Authors: Parsons BL, Myers MB, Meng F, Wang Y, McKinzie PB

Cancer risk assessment impacts a range of societal needs, from the regulation of chemicals to achieving the best possible human health outcomes. Because oncogene and tumor suppressor gene mutations are necessary for the development of cancer, such mutations are ideal biomarkers to use in cancer risk assessment. Consequently, DNA-based methods to quantify particular tumor-associated hotspot point mutations (i.e., oncomutations) have been developed, including allele-specific competitive blocker-PCR (ACB-PCR). Several studies using ACB-PCR and model mutagens have demonstrated that significant induction of tumor-associated oncomutations are measureable at earlier time points than are used to score tumors in a bioassay. In the particular case of benzo[a]pyrene induction of K-Ras codon 12 TGT mutation in the A/J mouse lung, measurement of tumor-associated oncomutation was shown to be an earlier and more sensitive endpoint than tumor response. The measurement of oncomutation by ACB-PCR led to two unexpected findings. First, oncomutations are present in various tissues of control rodents and "normal" human colonic mucosa samples at relatively high frequencies. Approximately 60% of such samples (88/146) have mutant fractions (MFs) >10(-5), and some have MFs as high as 10(-3) or 10(-4). Second, preliminary data indicate that oncomutations are present frequently as subpopulations in tumors. These findings are integrated into a hypothesis that the predominant preexisting mutations in particular tissues may be useful as generic reporters of carcinogenesis. Future research opportunities using oncomutation as an endpoint are described, including rodent to human extrapolation, dose-response assessment, and personalized medicine.

PMID: 20740637 [PubMed - indexed for MEDLINE]

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