7 research outputs found

    Systematic Screening for Occupational Exposures in Lung Cancer Patients: A Prospective French Cohort

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    Occupational lung cancers are under-reported and under-compensated worldwide. We assessed systematic screening for occupational exposure to carcinogens combining a self-administered questionnaire and an occupational consultation to improve the detection of occupational lung cancers and their compensation. Social deprivation and the costs of this investigation were estimated. Patients with lung cancer received a self-administered questionnaire to collect their job history, potential exposure to carcinogens and deprivation. A physician assessed the questionnaire and recommended an occupational consultation if necessary. During the consultation, a physician assessed if the lung cancer was work-related and, if it was, delivered a medical certificate to claim for compensation. Over 18 months, 440 patients received the self-administered questionnaire: 234 returned a completed questionnaire and a consultation was required for 120 patients. Compensation was judged possible for 41 patients. Among the 35 medical certificates delivered, 19 patients received compensation. Nearly half the patients (46%) were assessed as socially deprived and these patients took significantly longer to return the questionnaire compared with those who were not deprived. The mean cost of the process was €62.65 per patient. Our results showed a systematic self-administered questionnaire can be used to identify patients potentially exposed to carcinogens and to improve compensation

    EGFR-Mutated Breast Metastasis of Lung Adenocarcinoma: A Case Report

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    Breast metastasis from other primary carcinoma is very rare and could be difficult to identify despite immunohistochemistry analysis. Breast metastasis from lung adenocarcinoma can mimic triple-negative breast cancer. Given the prognosis and therapeutic challenges, a correct diagnosis appears essential, and molecular biomarkers could be useful. We report the case of a 52-year-old woman with a breast mass initially diagnosed as primary breast cancer and secondarily attached to breast metastasis from an EGFR-mutated lung adenocarcinoma. The same activating EGFR mutations were identified in both the primary lung carcinoma and the breast metastasis

    High expression levels of egfl7 correlate with low endothelial cell activation in peritumoral vessels of human breast cancer

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    International audienceTumor blood vessels participate in the immune response against cancer cells and we previously used pre-clinical models to demonstrate that egfl7 (VE-statin) promotes tumor cell evasion from the immune system by repressing endothelial cell activation, preventing immune cells from entering the tumor mass. In the present study, the expression levels of egfl7 and that of ICAM-1 as a marker of endothelium activation, were evaluated in peritumoral vessels of human breast cancer samples. Breast cancer samples (174 invasive and 30 in situ) from 204 patients treated in 2005 were immunostained for CD31, ICAM-1 and stained for egfl7 using in situ hybridization. The expression levels of ICAM-1 and egfl7 were assessed in peritumoral areas using semi-quantitative scales. There was a strong and significant inverse correlation between the expression of ICAM-1 and that of egfl7 in CD31 + blood vessels. When the ICAM-1 score increased, the egfl7 score reduced significantly (P=0.004), and vice-versa (Cuzick's test for trend across ordered groups). In order to determine which gene influenced the other gene between egfl7 and ICAM-1, the expression levels of either gene were modulated in endothelial cells. Egfl7 regulated ICAM-1 expression while ICAM-1 had no effects on egfl7 expression in the same conditions. Altogether, these results provide further results that egfl7 serves a regulatory role in endothelial cell activation in relation to immune infiltration and that it is a potential therapeutic target to consider for improving anticancer immunotherapies

    High expression levels of egfl7 correlate with low endothelial cell activation in peritumoral vessels of human breast cancer

    No full text
    Tumor blood vessels participate in the immune response against cancer cells and we previously used pre-clinical models to demonstrate that egfl7 (VE-statin) promotes tumor cell evasion from the immune system by repressing endothelial cell activation, preventing immune cells from entering the tumor mass. In the present study, the expression levels of egfl7 and that of ICAM-1 as a marker of endothelium activation, were evaluated in peritumoral vessels of human breast cancer samples. Breast cancer samples (174 invasive and 30 in situ) from 204 patients treated in 2005 were immunostained for CD31, ICAM-1 and stained for egfl7 using in situ hybridization. The expression levels of ICAM-1 and egfl7 were assessed in peritumoral areas using semi-quantitative scales. There was a strong and significant inverse correlation between the expression of ICAM-1 and that of egfl7 in CD31(+) blood vessels. When the ICAM-1 score increased, the egfl7 score reduced significantly (P=0.004), and vice-versa (Cuzick's test for trend across ordered groups). In order to determine which gene influenced the other gene between egfl7 and ICAM-1, the expression levels of either gene were modulated in endothelial cells. Egfl7 regulated ICAM-1 expression while ICAM-1 had no effects on egfl7 expression in the same conditions. Altogether, these results provide further results that egfl7 serves a regulatory role in endothelial cell activation in relation to immune infiltration and that it is a potential therapeutic target to consider for improving anticancer immunotherapies
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