Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| Name | Class |
|---|---|
| Henri Mondor University Hospital | OTHER |
| Institut National de la Santé Et de la Recherche Médicale, France | OTHER_GOV |
Not provided
Not provided
Not provided
Not provided
To evaluate the regenerative capacities of mesenchymal cells composing the microenvironment of alveolar type 2 cells in a population of patients, undergoing thoracic surgery for suspected cancer, who are smokers with and without COPD compared to non-smokers patients
Chronic obstructive pulmonary diseases (COPD) have a major public health impact, as evidenced by the 250 million patients affected by these diseases and the 50% 5-year mortality for severe stages of chronic obstructive pulmonary disease (COPD). One pathophysiological mechanism of COPD and emphysema is a depletion of alveolar progenitor cells inducing a loss of alveolar-reparation capacities after an aggression. The genesis of these alterations and the mechanisms involved remain unknown. Alveolar type 2 cells (AT2) are the alveolar epithelial progenitor cells. AT2 proliferate and differentiate into alveolar type 1 cells (AT1) which form the alveolar-capillary barrier, along with endothelial cells, through which respiratory gas exchanges take place. The proliferation and differentiation of AT2 into AT1 are under the control of mesenchymal cells and endothelial cells located in close proximity. Together these cells form the alveolar stem cell niche. The characteristics and interactions of the different cell populations have been well described during lung growth, in the normal adult lung or during pulmonary fibrosis; however, participants are poorly described during smoking exposure and chronic obstructive diseases.
Not provided
Not provided
Not provided
Not provided
Not provided
| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Thoracic resection surgery | Other | Smokers (active or ex-smokers) and non-smokers with COPD and without COPD undergoing thoracic resection surgery |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| Thoracic resection surgery | Other | Patients undergoing thoracic resection surgery (pneumonectomy, lobectomy, segmentectomy) for cancer or suspected cancer, including smokers (active or ex-smokers) and non-smokers, with COPD and without COPD, and non-smoking patients. |
| Measure | Description | Time Frame |
|---|---|---|
| Number of alveolar organoids | Comparison of the number of alveolar organoids formed 21 days after culture of fibroblasts with alveolar type II cells between smokers with and without COPD and non-smoking patients | through study completion, an average of 3 years |
| Measure | Description | Time Frame |
|---|---|---|
| Fibroblast proliferation capacity | Evaluated by their doubling time, number of cells collected compared to the number of cells seeded | through study completion, an average of 3 years |
| Differentiation into myofibroblasts |
Not provided
Inclusion Criteria:
Exclusion Criteria:
Not provided
Not provided
Not provided
Not provided
Not provided
| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| JUNG Camille, MD | Contact | 0145175000 | +33 | camille.jung@chiccreteil.fr |
Not provided
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Rousseau-Bussac | Recruiting | Créteil | 94000 | France |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| ID | Term |
|---|---|
| D029424 | Pulmonary Disease, Chronic Obstructive |
| ID | Term |
|---|---|
| D008173 | Lung Diseases, Obstructive |
| D008171 | Lung Diseases |
| D012140 | Respiratory Tract Diseases |
| D002908 | Chronic Disease |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
By immunofluorescence marking: number of alpha-smooth muscle actin (alpha-SMA) + cells compared to total cells
| through study completion, an average of 3 years |
| Fibroblast migration capacity | Evaluated in Boyden chamber | through study completion, an average of 3 years |
| Modulated signaling pathways in isolated fibroblasts between groups | Evaluated by Ribonucleic acid (RNA) sequencing of fibroblasts | through study completion, an average of 3 years |
| Modulated signaling pathways in endothelial cells between groups | Evaluated byRibonucleic acid (RNA) sequencing of endothelial cells | through study completion, an average of 3 years |
| Evaluation of cytokines in fibroblasts supernatant | Evaluated by Luminex Assay | through study completion, an average of 3 years |
| Tumor progression | By studying the migration and invasion of tumor cells | through study completion, an average of 3 years |
| Identification of different cell types on total lung | Cell types composing the lung stem cell microenvironment measured by single cell analysis | through study completion, an average of 3 years |
| Severity of pulmonary emphysema, | Change of lung density assessed by computed tomography scan | At inclusion, every year, up to 5 years after surgery |
| Type of pulmonary emphysema | Assessed by computed tomography scan : [centro-lobular or pan-lobular, para-septal] | At inclusion, every year, up to 5 years after surgery |
| Research of pulmonary biomarkers | Searched according to the results obtained during cell cultures (immunohistochemistry, immunofluorescence) | through study completion, an average of 3 years |
| Identification of biomarkers in the pre and postoperative circulating blood | Evaluated in laboratory by metagenomic analysis of 16s Ribonucleic acid (RNA) of bacteria for cluster analysis that correlate with lung injury and could be prognostic markers | through study completion, an average of 3 years |
| Identification of biomarkers in the intestinal microbiota | Evaluated in laboratory by metagenomic analysis of 16s Ribonucleic acid (RNA) of bacteria for cluster analysis that correlate with lung injury and could be prognostic markers | through study completion, an average of 3 years |
| Measurement of Forced expiratory volume at one second (FEV1) | Determine the relationship between respiratory disease phenotype and exercise impact by measurement of Forced expiratory volume at one second (FEV1) | through study completion, an average of 3 years |
| Measurement of Forced Vital Capacity (FVC ) | Determine the relationship between respiratory disease phenotype and exercise impact by measurement of Forced Vital Capacity (FVC ) | through study completion, an average of 3 years |
| Measurement of pulmonary diffusion capacity of CO (DLCO) | Determine the relationship between respiratory disease phenotype and exercise impact by measurement of pulmonary diffusion capacity of CO (DLCO) | through study completion, an average of 3 years |
| Measurement of CO transfer coefficient (KCO) | Determine the relationship between respiratory disease phenotype and exercise impact by measurement of CO transfer coefficient (KCO) | through study completion, an average of 3 years |
| Hopital Cochin | Active, not recruiting | Paris | 75014 | France |
| HEGP | Active, not recruiting | Paris | 75015 | France |
| Hopital Tenon | Active, not recruiting | Paris | 75020 | France |
| D020969 |
| Disease Attributes |
| D010335 | Pathologic Processes |
| D013568 | Pathological Conditions, Signs and Symptoms |