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Defective FGFR2 Signaling in the Small Airway Basal Progenitor Cells in COPD

NCT02341326 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 111

Last updated 2025-03-11

No results posted yet for this study

Summary

Early changes associated with the development of smoking-induced diseases, e.g., COPD and lung cancer (the two commonest causes of death in U.S.) are often characterized by abnormal airway epithelial differentiation. Airway basal cells (BC) are stem/progenitor cells necessary for generation of differentiated airway epithelium. Based on our preliminary observations on SAE BC cells and FGFR2 signaling, we hypothesized that suppression of FGFR2 signaling in the SAE BC stem/progenitor cells by cigarette smoking renders these cells less potent in generating and maintaining normally differentiated SAE, shifting these cells towards a COPD associated phenotype. To test this, SAE basal cells will be isolated from cultured cells obtained through bronchoscopic brushings and analyzed through in vitro assays for their stem/progenitor capacities.

Conditions

  • COPD
  • Smoking
  • Lung Disorder

Sponsors & Collaborators

  • National Heart, Lung, and Blood Institute (NHLBI)

    collaborator NIH

  • Weill Medical College of Cornell University

    lead OTHER

Principal Investigators

  • Renat Shaykhiev, MD · Weill Cornell Medical College, NY

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2014-07-31
Primary Completion
2024-10-29
Completion
2024-10-29

Countries

  • United States

Study Locations

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Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02341326 on ClinicalTrials.gov