Study of the Mechanisms of Asthma
MAST
Determining Mechanisms of Asthma Through Detailed Analysis of Airway Secretions and Tissues
1 other identifier
interventional
127
1 country
1
Brief Summary
The purpose of this study is to identify the causes of asthma that were not previously suspected, to better understand the effects of inhaled steroids on asthma and to identify new way to treat asthma. In order to take advantage of the most current scientific expertise, we (scientists at UCSF) plan to work together with Genentech Inc. We believe that working with Genentech will provide the best chance of developing new treatments for asthma.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P75+ for phase_1 asthma
Started Apr 2007
Longer than P75 for phase_1 asthma
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
Click on a node to explore related trials.
Study Timeline
Key milestones and dates
Study Start
First participant enrolled
April 1, 2007
CompletedFirst Submitted
Initial submission to the registry
January 2, 2008
CompletedFirst Posted
Study publicly available on registry
January 16, 2008
CompletedPrimary Completion
Last participant's last visit for primary outcome
June 1, 2011
CompletedStudy Completion
Last participant's last visit for all outcomes
June 1, 2011
CompletedResults Posted
Study results publicly available
January 20, 2014
CompletedJanuary 20, 2014
December 1, 2013
4.2 years
January 2, 2008
September 25, 2013
December 5, 2013
Conditions
Outcome Measures
Primary Outcomes (1)
Gene Expression in Airway Secretions and Tissues
The primary outcome measure for this study is the scaled mean value of three gene expression markers of IL-13 in the airway: PERIOSTIN, calcium-activated chloride channel regulator 1 (CLCA1), and plasminogen activator inhibitor-2 (SERPINB2). First, for each of the three interleukin-13 (IL-13) signature genes, the log (base-2) transformed relative expression value for each subject is measured using real-time polymerase chair reaction (PCR) and normalized with the geometric mean of 5 housekeeping genes. Next, these values are centered (by subtracting the mean for that gene) and scaled (by dividing by the standard deviation for that gene) so that each gene makes an equal, assay-independent contribution to the Th2 phenotype. Then, for each subject, the arithmetic mean of the three centered \& scaled genes is calculated, producing the "three-gene-mean" metric.
Healthy Control: Visit 2 (at 1 week); Steroid Naive Asthmatics: Visit 2 (at 1 week); Steroid Treated Asthmatics: Visit 5 (at 9 weeks)
Study Arms (3)
B
ACTIVE COMPARATORAsthmatics not on inhaled corticosteroids who will be put on an inhaled steroid during the study
A
NO INTERVENTIONHealthy, non-asthmatics who will not be put on any intervention
C
ACTIVE COMPARATORAsthmatics, who are already on inhaled corticosteroids who will be put on standardized dose of inhaled corticosteroids
Interventions
inhaled powder of inhaled corticosteroid, 1 puff (180mcg) twice a day for 8-10 weeks
Eligibility Criteria
You may qualify if:
- Group C:
- Male and female subjects between the ages of 18 and 70 years
- History of asthma
- Continuous treatment with inhaled corticosteroids for at least the 6-week
- Hyperreactivity to methacholine (provocative concentration of methacholine causing a 20% drop in forced expiratory volume in 1 second (PC20 FEV1) Methacholine ≤ 16.0 mg/mL).
You may not qualify if:
- History of asthma
- No use of oral or inhaled corticosteroids for the treatment of asthma in the past 6 weeks
- Hyperreactivity to methacholine (PC20 FEV1 Methacholine ≤ 8.0 mg/mL).
- At least one of the following symptoms, beta agonist use, or FEV1 criteria:
- Asthma symptoms on at least two days per week; OR
- Beta agonist use on at least two days per week; OR
- Forced expiratory volume in 1 second (FEV1) \< 85% predicted
- Subjects must be non-smokers (patients who have never smoked or patients who have not smoked for 1 year and have a total pack-year smoking history \< 15 packs).
Contact the study team to confirm eligibility.
Sponsors & Collaborators
- University of California, San Franciscolead
- Genentech, Inc.collaborator
Study Sites (1)
University of California, San Francisco
San Francisco, California, 94143, United States
Related Publications (1)
Solberg OD, Ostrin EJ, Love MI, Peng JC, Bhakta NR, Hou L, Nguyen C, Solon M, Nguyen C, Barczak AJ, Zlock LT, Blagev DP, Finkbeiner WE, Ansel KM, Arron JR, Erle DJ, Woodruff PG. Airway epithelial miRNA expression is altered in asthma. Am J Respir Crit Care Med. 2012 Nov 15;186(10):965-74. doi: 10.1164/rccm.201201-0027OC. Epub 2012 Sep 6.
PMID: 22955319DERIVED
Related Links
MeSH Terms
Conditions
Interventions
Condition Hierarchy (Ancestors)
Intervention Hierarchy (Ancestors)
Results Point of Contact
- Title
- John V. Fahy, MD, MSc
- Organization
- University of California, San Francisco
Study Officials
- PRINCIPAL INVESTIGATOR
John V Fahy, M.D., M.Sc.
University of California, San Francisco
Publication Agreements
- PI is Sponsor Employee
- No
- Restrictive Agreement
- No
Study Design
- Study Type
- interventional
- Phase
- phase 1
- Allocation
- NON RANDOMIZED
- Masking
- NONE
- Purpose
- BASIC SCIENCE
- Intervention Model
- PARALLEL
- Sponsor Type
- OTHER
- Responsible Party
- SPONSOR
Study Record Dates
First Submitted
January 2, 2008
First Posted
January 16, 2008
Study Start
April 1, 2007
Primary Completion
June 1, 2011
Study Completion
June 1, 2011
Last Updated
January 20, 2014
Results First Posted
January 20, 2014
Record last verified: 2013-12