Collaboration: COPDGene - Revision history

Marianna: /* References */

2016-12-13T21:17:16Z

References

Marianna at 19:49, 16 December 2009

2009-12-16T19:49:01Z

Raul: /* Key Personnel */

2009-12-16T19:29:26Z

Key Personnel

Marianna at 19:06, 16 December 2009

2009-12-16T19:06:21Z

Marianna at 18:58, 16 December 2009

2009-12-16T18:58:02Z

Raul: /* Specific Aims */

2009-12-16T18:11:56Z

Specific Aims

Raul: /* Grant # */

2009-12-16T18:01:04Z

Grant #

Raul: /* Specific Aims */

2009-12-16T18:00:05Z

Specific Aims

Raul at 17:59, 16 December 2009

2009-12-16T17:59:28Z

Raul at 17:59, 16 December 2009

2009-12-16T17:59:17Z

@@ Line 44: / Line 44: @@
 #     Friedlander AL, Lynch D, Dyar LA et al. Phenotypes of chronic obstructive pulmonary disease. COPD 2007; 4(4):355-84
 #     Gottlieb DJ, Wilk JB, Harmon M et al. Heritability of longitudinal change in lung function. The Framingham study. Am J Respir Crit Care Med 2001; 164(9):1655-9
-#     Hersh CP, Demeo DL, Lazarus R et al. Genetic association analysis of functional impairment in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006; 173(9):977-84
+#     Hersh CP, DeMeo DL, Lazarus R et al. Genetic association analysis of functional impairment in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006; 173(9):977-84
-#     Hersh CP, DeMeo DL, Reilly JJ et al. Xenobiotic metabolizing enzyme gene polymorphisms predict response to lung volume reduction surgery. Respir Res 2007; 8:59
+#     Hersh CP, DeMeo DL, Reilly JJ, Silverman EK. Xenobiotic metabolizing enzyme gene polymorphisms predict response to lung volume reduction surgery. Respir Res. 2007 Aug 8;8:59. PubMed PMID: 17686149; PubMed Central PMCID: PMC2048957.
-#     Hoffman EA, Simon BA, McLennan G. State of the Art. A structural and functional assessment of the lung via multidetector-row computed tomography: phenotyping chronic obstructive pulmonary disease. Proc Am Thorac Soc 2006; 3(6):519-32
+#     Hoffman EA, Simon BA, McLennan G. State of the Art. A structural and functional assessment of the lung via multidetector-row computed tomography: phenotyping chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2006 Aug;3(6):519-32. Review. PubMed PMID: 16921136; PubMed Central PMCID: PMC2647643.
-#     Hoyert DL, Arias E, Smith BL et al. Deaths: final data for 1999. Natl Vital Stat Rep 2001; 49(8):1-113
+#     Hoyert DL, Arias E, Smith BL, Murphy SL, Kochanek KD. Deaths: final data for 1999. Natl Vital Stat Rep. 2001 Sep 21;49(8):1-113. PubMed PMID: 11591077.
-#     Kueppers F, Miller RD, Gordon H et al. Familial prevalence of chronic obstructive pulmonary disease in a matched pair study. Am J Med 1977; 63(3):336-42
+#     Kueppers F, Miller RD, Gordon H et al. Familial prevalence of chronic obstructive pulmonary disease in a matched pair study. Am J Med. 1977 Sep;63(3):336-42. PMID: 302643.
 #     Lokke A, Lange P, Scharling H et al. Developing COPD: a 25 year follow up study of the general population. Thorax 2006; 61(11):935-9
 #     Mannino DM, Buist AS. Global burden of COPD: risk factors, prevalence, and future trends. Lancet 2007; 370(9589):765-73

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-Back to [[NA-MIC_External_Collaborations]]
+Back to [[NA-MIC_External_Collaborations|NA-MIC External Collaborations]]
-__TOC__
+__NOTOC__
 [[Image:LungCover-LowRes.png|thumb|right|300px|Burden of emphysema in a COPD subject]]

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 The project described is being supported by Award Numbers U01HL089897 and U01HL089856 from the National Heart, Lung, And Blood Institute.
 ==Key Personnel==
-*National Jewish Health: James D. Crapo
+*National Jewish Health: James D. Crapo (PI)
-*NA-MIC: Raul San Jose estepar
+*Brigham and Women's Hospital: Edwin K. Silverman (PI)
 ==Grant Duration==
 /27/2007-07/31/2012

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 Finally, the wealth of data to be accrued in COPDGene® will be stored and made available to the broader scientific community for future studies.  This will include the detailed phenotypic subject information, whole genome data and the imaging data from CT scans.
-== Grant #==
+== Grant#==
 The project described is being supported by Award Numbers U01HL089897 and U01HL089856 from the National Heart, Lung, And Blood Institute.
 ==Key Personnel==

@@ Line 32: / Line 32: @@
 == Grant #==
 The project described is being supported by Award Numbers U01HL089897 and U01HL089856 from the National Heart, Lung, And Blood Institute.
+==Key Personnel==
 == References ==
 #     Cohen BH, Ball WC Jr, Brashears S et al. Risk factors in chronic obstructive pulmonary disease (COPD). Am J Epidemiol 1977; 105(3):223-32

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 == Specific Aims ==
-* Specific Aim 1: Cohort Building.  The enrollment of 10,000 subjects is balanced with 2/3 non-Hispanic White and 1/3 African American, distributed across the full spectrum of disease severity and both genders (Table 4).    The cohort is specifically being recruited for a genome wide association study (GWAS) analysis and is large enough to provide adequate statistical power to detect genes exerting modest effects on risk.
+* Specific Aim 1: Cohort Building.  The enrollment of 10,000 subjects is balanced with 2/3 non-Hispanic White and 1/3 African American, distributed across the full spectrum of disease severity and both genders.    The cohort is specifically being recruited for a genome wide association study (GWAS) analysis and is large enough to provide adequate statistical power to detect genes exerting modest effects on risk.
 * Specific Aim 2: Characterization of Subtypes of COPD.   The main characterization of COPD subtypes will be based on the presence and severity of parenchymal and airway disease based on inspiratory and expiratory high-resolution chest CT scans.
-* Specific Aim3: Genome-Wide Association Study (See Figure 2).   The initial study plan for the GWAS involves four phases.  There will be an initial GWAS on a balanced group of 3000 subjects of current or former smoker case and control subjects (2000 White and 1000 African American) in Phase 1.  Statistical signals (SNPs in or between genes) identified in Phase I will be confirmed in Phase II with a custom SNP array that will provide greater coverage of genes.  In Phase III SNPs in genes/regions identified and confirmed in Phases I and II will be investigated with regional fine mapping and tests of associations to identify causal genes.  The final group of candidate genes will be replicated in other COPD cohorts as Phase IV.  With continued improvements in SNP genotyping technology additional phases (beyond Phase 1) may be analyzed at the genome-wide level.
+* Specific Aim3: Genome-Wide Association Study.   The initial study plan for the GWAS involves four phases.  There will be an initial GWAS on a balanced group of 3000 subjects of current or former smoker case and control subjects (2000 White and 1000 African American) in Phase 1.  Statistical signals (SNPs in or between genes) identified in Phase I will be confirmed in Phase II with a custom SNP array that will provide greater coverage of genes.  In Phase III SNPs in genes/regions identified and confirmed in Phases I and II will be investigated with regional fine mapping and tests of associations to identify causal genes.  The final group of candidate genes will be replicated in other COPD cohorts as Phase IV.  With continued improvements in SNP genotyping technology additional phases (beyond Phase 1) may be analyzed at the genome-wide level.
 * Specific Aim 4: Natural history of COPD and Risk Factors for Progression.  The COPDGene cohort will be established for longitudinal follow-up with regular contact made to determine mortality, comorbid disease events and disease status based on clinical and/or chest CT evidence of progression.

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 __TOC__
-[[Image:LungCover-LowRes|thumb|right|300px|Burden of emphysema in a COPD subject]]
+[[Image:LungCover-LowRes.png|thumb|right|300px|Burden of emphysema in a COPD subject]]
 ==Abstract==
 Chronic Obstructive Pulmonary Disease (COPD) is the fourth leading cause of death in the United States and an important public health issue [8].  An estimated 24 million individuals in the U.S. may be affected by COPD [12]. Both the number of affected individuals and the number of deaths from COPD are expected to increase as the population ages [11].  COPD is a heterogeneous condition, with a variety of disease-related phenotypes [3,16]. Better understanding of the disease mechanisms is needed to develop effective treatments and prevention strategies.  To accomplish this, we need improved understanding of the etiology of COPD, clinical classifications of the disease that are biologically and medically coherent, and knowledge of genetic factors that influence risk of COPD.