PMID- 14749602
OWN - NLM
STAT- MEDLINE
DCOM- 20040308
LR  - 20191108
IS  - 1070-5287 (Print)
IS  - 1070-5287 (Linking)
VI  - 10
IP  - 1
DP  - 2004 Jan
TI  - Recent development in genomic and proteomic research for asthma.
PG  - 22-30
AB  - PURPOSE OF REVIEW: Asthma is a complex genetic disorder with a heterogeneous 
      phenotype attributed to the interactions among many genes and the environment. 
      This review highlights recent developments in asthma genomic and proteomic 
      research. RECENT FINDINGS: Numerous loci and candidate genes have been reported 
      to show linkage and association of asthma and the asthma-associated phenotypes, 
      atopy, elevated immunoglobulin E (IgE) levels, and bronchial hyperresponsiveness 
      to alleles of microsatellite markers and single nucleotide polymorphisms within 
      specific cytokine/chemokine, and IgE regulating genes. Although many studies 
      reporting these observations are compelling, only a few genes conferring 
      significant risk have been mapped. Although significant progress has been made in 
      the field of asthma genetics in the past decade, the clinical implications of the 
      genetic variations within the numerous candidate asthma genes, which have been 
      found to associate with the expression of the asthmatic phenotype, remain largely 
      undetermined. However, in the past year the scientific community has benefited 
      from postgenomic discoveries, with the recent cloning of two asthma genes, ADAM 
      33 and PHF11, and this has generated new information that is benefiting others. 
      SUMMARY: The asthma genetics field has advanced considerably in recent years, 
      with new information being generated that has led to improved understanding of 
      the pathobiology underlying this complex disorder. This has also generated 
      interest in the study of gene-gene interaction and how linkage disequilibrium 
      blocks and haplotypes can be used as functional units to pinpoint mutations and 
      capture relative risk of mutated genes in complex disorders.
FAU - Halapi, Eva
AU  - Halapi E
AD  - Division of Respiratory and Pharmacogenomic Research, deCODE genetics, Inc., 
      Reykjavik, Iceland.
FAU - Hakonarson, Hakon
AU  - Hakonarson H
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Opin Pulm Med
JT  - Current opinion in pulmonary medicine
JID - 9503765
RN  - 0 (Transcription Factors)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.- (ADAM33 protein, human)
RN  - EC 3.4.24.- (Metalloendopeptidases)
SB  - IM
MH  - ADAM Proteins
MH  - Asthma/*genetics/physiopathology
MH  - Bronchial Hyperreactivity/genetics
MH  - Chromosomes, Human/genetics
MH  - Dermatitis, Atopic/genetics
MH  - Haplotypes
MH  - Humans
MH  - Linkage Disequilibrium
MH  - Metalloendopeptidases
MH  - Polymorphism, Single Nucleotide
MH  - Proteomics
MH  - Transcription Factors/genetics
RF  - 104
EDAT- 2004/01/30 05:00
MHDA- 2004/03/09 05:00
CRDT- 2004/01/30 05:00
PHST- 2004/01/30 05:00 [pubmed]
PHST- 2004/03/09 05:00 [medline]
PHST- 2004/01/30 05:00 [entrez]
AID - 10.1097/00063198-200401000-00005 [doi]
PST - ppublish
SO  - Curr Opin Pulm Med. 2004 Jan;10(1):22-30. doi: 10.1097/00063198-200401000-00005.