Population Genomics of Drug Response
Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidat...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Halapi, Eva [verfasserIn] Stefansson, Kari [verfasserIn] Hakonarson, Hakon [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2004 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: American Journal of Pharmacogenomics - Springer International Publishing, 2001, 4(2004), 2 vom: Apr., Seite 73-82 |
|---|---|
| Übergeordnetes Werk: |
volume:4 ; year:2004 ; number:2 ; month:04 ; pages:73-82 |
| Links: |
|---|
| DOI / URN: |
10.2165/00129785-200404020-00002 |
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| 520 | |a Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. | ||
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10.2165/00129785-200404020-00002 doi (DE-627)SPR033298920 (SPR)00129785-200404020-00002-e DE-627 ger DE-627 rakwb eng Halapi, Eva verfasserin aut Population Genomics of Drug Response 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. Asthma (dpeaa)DE-He213 Schizophrenia (dpeaa)DE-He213 Clozapine (dpeaa)DE-He213 Drug Response (dpeaa)DE-He213 Founder Population (dpeaa)DE-He213 Stefansson, Kari verfasserin aut Hakonarson, Hakon verfasserin aut Enthalten in American Journal of Pharmacogenomics Springer International Publishing, 2001 4(2004), 2 vom: Apr., Seite 73-82 (DE-627)SPR033297754 nnns volume:4 year:2004 number:2 month:04 pages:73-82 https://dx.doi.org/10.2165/00129785-200404020-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 4 2004 2 04 73-82 |
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10.2165/00129785-200404020-00002 doi (DE-627)SPR033298920 (SPR)00129785-200404020-00002-e DE-627 ger DE-627 rakwb eng Halapi, Eva verfasserin aut Population Genomics of Drug Response 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. Asthma (dpeaa)DE-He213 Schizophrenia (dpeaa)DE-He213 Clozapine (dpeaa)DE-He213 Drug Response (dpeaa)DE-He213 Founder Population (dpeaa)DE-He213 Stefansson, Kari verfasserin aut Hakonarson, Hakon verfasserin aut Enthalten in American Journal of Pharmacogenomics Springer International Publishing, 2001 4(2004), 2 vom: Apr., Seite 73-82 (DE-627)SPR033297754 nnns volume:4 year:2004 number:2 month:04 pages:73-82 https://dx.doi.org/10.2165/00129785-200404020-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 4 2004 2 04 73-82 |
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10.2165/00129785-200404020-00002 doi (DE-627)SPR033298920 (SPR)00129785-200404020-00002-e DE-627 ger DE-627 rakwb eng Halapi, Eva verfasserin aut Population Genomics of Drug Response 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. Asthma (dpeaa)DE-He213 Schizophrenia (dpeaa)DE-He213 Clozapine (dpeaa)DE-He213 Drug Response (dpeaa)DE-He213 Founder Population (dpeaa)DE-He213 Stefansson, Kari verfasserin aut Hakonarson, Hakon verfasserin aut Enthalten in American Journal of Pharmacogenomics Springer International Publishing, 2001 4(2004), 2 vom: Apr., Seite 73-82 (DE-627)SPR033297754 nnns volume:4 year:2004 number:2 month:04 pages:73-82 https://dx.doi.org/10.2165/00129785-200404020-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 4 2004 2 04 73-82 |
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10.2165/00129785-200404020-00002 doi (DE-627)SPR033298920 (SPR)00129785-200404020-00002-e DE-627 ger DE-627 rakwb eng Halapi, Eva verfasserin aut Population Genomics of Drug Response 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. Asthma (dpeaa)DE-He213 Schizophrenia (dpeaa)DE-He213 Clozapine (dpeaa)DE-He213 Drug Response (dpeaa)DE-He213 Founder Population (dpeaa)DE-He213 Stefansson, Kari verfasserin aut Hakonarson, Hakon verfasserin aut Enthalten in American Journal of Pharmacogenomics Springer International Publishing, 2001 4(2004), 2 vom: Apr., Seite 73-82 (DE-627)SPR033297754 nnns volume:4 year:2004 number:2 month:04 pages:73-82 https://dx.doi.org/10.2165/00129785-200404020-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 4 2004 2 04 73-82 |
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10.2165/00129785-200404020-00002 doi (DE-627)SPR033298920 (SPR)00129785-200404020-00002-e DE-627 ger DE-627 rakwb eng Halapi, Eva verfasserin aut Population Genomics of Drug Response 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. Asthma (dpeaa)DE-He213 Schizophrenia (dpeaa)DE-He213 Clozapine (dpeaa)DE-He213 Drug Response (dpeaa)DE-He213 Founder Population (dpeaa)DE-He213 Stefansson, Kari verfasserin aut Hakonarson, Hakon verfasserin aut Enthalten in American Journal of Pharmacogenomics Springer International Publishing, 2001 4(2004), 2 vom: Apr., Seite 73-82 (DE-627)SPR033297754 nnns volume:4 year:2004 number:2 month:04 pages:73-82 https://dx.doi.org/10.2165/00129785-200404020-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 4 2004 2 04 73-82 |
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Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. |
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Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. |
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Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. Collectively, these studies support the value of leveraging information available within population-based data systems to map and isolate genes for common complex disease and drug response. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR033298920</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519084352.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2004 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/00129785-200404020-00002</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR033298920</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)00129785-200404020-00002-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Halapi, Eva</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Population Genomics of Drug Response</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2004</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Genetic diversity contributes to both disease susceptibility and variability in response to drugs. However, it has proven difficult to isolate genes that underlie common complex disease, and genetic variations that influence clinical responses to drugs remain largely uncovered. The candidate gene approach to uncover genetic variations that contribute to disease susceptibility or variations in response to common drugs has not met expectations. Although the sib-pair linkage approach has certain theoretical advantages in dealing with common/complex disease, success has been slow in coming. Meanwhile family studies including siblings, cousins and second cousins, and studies in well-defined founder populations, have increasingly gained popularity and enabled scientists to map and isolate genes for common complex disease, such as schizophrenia and asthma. The latter method has generated new hope that this approach may also be effective in mapping genes that regulate drug response. Indeed, there is compelling evidence that corticosteroid sensitivity is a mapable trait in patients with asthma. 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