Gene signature: Difference between revisions
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A condition's '''gene signature''' is the group of [[gene]]s in a type of [[Cell (biology)|cell]] whose combined [[Gene expression|expression]] pattern<ref>Itadani H, Mizuarai S, Kotani H. Can [[systems biology]] understand pathway activation? [[Gene expression]] signatures as surrogate markers for understanding the complexity of pathway activation. Curr Genomics. 2008 Aug;9(5):349-60.PMID |
A condition's '''gene signature''' is the group of [[gene]]s in a type of [[Cell (biology)|cell]] whose combined [[Gene expression|expression]] pattern<ref>Itadani H, Mizuarai S, Kotani H. Can [[systems biology]] understand pathway activation? [[Gene expression]] signatures as surrogate markers for understanding the complexity of pathway activation. Curr Genomics. 2008 Aug;9(5):349-60.PMID 19517027</ref> is uniquely characteristic of that condition.<ref>Liu J, Campen A, Huang S, Peng SB, Ye X, Palakal M, Dunker AK, Xia Y, Li S. Identification of a gene signature in [[cell cycle]] pathway for [[breast cancer]] prognosis using gene expression profiling data. BMC Med Genomics. 2008 Sep 11;1:39. PMID 18786252</ref> Ideally, the gene signature can be used to select a group of patients<ref>Wouters BJ, Löwenberg B, Erpelinck-Verschueren CA, van Putten WL, Valk PJ, Delwel R. Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of [[acute myeloid leukemia]] with a distinctive gene expression profile that is uniquely associated with a favorable outcome. Blood. 2009 Mar 26;113(13):3088-91. Epub 2009 Jan 26.PMID 19171880</ref> at a specific state of a disease with accuracy that facilitates selection of treatments.<ref>Hassane DC, Guzman ML, Corbett C, Li X, Abboud R, Young F, Liesveld JL, Carroll M, Jordan CT. Discovery of agents that eradicate leukemia [[stem cell]]s using an [[in silico]] screen of public gene expression data. Blood. 2008 Jun 15;111(12):5654-62. Epub 2008 Feb 27.PMID 18305216</ref><ref>Corsello SM, Roti G, Ross KN, Chow KT, Galinsky I, DeAngelo DJ, Stone RM, Kung AL, Golub TR, Stegmaier K. Identification of AML1-ETO modulators by [[Chemogenomics|chemical genomics]]. Blood. 2009 Jun 11;113(24):6193-205. Epub 2009 Apr 17. PMID 19377049</ref> |
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== See also == |
== See also == |
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Revision as of 10:53, 3 December 2011
A condition's gene signature is the group of genes in a type of cell whose combined expression pattern[1] is uniquely characteristic of that condition.[2] Ideally, the gene signature can be used to select a group of patients[3] at a specific state of a disease with accuracy that facilitates selection of treatments.[4][5]
See also
References
- ^ Itadani H, Mizuarai S, Kotani H. Can systems biology understand pathway activation? Gene expression signatures as surrogate markers for understanding the complexity of pathway activation. Curr Genomics. 2008 Aug;9(5):349-60.PMID 19517027
- ^ Liu J, Campen A, Huang S, Peng SB, Ye X, Palakal M, Dunker AK, Xia Y, Li S. Identification of a gene signature in cell cycle pathway for breast cancer prognosis using gene expression profiling data. BMC Med Genomics. 2008 Sep 11;1:39. PMID 18786252
- ^ Wouters BJ, Löwenberg B, Erpelinck-Verschueren CA, van Putten WL, Valk PJ, Delwel R. Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with a favorable outcome. Blood. 2009 Mar 26;113(13):3088-91. Epub 2009 Jan 26.PMID 19171880
- ^ Hassane DC, Guzman ML, Corbett C, Li X, Abboud R, Young F, Liesveld JL, Carroll M, Jordan CT. Discovery of agents that eradicate leukemia stem cells using an in silico screen of public gene expression data. Blood. 2008 Jun 15;111(12):5654-62. Epub 2008 Feb 27.PMID 18305216
- ^ Corsello SM, Roti G, Ross KN, Chow KT, Galinsky I, DeAngelo DJ, Stone RM, Kung AL, Golub TR, Stegmaier K. Identification of AML1-ETO modulators by chemical genomics. Blood. 2009 Jun 11;113(24):6193-205. Epub 2009 Apr 17. PMID 19377049
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