Invention Grant
US08110361B2 DNA methylation markers associated with the CpG island methylator phenotype (CIMP) in human colorectal cancer
失效
与人结肠直肠癌中CpG岛甲基化表型(CIMP)相关的DNA甲基化标记
- Patent Title: DNA methylation markers associated with the CpG island methylator phenotype (CIMP) in human colorectal cancer
- Patent Title (中): 与人结肠直肠癌中CpG岛甲基化表型(CIMP)相关的DNA甲基化标记
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Application No.: US11913535Application Date: 2006-05-02
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Publication No.: US08110361B2Publication Date: 2012-02-07
- Inventor: Peter W. Laird , Kimberly D. Siegmund , Mihaela Campan , Daniel J. Weisenberger , Tiffany I. Long
- Applicant: Peter W. Laird , Kimberly D. Siegmund , Mihaela Campan , Daniel J. Weisenberger , Tiffany I. Long
- Applicant Address: US CA Los Angeles
- Assignee: University of Southern California USC Stevens Center for Innovation
- Current Assignee: University of Southern California USC Stevens Center for Innovation
- Current Assignee Address: US CA Los Angeles
- Agency: Davis Wright Tremaine LLP
- Agent Barry L. Davison
- International Application: PCT/US2006/017160 WO 20060502
- International Announcement: WO2006/119434 WO 20061109
- Main IPC: C12Q1/68
- IPC: C12Q1/68

Abstract:
Particular aspects confirm the existence of a CpG island methylator phenotype (CIMP) in colorectal cancer, and provide novel validated DNA methylation markers associated with CIMP. Additional aspects provide novel methods and compositions for: determining CIMP status in colorectal cancers, determining the relationship between CIMP status and other molecular features of the cancers (e.g., BRAF mutation, KRAS mutation and MSI status); determining the relationship between CIMP status and other variables (e.g., age, sex, tumor location, family history, race, country of origin, tumor characteristics (including, tumor type, tumor grade, invasive margin characteristics, lymphocyte infiltration characteristics, direct spread, lymph node spread, venous spread and type of residual adjacent polyp, if present)); and determining, between subgroups defined by CIMP status and BRAF mutations, effects of selected risk factors (e.g., body mass index, smoking history, alcohol intake, dietary folate intake, folate metabolic enzyme polymorphisms and history of hormonal use).
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