The Molecular Analysis of Genome Instability Core will perform cytological assays to detect chromosome rearrangements, and assays to detect resection of double-strand breaks (DSBs) for program project participants. The Core Directors will consult with the program project investigators in the development of new procedures within our areas of expertise. By centralizing services under the leadership of two experts in chromosome cytology and DNA end resection, the Core will enhance the productivity of the program project members and promote synergy among the projects by providing access to critical methodologies and reagents. To accomplish these goals. Core B will pursue the following specofoc aims:
Specific Aim 1 : To provide services to analyze DNA end resection by direct physical methods.
Specific Aim 2 : To perform molecular cytogenetic assays to characterize chromosomal changes in cells derived from in vitro and in vivo experimental models.

Public Health Relevance

The Molecular Analysis of Genomic Instability Core will carry out assays to detect DNA end resection and chromosome translocations, allowing Project Leaders to use their staff and facilities more efficiently and advance the overall goal ofthe Program to understand how DNA end resection and translocations contribute to cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
1P01CA174653-01A1
Application #
8608850
Study Section
Special Emphasis Panel ()
Project Start
Project End
Budget Start
2013-09-01
Budget End
2014-08-31
Support Year
1
Fiscal Year
2014
Total Cost
$123,317
Indirect Cost
$46,244
Name
Columbia University
Department
Type
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Symington, Lorraine S (2016) Mechanism and regulation of DNA end resection in eukaryotes. Crit Rev Biochem Mol Biol 51:195-212
Yamamoto, Kenta; Wang, Jiguang; Sprinzen, Lisa et al. (2016) Kinase-dead ATM protein is highly oncogenic and can be preferentially targeted by Topo-isomerase I inhibitors. Elife 5:
Oh, Julyun; Al-Zain, Amr; Cannavo, Elda et al. (2016) Xrs2 Dependent and Independent Functions of the Mre11-Rad50 Complex. Mol Cell 64:405-415
Aparicio, Tomas; Baer, Richard; Gottesman, Max et al. (2016) MRN, CtIP, and BRCA1 mediate repair of topoisomerase II-DNA adducts. J Cell Biol 212:399-408
Reczek, Colleen R; Shakya, Reena; Miteva, Yana et al. (2016) The DNA resection protein CtIP promotes mammary tumorigenesis. Oncotarget 7:32172-83
Deng, Sarah K; Chen, Huan; Symington, Lorraine S (2015) Replication protein A prevents promiscuous annealing between short sequence homologies: Implications for genome integrity. Bioessays 37:305-13
Yamamoto, K; Lee, B J; Li, C et al. (2015) Early B-cell-specific inactivation of ATM synergizes with ectopic CyclinD1 expression to promote pre-germinal center B-cell lymphomas in mice. Leukemia 29:1414-24
Chen, Huan; Donnianni, Roberto A; Handa, Naofumi et al. (2015) Sae2 promotes DNA damage resistance by removing the Mre11-Rad50-Xrs2 complex from DNA and attenuating Rad53 signaling. Proc Natl Acad Sci U S A 112:E1880-7
Deng, Sarah K; Yin, Yi; Petes, Thomas D et al. (2015) Mre11-Sae2 and RPA Collaborate to Prevent Palindromic Gene Amplification. Mol Cell 60:500-8
Sato, Mai; Rodriguez-Barrueco, Ruth; Yu, Jiyang et al. (2015) MYC is a critical target of FBXW7. Oncotarget 6:3292-305

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