The Biostatistics and Bioinformatics Core B will provide statistics and bioinformatics support and expertise in experimental design, data analysis and interpretation ofthe results as needed by the Projects and other Cores to achieve their Specific Aims. The studies in this POl require a variety of statistical and bioinformatic data analysis strategies such as modeling time course experiment data, tesfing synergisfic effect of kinase inhibitor combination, and analyzing genomic profiling data of RNA expression and DNA copy number. In addition. Core B will develop and maintain a bioinformatics infrastructure to enable collaboration and data sharing among research projects. This infrastructure includes: 1) a gene signature database 2) a somafic mutation database and functional characterization tools, and 3) a virtual cell line repository. A broad range of bioinformatics, computational, and statistical techniques will be applied to create this infrastructure.

Public Health Relevance

The Biostatistics and Bioinformatics Core B forms an integral part ofthe P01 and will provide services that are essential for many of the different projects within the POl, assisting the POl investigators in their achievement of the overall research objective: developing new targets for therapy for carcinomas of the lung.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
2P01CA129243-06
Application #
8393595
Study Section
Special Emphasis Panel (ZCA1-RPRB-J (M1))
Project Start
2007-07-23
Project End
2017-08-31
Budget Start
2012-09-12
Budget End
2013-08-31
Support Year
6
Fiscal Year
2012
Total Cost
$143,832
Indirect Cost
$51,979
Name
Sloan-Kettering Institute for Cancer Research
Department
Type
DUNS #
064931884
City
New York
State
NY
Country
United States
Zip Code
10065
Yu, Helena A; Perez, Leslie; Chang, Qing et al. (2017) A Phase 1/2 Trial of Ruxolitinib and Erlotinib in Patients with EGFR-Mutant Lung Adenocarcinomas with Acquired Resistance to Erlotinib. J Thorac Oncol 12:102-109
Ichihara, Eiki; Westover, David; Meador, Catherine B et al. (2017) SFK/FAK Signaling Attenuates Osimertinib Efficacy in Both Drug-Sensitive and Drug-Resistant Models of EGFR-Mutant Lung Cancer. Cancer Res 77:2990-3000
Yaeger, Rona; Yao, Zhan; Hyman, David M et al. (2017) Mechanisms of Acquired Resistance to BRAF V600E Inhibition in Colon Cancers Converge on RAF Dimerization and Are Sensitive to Its Inhibition. Cancer Res 77:6513-6523
Weigelt, Britta; Comino-Méndez, Iñaki; de Bruijn, Ino et al. (2017) Diverse BRCA1 and BRCA2 Reversion Mutations in Circulating Cell-Free DNA of Therapy-Resistant Breast or Ovarian Cancer. Clin Cancer Res 23:6708-6720
Pal, Debjani; Pertot, Anja; Shirole, Nitin H et al. (2017) TGF-? reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24- cancer cells. Elife 6:
Yu, H A; Sima, C; Feldman, D et al. (2017) Phase 1 study of twice weekly pulse dose and daily low-dose erlotinib as initial treatment for patients with EGFR-mutant lung cancers. Ann Oncol 28:278-284
Boire, Adrienne; Zou, Yilong; Shieh, Jason et al. (2017) Complement Component 3 Adapts the Cerebrospinal Fluid for Leptomeningeal Metastasis. Cell 168:1101-1113.e13
Nieto, Patricia; Ambrogio, Chiara; Esteban-Burgos, Laura et al. (2017) A Braf kinase-inactive mutant induces lung adenocarcinoma. Nature 548:239-243
Yao, Zhan; Yaeger, Rona; Rodrik-Outmezguine, Vanessa S et al. (2017) Tumours with class 3 BRAF mutants are sensitive to the inhibition of activated RAS. Nature 548:234-238
Drilon, Alexander; Somwar, Romel; Wagner, Jacob P et al. (2016) A Novel Crizotinib-Resistant Solvent-Front Mutation Responsive to Cabozantinib Therapy in a Patient with ROS1-Rearranged Lung Cancer. Clin Cancer Res 22:2351-8

Showing the most recent 10 out of 168 publications