Informatics Core C (Informatics/Biostatistics) The specialized research of the SPORE involves translational research integrating laboratory and clinical studies, interdisciplinary research, inter- project collaboration, and use of specialized resources like the Pathology and Tissue Resource by the projects. These endeavors require biostatistical experience, a facile means of communication, and the ability to share, analyze, and rigorously audit data, particularly clinical data. The Informatics Core was thus devised as a central and essential specialized resource that would be used by all the established and developmental projects of the SPORE as well as in its career development program to meet these needs. The collaborative interaction of UTSW and UTMDA in creating the University of Texas Lung Cancer SPORE makes the Informatics Core of even greater importance to facilitate inter-institutional integration. The purposes of the Informatics Core are as follows: l) To provide the statistical analysis required to achieve the specific aims of each project. 2) To assist in the design and analysis of new research arising from individual projects. 3) To facilitate electronic communication including the sharing of data and results between projects, cores and investigators and thus promote interdisciplinary, inter-project, and inter-institutional integration and collaboration. 4) To supervise and coordinate the collection, entry, and maintenance of data required for each project. 5) To provide for rigorous data management, quality assurance, auditing procedures, and confidentiality of clinical trials data. 6) To coordinate the data acquisition and biostatistical analysis and audit planning for the Internal Data Monitoring Committee. 7) To provide the above informatics support for the Developmental

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
2P50CA070907-04
Application #
6198706
Study Section
Project Start
1999-09-08
Project End
2000-08-31
Budget Start
Budget End
Support Year
4
Fiscal Year
1999
Total Cost
Indirect Cost
City
Dallas
State
TX
Country
United States
Zip Code
75390
Song, Kai; Bi, Jia-Hao; Qiu, Zhe-Wei et al. (2018) A quantitative method for assessing smoke associated molecular damage in lung cancers. Transl Lung Cancer Res 7:439-449
Ji, Xuemei; Bossé, Yohan; Landi, Maria Teresa et al. (2018) Identification of susceptibility pathways for the role of chromosome 15q25.1 in modifying lung cancer risk. Nat Commun 9:3221
He, Min; Liu, Shanshan; Gallolu Kankanamalage, Sachith et al. (2018) The Epithelial Sodium Channel (?ENaC) Is a Downstream Therapeutic Target of ASCL1 in Pulmonary Neuroendocrine Tumors. Transl Oncol 11:292-299
Parra, Edwin R; Villalobos, Pamela; Behrens, Carmen et al. (2018) Effect of neoadjuvant chemotherapy on the immune microenvironment in non-small cell lung carcinomas as determined by multiplex immunofluorescence and image analysis approaches. J Immunother Cancer 6:48
Guo, Hou-Fu; Tsai, Chi-Lin; Terajima, Masahiko et al. (2018) Pro-metastatic collagen lysyl hydroxylase dimer assemblies stabilized by Fe2+-binding. Nat Commun 9:512
Meraz, Ismail M; Majidi, Mourad; Cao, Xiaobo et al. (2018) TUSC2 Immunogene Therapy Synergizes with Anti-PD-1 through Enhanced Proliferation and Infiltration of Natural Killer Cells in Syngeneic Kras-Mutant Mouse Lung Cancer Models. Cancer Immunol Res 6:163-177
Zhang, Liren; Lin, Jing; Ye, Yuanqing et al. (2018) Serum MicroRNA-150 Predicts Prognosis for Early-Stage Non-Small Cell Lung Cancer and Promotes Tumor Cell Proliferation by Targeting Tumor Suppressor Gene SRCIN1. Clin Pharmacol Ther 103:1061-1073
Bayo, Juan; Tran, Tram Anh; Wang, Lei et al. (2018) Jumonji Inhibitors Overcome Radioresistance in Cancer through Changes in H3K4 Methylation at Double-Strand Breaks. Cell Rep 25:1040-1050.e5
Ludlow, Andrew T; Wong, Mandy Sze; Robin, Jerome D et al. (2018) NOVA1 regulates hTERT splicing and cell growth in non-small cell lung cancer. Nat Commun 9:3112
Chen, Limo; Diao, Lixia; Yang, Yongbin et al. (2018) CD38-Mediated Immunosuppression as a Mechanism of Tumor Cell Escape from PD-1/PD-L1 Blockade. Cancer Discov 8:1156-1175

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