The principal objective of the Biostatistics Core will be to provide project investigators a centralized resource for biostatistics expertise. Statistical issues will be addressed at all levels of investigation: from the design of clinically based studies and laboratory experiments, to the maintenance of data quality;and from conclusions based on formal hypothesis testing, to important leads discovered by thorough data exploration. In support of this objective, the specific aims of the Core include: 1. Design: collaborate with project investigators in the design of laboratory experiments and clinical studies and the formulation of unambiguous hypotheses and hypothesis testing strategies. 2. Analysis: provide support for formal hypothesis tests in clinical and experimental data that ensure strong conclusions;statistical modeling and sensitivity analyses of prospective and retrospective studies; exploratory analyses that lead to further studies and experiments;and visual displays of data that clarify conclusions and uncover leads. 3. Data Quality Assurance: manage data and coordinate services with the Clinical Core A to ensure high quality, security and investigator accessibility for all clinical and experimental data. 4. Methods Research: Investigate new methodologies to directly address difficult data or design problems.
The Biostatistics Core will provide critical support for planning and design of experiments and clinically based studies, statistical analyses and display of data, and data management and integrity. This support is designed to ensure that studies yield reliable conclusions, resources are efficiently used, and exploratory analyses uncover important leads.
|Mahdi, Haider; Mester, Jessica L; Nizialek, Emily A et al. (2015) Germline PTEN, SDHB-D, and KLLN alterations in endometrial cancer patients with Cowden and Cowden-like syndromes: an international, multicenter, prospective study. Cancer 121:688-96|
|Lakshmanan, Aparna; Doseff, Andrea I; Ringel, Matthew D et al. (2014) Apigenin in combination with Akt inhibition significantly enhances thyrotropin-stimulated radioiodide accumulation in thyroid cells. Thyroid 24:878-87|
|Wójcicka, Anna; Czetwerty?ska, Ma?gorzata; ?wierniak, Micha? et al. (2014) Variants in the ATM-CHEK2-BRCA1 axis determine genetic predisposition and clinical presentation of papillary thyroid carcinoma. Genes Chromosomes Cancer 53:516-23|
|Pringle, Daphne R; Vasko, Vasily V; Yu, Lianbo et al. (2014) Follicular thyroid cancers demonstrate dual activation of PKA and mTOR as modeled by thyroid-specific deletion of Prkar1a and Pten in mice. J Clin Endocrinol Metab 99:E804-12|
|McCarty, Samantha K; Saji, Motoyasu; Zhang, Xiaoli et al. (2014) BRAF activates and physically interacts with PAK to regulate cell motility. Endocr Relat Cancer 21:865-77|
|Lakshmanan, Aparna; Scarberry, Daniel; Shen, Daniel H et al. (2014) Modulation of sodium iodide symporter in thyroid cancer. Horm Cancer 5:363-73|
|Wojcicka, A; de la Chapelle, A; Jazdzewski, K (2014) MicroRNA-related sequence variations in human cancers. Hum Genet 133:463-9|
|Stechschulte, Lance A; Wuescher, Leah; Marino, Joseph S et al. (2014) Glucocorticoid receptor ? stimulates Akt1 growth pathway by attenuation of PTEN. J Biol Chem 289:17885-94|
|Ngeow, Joanne; Stanuch, Kim; Mester, Jessica L et al. (2014) Second malignant neoplasms in patients with Cowden syndrome with underlying germline PTEN mutations. J Clin Oncol 32:1818-24|
|Medici, Marco; Porcu, Eleonora; Pistis, Giorgio et al. (2014) Identification of novel genetic Loci associated with thyroid peroxidase antibodies and clinical thyroid disease. PLoS Genet 10:e1004123|
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