Program 1. Cancer Genetics and Epigenetics (CGE): DNA damage, genetic mutations, genomic instability and alterations in DNA/chromatin modifications that modify gene expression are all critical events that contribute to the development of cancers in humans. The primary themes of the CGE Program reflect a major emphasis on basic science investigations directly related to oncogenesis. The CGE Program's four main thematic areas are: (1) DNA damage, repair, mutagenesis and genetic instability;(2) epigenetics, including DNA and chromatin modification and chromatin remodeling;(3) chromosome instability and nuclear architecture;(4) cancer genetics and functional genomics.
The aims of the CGE Program are: (1) To elucidate the underlying molecular and biochemical mechanisms that result in the establishment and maintenance of genetic instability during tumor development and progression. (2) To elucidate and understand how epigenetic modifications of DNA and chromatin structural components impact gene expression programs and other nucleic acid transactions during tumorigenesis. (3) To understand the mechanisms underlying chromosomal aberrations, allelic imbalances and alterations in nuclear architecture and their contributions to multi-step tumorigenesis. (4) To identify and characterize novel oncogenes and tumor suppressor genes and to develop genome-scale discovery and analysis platforms and computational models to identify genetic loci and genetic variants involved in tumorigenesis. The CGE Program is comprised of 26 members from 10 departments within the School of Medicine and Emory College. Currently, there are 24 funded program members with total support of approximately $9 million per year, of which NCI funding represents $3.9M ($2.6M direct). From 2003-2008 the CGE program members published 400 articles. Of these total publications, 39 (9.75%) are intraprogrammatic collaborations and 82 (20.5%) are interprogrammatic collaborations. From 2006-2008, CGE members published 183 articles. Intraprogrammatic collaborations account for 21 (11.5 %) and interprogrammatic collaborations account for 39 (21.3 %) of these publications.
|Xiao, Canhua; Beitler, Jonathan J; Higgins, Kristin A et al. (2018) Differential regulation of NF-kB and IRF target genes as they relate to fatigue in patients with head and neck cancer. Brain Behav Immun 74:291-295|
|Cassidy, Richard J; Zhang, Xinyan; Switchenko, Jeffrey M et al. (2018) Health care disparities among octogenarians and nonagenarians with stage III lung cancer. Cancer 124:775-784|
|Jhaveri, Jaymin; Chowdhary, Mudit; Zhang, Xinyan et al. (2018) Does size matter? Investigating the optimal planning target volume margin for postoperative stereotactic radiosurgery to resected brain metastases. J Neurosurg :1-7|
|Jhaveri, Jaymin; Rayfield, Lael; Liu, Yuan et al. (2018) Impact of intensity modulated radiation therapy on survival in anal cancer. J Gastrointest Oncol 9:618-630|
|Bilen, Mehmet Asim; Dutcher, Giselle Marie Almeida; Liu, Yuan et al. (2018) Association Between Pretreatment Neutrophil-to-Lymphocyte Ratio and Outcome of Patients With Metastatic Renal-Cell Carcinoma Treated With Nivolumab. Clin Genitourin Cancer 16:e563-e575|
|Chowdhary, Mudit; Switchenko, Jeffrey M; Press, Robert H et al. (2018) Post-treatment neutrophil-to-lymphocyte ratio predicts for overall survival in brain metastases treated with stereotactic radiosurgery. J Neurooncol 139:689-697|
|Lin, Songbai; Han, Yiran; Jenkin, Kayte et al. (2018) Lysophosphatidic Acid Receptor 1 Is Important for Intestinal Epithelial Barrier Function and Susceptibility to Colitis. Am J Pathol 188:353-366|
|Morgan, T M; Wang, X; Qian, X et al. (2018) Measurement of circulating tumor cells in squamous cell carcinoma of the head and neck and patient outcomes. Clin Transl Oncol :|
|Bekhbat, Mandakh; Chu, Karen; Le, Ngoc-Anh et al. (2018) Glucose and lipid-related biomarkers and the antidepressant response to infliximab in patients with treatment-resistant depression. Psychoneuroendocrinology 98:222-229|
|Zhu, Dan; Osuka, Satoru; Zhang, Zhaobin et al. (2018) BAI1 Suppresses Medulloblastoma Formation by Protecting p53 from Mdm2-Mediated Degradation. Cancer Cell 33:1004-1016.e5|
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