The Tissue Biorepository Core has and continues to restructure itself as the most recently added Core Facility of the Center for Colon Cancer Research. It is an IRB-approved biorepository that collects and banks excess surgical specimens. Over the past few years we have initiated and modified protocols for collecting, storing, and distribufing tissue samples and relevant de-identified clinical data to researchers. As such we have been instrumental in the development of a number of research programs that otherwise would not have been feasible without the contributions of the Biorepository. The objective of the Biorepository is to facilitate cancer research, particularly in colon cancer, by providing high quality normal and tumor-derived human tissue along with robust de-identified clinical data to researchers. Our overall long-term goal is to establish this core as a fully functional, efficient and sustainable facility that can confine to efficiently provide high quality de-identified tissue samples and biospecimens to researchers. The CCCR Biorepository is also in an excellent position to contribute important and novel biospecimens to the research community derived from racial/ethnic and underserved populations. Compared to most other states in the US, South Carolina (SC) has a rather large African-American population (31% of the total) living predominantly in rural areas of the state. The demographics of the patient population in SC allow us to develop an inventory of biospecimens that will enable researchers to begin to dissect cancer disparities, one of the major goals of the NCI's 2007 Strategic Plan for Leading the Nation to Eliminate the Suffering and Death Due to Cancer.
The CCCR Biorepository has been operational since 2003 and is an important new Core Facility for the CCCR. The use of human specimens from donor matched sets, combined with information of clinical status and outcome, can provide both genetic and population-based information that will be critical for diagnostics, prognostics and therapeutics as well as the understanding of underlying mechanisms that lead to cancer.
|Oliver, David; Ji, Hao; Liu, Piaomu et al. (2017) Identification of novel cancer therapeutic targets using a designed and pooled shRNA library screen. Sci Rep 7:43023|
|Farmaki, Elena; Kaza, Vimala; Papavassiliou, Athanasios G et al. (2017) Induction of the MCP chemokine cluster cascade in the periphery by cancer cell-derived Ccl3. Cancer Lett 389:49-58|
|Brown, Jacob L; Rosa-Caldwell, Megan E; Lee, David E et al. (2017) Mitochondrial degeneration precedes the development of muscle atrophy in progression of cancer cachexia in tumour-bearing mice. J Cachexia Sarcopenia Muscle 8:926-938|
|Alexander, M; Burch, J B; Steck, S E et al. (2017) Case-control study of candidate gene methylation and adenomatous polyp formation. Int J Colorectal Dis 32:183-192|
|McDermott, Martina S J; Chumanevich, Alexander A; Lim, Chang-Uk et al. (2017) Inhibition of CDK8 mediator kinase suppresses estrogen dependent transcription and the growth of estrogen receptor positive breast cancer. Oncotarget 8:12558-12575|
|Zhang, Yu; Davis, Celestia; Shah, Sapana et al. (2017) IL-33 promotes growth and liver metastasis of colorectal cancer in mice by remodeling the tumor microenvironment and inducing angiogenesis. Mol Carcinog 56:272-287|
|Chandrashekaran, Varun; Seth, Ratanesh K; Dattaroy, Diptadip et al. (2017) HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease. Redox Biol 13:8-19|
|Farmaki, E; Chatzistamou, I; Kaza, V et al. (2016) A CCL8 gradient drives breast cancer cell dissemination. Oncogene 35:6309-6318|
|Narsale, Aditi A; Puppa, Melissa J; Hardee, Justin P et al. (2016) Short-term pyrrolidine dithiocarbamate administration attenuates cachexia-induced alterations to muscle and liver in ApcMin/+ mice. Oncotarget 7:59482-59502|
|Peña, Edsel A (2016) Asymptotics for a Class of Dynamic Recurrent Event Models. J Nonparametr Stat 28:716-735|
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