According to the recent Institute of Medicine (IOM) report on Relieving Pain in America (2011), chronic pain is a public health epidemic affecting more than 116 million Americans and costing more than $600 billion per year in healthcare expenses and lost work productivity. More Americans suffer from pain than those afflicted with heart disease, diabetes and cancer combined. Despite recent advances in treatment, most people do not obtain adequate pain relief. An important focus has been on understanding the basic biology of chronic pain, so that new mechanistically based therapeutics can be developed. Unfortunately, standard research and development pipelines that start at the bench with several hundred known signaling pathways have not yielded many new targets in pain research. In a recent commentary, the NIH Director Francis Collins argued that these failures may be due to the feed-forward translational continuum from bench to beside that relies on biologically well-understood pathways. The result, in terms of drug development, is prolonged time to clinic, high failure rates and exorbitant cost. In this era of """"""""omics"""""""" research, studies that incorporate geneti and genomic data may yield thousands of new, potentially druggable targets. The purpose of this Center for the Genomics of Pain is to combine rigorous phenotyping of pain and comorbid conditions with cutting edge genomics to more fully understand how individual differences can reduce or amplify pain. The Center's conceptual framework, adapted from Dr. William Maixner's model, incorporates comorbid pain conditions (intermediate risk factors), epigenetics, genomics, environment and gender to explain pain phenotypes. For the first time on the University of Maryland Baltimore Campus, geneticists, genomicists and pain researchers will combine their expertise to identify critical new therapeutic targets that can be exploited to reduce or eliminate chronic pain.
Chronic pain has no biological purpose, and can last for years. Unlike acute pain, which can be treated with conventional pain medicines, chronic pain is very difficult to treat and many patients do not obtain adequate pain relief. The formation of this new Center will combine cutting edge pain research with genomics so that new information about chronic pain may be used to develop better pain medicine.
|Marmiroli, Paola; Riva, Beatrice; Pozzi, Eleonora et al. (2017) Susceptibility of different mouse strains to oxaliplatin peripheral neurotoxicity: Phenotypic and genotypic insights. PLoS One 12:e0186250|
|Griffith, Kathleen A; Zhu, Shijun; Johantgen, Meg et al. (2017) Oxaliplatin-Induced Peripheral Neuropathy and Identification of Unique Severity Groups in Colorectal Cancer. J Pain Symptom Manage 54:701-706.e1|
|Starkweather, Angela R; Heineman, Amy; Storey, Shannon et al. (2016) Methods to measure peripheral and central sensitization using quantitative sensory testing: A focus on individuals with low back pain. Appl Nurs Res 29:237-41|
|Moore, Shirley M; Schiffman, Rachel; Waldrop-Valverde, Drenna et al. (2016) Recommendations of Common Data Elements to Advance the Science of Self-Management of Chronic Conditions. J Nurs Scholarsh 48:437-47|
|Wu, Junfang; Zhao, Zaorui; Zhu, Xiya et al. (2016) Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury. Pain 157:488-503|
|Starkweather, Angela R; Lyon, Debra E; Kinser, Patricia et al. (2016) Comparison of Low Back Pain Recovery and Persistence: A Descriptive Study of Characteristics at Pain Onset. Biol Res Nurs 18:401-10|
|Resnick, Barbara; Klinedinst, N Jennifer; Yerges-Armstrong, Laura et al. (2016) Pain, Genes, and Function in the Post-Hip Fracture Period. Pain Manag Nurs 17:181-96|
|Wu, Junfang; Zhao, Zaorui; Kumar, Alok et al. (2016) Endoplasmic Reticulum Stress and Disrupted Neurogenesis in the Brain Are Associated with Cognitive Impairment and Depressive-Like Behavior after Spinal Cord Injury. J Neurotrauma 33:1919-1935|
|Starkweather, Angela R; Ramesh, Divya; Lyon, Debra E et al. (2016) Acute Low Back Pain: Differential Somatosensory Function and Gene Expression Compared With Healthy No-Pain Controls. Clin J Pain 32:933-939|
|Hertz, Daniel L; Owzar, Kouros; Lessans, Sherrie et al. (2016) Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy. Clin Cancer Res 22:4890-4900|
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