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Baldassarri S.R.,Yale University | Toll B.A.,Medical University of South Carolina | Toll B.A.,Hollings Cancer Center | Toll B.A.,Yale University | Leone F.T.,University of Pennsylvania
Journal of Allergy and Clinical Immunology: In Practice | Year: 2015

Tobacco smoking remains the leading preventable cause of death and illness in the United States. Smoking cessation is particularly relevant for individuals with chronic obstructive pulmonary disease because it is known from multiple studies that individuals who quit smoking experience an initial improvement in pulmonary function, a decreased rate of normal age-related decline in FEV1, a lower risk of hospital admission, and improved survival. Tobacco dependence must be recognized as a chronic disease, and comprehensive treatment for the tobacco-dependent patient with chronic obstructive pulmonary disease begins with a physician's inquiry into smoking and encouragement to quit, followed by an assessment of the level of dependence and the severity of withdrawal symptoms during previous quit attempts. Combination pharmacotherapy is recommended for the initial treatment of most smokers, especially those with moderate to high baseline levels of tobacco dependence. The patient's history, combined with his or her personal preference, can guide the clinician in initiating an appropriate treatment regimen. Given the chronic nature of tobacco dependence, clinicians must anticipate relapses and the need for recurrent, long-term follow-up. Comprehensive tobacco treatment consultation should be sought whenever possible for patients with high levels of tobacco dependence and multiple relapses or failed quit attempts. © 2015 American Academy of Allergy, Asthma & Immunology. Source

Wu J.,Medical University of South Carolina | Wu J.,Hollings Cancer Center | Wu J.,University of Washington
OncoImmunology | Year: 2016

ABSTRACT: Human tumor-derived soluble NKG2D sMIC paralyzes the immune system through multiple pathways. Targeting soluble MIC with a nonblocking sMIC-neutralizing anti-MIC antibody effectuated and revamped endogenous innate and adoptive antitumor responses. Therapy induced regression of primary tumors and eliminated metastasis in preclinical models. © 2016, © Taylor & Francis Group, LLC. Source

Addicott M.A.,Duke University | Froeliger B.,Medical University of South Carolina | Froeliger B.,Hollings Cancer Center | Kozink R.V.,Duke University | And 4 more authors.
Neuropsychopharmacology | Year: 2014

Smoking cessation results in withdrawal symptoms such as craving and negative mood that may contribute to lapse and relapse. Little is known regarding whether these symptoms are associated with the nicotine or non-nicotine components of cigarette smoke. Using arterial spin labeling, we measured resting-state cerebral blood flow (CBF) in 29 adult smokers across four conditions: (1) nicotine patch+denicotinized cigarette smoking, (2) nicotine patch+abstinence from smoking, (3) placebo patch+denicotinized cigarette smoking, and (4) placebo patch+abstinence from smoking. We found that changes in self-reported craving positively correlated with changes in CBF from the denicotinized cigarette smoking conditions to the abstinent conditions. These correlations were found in several regions throughout the brain. Self-reported craving also increased from the nicotine to the placebo conditions, but had a minimal relationship with changes in CBF. The results of this study suggest that the non-nicotine components of cigarette smoke significantly impact withdrawal symptoms and associated brain areas, independently of the effects of nicotine. As such, the effects of non-nicotine factors are important to consider in the design and development of smoking cessation interventions and tobacco regulation. © 2014 American College of Neuropsychopharmacology. All rights reserved. Source

Zhang J.,Medical University of South Carolina | Basher F.,Medical University of South Carolina | Wu J.D.,Medical University of South Carolina | Wu J.D.,Hollings Cancer Center
Frontiers in Immunology | Year: 2015

The activating/co-stimulatory receptor NKG2D (natural-killer group 2, member D) is expressed on the surface of all human NK, NKT, CD8+ T, and subsets of γδ+ T cells. The significance of NKG2D function in tumor immunity has been well demonstrated in experimental animal models. However, the role of human NKG2D ligands in regulating tumor immunity and cancer prognosis had been controversial in the literature. In this review, we summarize the latest advancement, discuss the controversies, and present evidence that membrane-bound and soluble NKG2D ligands oppositely regulate tumor immunity. We also discuss new perspectives of targeting NKG2D ligands for cancer immunotherapy. © 2015 Zhang, Basher and Wu. Source

Meyers-Needham M.,Medical University of South Carolina | Ponnusamy S.,Medical University of South Carolina | Gencer S.,Medical University of South Carolina | Jiang W.,Medical University of South Carolina | And 4 more authors.
EMBO Molecular Medicine | Year: 2012

Histone deacetylases (HDACs) and microRNAs (miRs) have pro-survival roles, but the mechanism behind this is unclear. Repression of ceramide synthase 1 (CerS1), altering C 18-ceramide generation, was linked to drug resistance and metastasis. Here we report that the CerS1 promoter was repressed by HDAC1-dependent inhibition of Sp1 recruitment to two specific GC-boxes spanning the -177 and -139 region. Moreover, an alternatively spliced variant CerS1 mRNA (CerS1-2) was detected mainly in cancer cells or primary tumour tissues compared to controls, which was targeted by miR-574-5p for degradation. A specific 3′UTR-targeting site, localized within the retained intron between exons 6 and 7, was identified, and its mutation, or miR-574-5p knockdown prevented the degradation of CerS1-2 mRNA. Interference with HDAC1 and miR-574-5p reconstituted CerS1-2 expression and C 18-ceramide generation in multiple human cancer cell lines, which subsequently inhibited proliferation and anchorage-independent growth. Accordingly, knockdown of CerS1 partially protected cancer cells from MS-275/miR-574-5p siRNA-mediated growth inhibition. Thus, these data suggest that the HDAC1/miR-574-5p axis might provide a novel therapeutic target to reconstitute tumour suppressor CerS1/ceramide signalling. © 2012 EMBO Molecular Medicine. Source

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