Mark O Lively

Wake Forest School of Medicine, Winston-Salem, North Carolina, United States

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Publications (4)10.32 Total impact

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    ABSTRACT: Tumor associated macrophages (TAMS) have been suggested to be key players in the tumor microenvironment. The M2 activation phenotype is believed to be the predominant TAM phenotype in solid tumors. To further define the role of M2 TAMs and analyze the cross-talk between tumor cells and TAMs, we examined the presence of macrophage markers in glioblastoma (GBM) tumors, their responses to various treatments, the genetic profile of M2 macrophages and also potential mediators of tumor cells communication with TAMs.
    Neuro-oncology. 07/2014; 16 Suppl 3:iii40-iii41.
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    ABSTRACT: WHO grade II low-grade gliomas (LGGs) with high risk factors for recurrence are mostly lethal despite current treatments, and novel approaches are needed. We conducted a phase I study to evaluate the safety and immunogenicity of subcutaneous vaccinations with synthetic peptides for glioma-associated antigen (GAA) epitopes in human leukocyte antigen (HLA)-A2+ adults with high-risk LGGs in the following three cohorts: 1) newly diagnosed patients without prior radiation therapy (RT); 2) newly diagnosed patients with prior RT, and 3) recurrent patients.
    Neuro-Oncology 07/2014; 16 Suppl 3:iii39. · 5.29 Impact Factor
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    ABSTRACT: EphrinA1 is a glycosylphosphatidylinositol (GPI)-linked ligand for the EphA2 receptor, which is overexpressed in glioblastoma (GBM), among other cancers. Activation of the receptor by ephrinA1 leads to a suppression of oncogenic properties of GBM cells. We documented that a monomeric functional form of ephrinA1 is released from cancer cells and thus explored the mechanism of ephrinA1 release and the primary protein sequence. We demonstrate here that multiple metalloproteases (MMPs) are able to cleave ephrinA1, most notably MMP-1, -2, -9, and -13. The proteolytic cleavage that releases ephrinA1 occurs at three positions near the C terminus, producing three forms ending in valine-175, histidine-177, or serine-178. Moreover, deletion of amino acids 174 to 181 or 175 to 181 yields ephrinA1 that is still GPI linked but not released by proteolysis, underlining the necessity of amino acids 175 to 181 for release from the membrane. Furthermore, recombinant ephrinA1 ending at residue 175 retains activity toward the EphA2 receptor. These findings suggest a mechanism of release and provide evidence for the existence of several forms of monomeric ephrinA1. Moreover, ephrinA1 should be truncated at a minimum at amino acid 175 in fusions or conjugates with other molecules in order to prevent likely proteolysis within physiological and pathobiological environments.
    Molecular and Cellular Biology 06/2012; 32(16):3253-64. · 5.04 Impact Factor
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    ABSTRACT: BACKGROUND: Coenzyme Q(10) (CoQ(10)) is a common antioxidant supplement with known cardioprotective effects and potential anticancer benefits. OBJECTIVES: We performed a randomized, double-blind, placebo-controlled study of oral CoQ(10) in female breast cancer patients with the primary objective of determining CoQ(10)'s effects on self-reported fatigue, depression, and quality of life (QOL). METHODS: Eligible women with newly diagnosed breast cancer and planned adjuvant chemotherapy were randomized to oral supplements of 300 mg CoQ(10) or placebo, each combined with 300 IU vitamin E, divided into 3 daily doses. Treatment was continued for 24 weeks. Blood tests, QOL measures, and levels of plasma CoQ(10) and vitamin E were obtained at baseline and at 8, 16, and 24 weeks. Mixed-effects models were used to assess treatment differences in outcomes over time. RESULTS: Between September 2004 and March 2009, 236 women were enrolled. Treatment arms were well balanced with respect to age (range, 28-85 years), pathologic stage (stage 0, 91%; stage I, 8%; stage II, 1%), ethnicity (white, 87%; black, 11%; Hispanic, 2%), and planned therapy. Baseline CoQ(10) levels in the CoQ(10) and placebo arms were 0.70 and 0.73 μg/mL, respectively; the 24-week CoQ(10) levels were 1.83 and 0.79 μg/mL, respectively. There were no significant differences between the CoQ(10) and placebo arms at 24 weeks for scores on the Profile of Mood States-Fatigue questionnaire (least squares means, 7.08 vs 8.24, P = .257), the Functional Assessment of Chronic Illness Therapy-Fatigue tool (37.6 vs 37.6, P = .965), the Functional Assessment of Cancer Therapy-Breast Cancer instrument (111.9 vs 110.4, P = .577), or the Center for Epidemiologic Studies-Depression scale (11.6 vs 12.3, P = .632). CONCLUSIONS: Supplementation with conventional doses of CoQ(10) led to sustained increases in plasma CoQ(10) levels but did not result in improved self-reported fatigue or QOL after 24 weeks of treatment.
    The journal of supportive oncology 06/2012;