Suboxone Pharma Foibles/FDA Does Its Job Well.

Suboxone Pharma Foibles/FDA Does Its Job Well.

R I Med J (2013). 2013; 96(4): 13
Gordon A, Kretzschmar A, Gilbert E

HubMed – addiction


Pyrvinium targets autophagy addiction to promote cancer cell death.

Cell Death Dis. 2013; 4: e614
Deng L, Lei Y, Liu R, Li J, Yuan K, Li Y, Chen Y, Liu Y, Lu Y, Edwards Iii CK, Huang C, Wei Y

Autophagy is a cellular catabolic process by which long-lived proteins and damaged organelles are degradated by lysosomes. Activation of autophagy is an important survival mechanism that protects cancer cells from various stresses, including anticancer agents. Recent studies indicate that pyrvinium pamoate, an FDA-approved antihelminthic drug, exhibits wide-ranging anticancer activity. Here we demonstrate that pyrvinium inhibits autophagy both in vitro and in vivo. We further demonstrate that the inhibition of autophagy is mammalian target of rapamycin independent but depends on the transcriptional inhibition of autophagy genes. Moreover, the combination of pyrvinium with autophagy stimuli improves its toxicity against cancer cells, and pretreatment of cells with 3-MA or siBeclin1 partially protects cells from pyrvinium-induced cell death under glucose starvation, suggesting that targeted autophagy addiction is involved in pyrvinium-mediated cytotoxicity. Finally, in vivo studies show that the combination therapy of pyrvinium with the anticancer and autophagy stimulus agent, 2-deoxy-D-glucose (2-DG), is significantly more effective in inhibiting tumor growth than pyrvinium or 2-DG alone. This study supports a novel cancer therapeutic strategy based on targeting autophagy addiction and implicates using pyrvinium as an autophagy inhibitor in combination with chemotherapeutic agents to improve their therapeutic efficacy. HubMed – addiction


Cigarette Smoking Among Asian American and Pacific Islander College Students: Implications for College Health Promotion.

Health Promot Pract. 2013 May 2;
Romero DR, Pulvers K

Asian Americans (AA) and Pacific Islanders (PI) are an understudied population for health and tobacco use, which is alarming for a fast growing U.S. population. Research in smoking among AA and PI college students is limited, despite 50% of AA and 20% of PI having obtained a college degree. A cross-sectional tobacco survey was administered in a large racially diverse Southern California university (N = 490) that examined smoking behavior, psychosocial, and perceptual factors related to smoking among AA and PI compared with Caucasians. Overall, 19% of participants were smokers. The prevalence of current smoking by race was 26% PI, 19% AA, and 17% Caucasian. AA and PI are light, infrequent smokers who smoke mainly for social reasons and in social locations. Most AA and PI made quit attempts and reported intention to quit smoking. Low to moderate risk perceptions for addiction, disease and difficulty in quitting were observed. Social norms center on family influences, therefore it is recommended that cessation approaches target cigarette smoking norms within this social environment to increase perceptual risks of smoking. Smoking cessation should be placed in college health outreach programs based on culturally tailored approaches for AA and PI that target their unique smoking characteristics. HubMed – addiction


MEK1/2 inhibition decreases lactate in BRAF-driven human cancer cells.

Cancer Res. 2013 May 2;
Falck Miniotis M, Arunan V, Eykyn TR, Marais R, Workman P, Leach MO, Beloueche-Babari M

The RAS-BRAF-MEK-ERK signaling pathway is a central driver in cancer with many BRAF and MEK inhibitors being evaluated in clinical trials. Identifying non-invasive biomarkers of early pharmacodynamic (PD) responses is important for development of these targeted drugs. Since increased aerobic glycolysis is often observed in cancer, we hypothesized that MEK1/2 (MAP2K1/MAP2K2) inhibitors may reduce lactate levels as detected by magnetic resonance spectroscopy (MRS), as a metabolic biomarker for the PD response. MRS was used to monitor intracellular and extracellular levels of lactate in human cancer cells in vitro and in melanoma tumors ex vivo. Additionally, we used 1H MRS and a fluorescent glucose analogue to evaluate the effect of MEK inhibition on glucose uptake. MEK1/2 signaling inhibition reduced extracellular lactate levels in BRAF-dependent cells but not BRAF-independent cells. The reduction in extracellular lactate in BRAF-driven melanoma cells was time-dependent and associated with reduced expression of hexokinase-II driven by c-Myc depletion. Taken together, these results reveal how MEK1/2 inhibition affects cancer cell metabolism in the context of BRAF oncogene addiction. Further, they offer a preclinical proof of concept for the use of MRS to measure lactate as a non-invasive metabolic biomarker for PD response to MEK1/2 inhibition in BRAF-driven cancers. HubMed – addiction



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