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Biology subjects

Fulco, C.

Publications and source records attributed to Fulco, C..

2 recordsLinked to original sources

Amphetamine and Nicotine Reduce Sucrose Self-Administration Independent of Sex

Amphetamine and nicotine are two widely used and abused drugs that are taken for legitimate pharmaceutical purposes but are also highly abused through illicit recreational use. Both of these drugs have been widely shown to decrease food intake in both humans and pre-clinical models, and although amphetamine and nicotine clearly affect food intake under normal baseline ( homeostatic) conditions, there has been limited examination of the ability of these drugs to affect reward-related ( hedonic) aspects of feeding. Furthermore, there are sex differences in the behavioral responses to both drugs, but it is unclear if these sex differences also translate to their effects on feeding. This study examined whether nicotine and amphetamine regulate sucrose intake in a food self-administration paradigm in a sex-dependent manner across both fixed and progressive schedules of reinforcement. Amphetamine reduced operant responding for sucrose pellets and decreased acute intake of sucrose during ad libitum free-feeding access in a dose-dependent manner, whereas nicotine reduced sucrose self-administration and free intake only at higher doses that also impaired locomotor activity in open field tests. The effects of both amphetamine and nicotine did not differ by sex for either drug. Overall, these results suggest that the mechanisms mediating the addictive qualities of these drugs and their appetite suppressing effects may be distinct and therefore could be a potential target for future obesity therapeutics.

neuroscience↗

Novel mechanism of MYC deregulation in Multiple Myeloma

MYC deregulation occurs in 67% of multiple myeloma (MM) cases and associates with progression and worse prognosis in MM. Enhanced MYC expression is known to be driven by translocation or amplification events, but it only occurs in 40% of MM patients. Here, we describe a new mechanism of MYC regulation, whereby epigenetic regulation of MYC by increased accessibility of a cell-type specific enhancer leads to increased MYC expression. We found enhancer activity does not associate with enhancer hijacking events. We identified specific binding of c-MAF, IRF4, and SPIB transcription factors to the enhancer can activate MYC. In addition, we discovered focal amplification of this specific enhancer in approximately 4% of MM patients. Together, our findings define a new epigenetic mechanism of MYC deregulation in MM beyond known translocations or amplifications and point to the importance of non-coding regulatory elements and their associated transcription factor networks as drivers of MM progression.

cancer biology↗