The Use of CyberKnife Stereotactic Body Radiation Therapy in Treating Hepatocellular Carcinoma

Radiation therapy is an ever-changing field, making it easier and safer to treat a broader range of cancers. With the advancement of the CyberKnife System, we can now investigate how effective stereotactic body radiation therapy (SBRT) treatments are in terms of treating hepatocellular carcinoma (HCC) patients. HCC is the most common liver cancer as well as one of the most prominent cancer-related deaths in the world. Several studies indicated that, previously, treating HCC with ionizing radiation was not an effective option due to the liver’s sensitivity to radiation, among other factors. After conducting research and examining nine different sources, there seems to be a common theme with patients who have started treatment with CyberKnife SBRT. Studies show a high percentage of in-field recurrence free rates after one and two years, as well as encouraging overall survival rates. In some studies, results also showed higher local control rates and lower toxicity reaction rates. CyberKnife SBRT can be used to treat patientshttps://digitalcommons.misericordia.edu/research_posters2020/1068/thumbnail.jp

Nicotine exploits a COPI-mediated process for chaperone-mediated up-regulation of its receptors

Chronic exposure to nicotine up-regulates high sensitivity nicotinic acetylcholine receptors (nAChRs) in the brain. This up-regulation partially underlies addiction and may also contribute to protection against Parkinson’s disease. nAChRs containing the α6 subunit (α6* nAChRs) are expressed in neurons in several brain regions, but comparatively little is known about the effect of chronic nicotine on these nAChRs. We report here that nicotine up-regulates α6* nAChRs in several mouse brain regions (substantia nigra pars compacta, ventral tegmental area, medial habenula, and superior colliculus) and in neuroblastoma 2a cells. We present evidence that a coat protein complex I (COPI)-mediated process mediates this up-regulation of α6* or α4* nAChRs but does not participate in basal trafficking. We show that α6β2β3 nAChR up-regulation is prevented by mutating a putative COPI-binding motif in the β3 subunit or by inhibiting COPI. Similarly, a COPI-dependent process is required for up-regulation of α4β2 nAChRs by chronic nicotine but not for basal trafficking. Mutation of the putative COPI-binding motif or inhibition of COPI also results in reduced normalized Förster resonance energy transfer between α6β2β3 nAChRs and εCOP subunits. The discovery that nicotine exploits a COPI-dependent process to chaperone high sensitivity nAChRs is novel and suggests that this may be a common mechanism in the up-regulation of nAChRs in response to chronic nicotine