Putting pain out of mind with an 'out of body' illusion.

BACKGROUND: Chronic pain is a growing societal concern that warrants scientific investigation, especially given the ineffectiveness of many treatments. Given evidence that pain experience relies on multisensory integration, there is interest in using body ownership illusions for reducing acute pain. AIM: In the present study, we investigate whether patients' experience of chronic pain could be reduced by full body illusions (FBIs) that cause participants to dissociate from their own body. METHODS: Participants with chronic pain (including sciatica, osteoarthritis, fibromyalgia, muscular pain, IBS and back pain) viewed their own 'virtual' bodies via a video camera and head-mounted display for two minutes. In the 'back-stroking FBI', their backs were stroked with a stick while they viewed synchronous or asynchronous stroking on the virtual body and in the 'front-stroking FBI', they were stroked near their collarbone while viewing the stick approach their field of view in a synchronous or asynchronous fashion. Illusion strength and pain intensity were measured with self-report questionnaires. RESULTS: We found that full body illusions were experienced by patients with chronic pain and further, that pain intensity was reduced by an average of 37% after illusion (synchronous) conditions. CONCLUSION: These findings add support to theories that high-level multisensory body representations can interact with homeostatic regulation and pain perception. SIGNIFICANCE: Pain intensity in chronic pain patients was reduced by 37% by 'out of body' illusions. These data demonstrate the potential of such illusions for the management of chronic pain.

Enhanced epidermal growth factor receptor signaling in MCF7 breast cancer cells after long-term culture in the presence of the pure antiestrogen ICI 182,780 (Faslodex).

This paper describes the establishment of an antiestrogen-resistant MCF7 breast cancer cell subline (FASMCF) by continuous culture of the estrogen-responsive parental line in steroid-depleted, ICI 182,780 (Faslodex; 10(-7) M)-supplemented medium. After a 3-month period of growth suppression, cells began to proliferate in ICI 182,780 at rates similar to those of untreated wild-type cells. Immunocytochemistry showed these cells to have reduced estrogen receptor and an absence of progesterone receptor proteins. RT-PCR and transient transfection studies with estrogen response element-reporter constructs confirmed that ICI 182,780-suppressed estrogen response element-mediated signaling. FASMCF cells show increased dependence upon epidermal growth factor receptor (EgfR)/mitogen-activated protein kinase (MAPK)-mediated signaling. Thus, EgfR protein and messenger RNA, growth responses to transforming growth factor-alpha, and extracellular signal-regulated kinase 1/2 MAPK activation levels are all increased. Unlike wild-type cells, FASMCF cells are highly sensitive to growth inhibition by an EgfR-specific tyrosine-kinase inhibitor (TKI), ZD1839 (Iressa), and an inhibitor of the activation of MEK1 (MAPKK), PD098059. Short-term ( approximately 3 weeks) withdrawal of cells from antiestrogen had no effect on growth or phenotype, whereas longer withdrawal (>10 weeks) appeared to partially reverse the cellular phenotype with increasing estrogen receptor and decreasing EgfR levels. In subsequent studies FASMCF cells were maintained in TKI, where their growth was again suppressed and secondary TKI resistance failed to develop within the 3-month period in which initial ICI 182,780 resistance arose. Furthermore, wild-type cells similarly maintained in combination ICI 182,780 and TKI treatment conditions remained growth arrested (>6 months), with notable cell loss through both reduced rates of cellular proliferation and increased cell death.