RESUMEN
Art is an instrument created by humans as an alternative way of expression. For this reason, it has found its use in clinical contexts to improve mood, increase participation in therapy, or improve communication for patients with different pathologies. In this systematic mini-review, the Preferred Reporting Item for Systematic Reviews and Meta-Analysis (PRISMA) guidelines were adopted. Internet-based bibliographic searches were conducted via major electronic databases (Web of Science and PubMed). We analyzed the quantitative studies in which art figures as a neurorehabilitation treatment to identify whether standard art therapy protocols exist and whether these are based on the principles of neuroaesthetics. Our review identified 8 quantitative and 18 qualitative studies. Although art therapy has been used for more than 20 years as a clinical tool, there are no standard protocols to refer to when planning interventions. Although the effectiveness of using arts as therapy has been reported in many qualitative or feasibility studies, there is still a lack of quantitative studies in which the outcomes of art therapy are directly based on the principles of neuroaesthetics.
RESUMEN
Doxorubicin is an anthracycline antibiotic used for cancer chemotherapy. The utility of doxorubicin is limited by its inability to kill all of the cells within a tumor and by resistant cells emerging from the treated population. We have screened for genes that regulate doxorubicin susceptibility in highly tumorigenic breast cancer cells by cDNA microarray and RNA interference (RNAi) analysis, and we have identified genes associated with both proliferation and cell cycle arrest after doxorubicin treatment. We confirmed that MDA-MB-231 cells treated with doxorubicin induce the expression of carbonic anhydrase II (CAII), inhibitor of differentiation/DNA binding 2 (Id2), activating transcription factor 3 (Atf3), and the phosphatidylinositol 3-kinase 55-kDa regulatory subunit p55PIK. These genes were induced at different times and with varying specificities to different chemotherapeutic drugs. In addition to being induced at the transcriptional level, the CAII and clusterin proteins were elevated after doxorubicin treatment. CAII, Id2, p55PIK, and clusterin were not altered by doxorubicin in MCF-7 cells, a weakly tumorigenic cell line used in previous studies of doxorubicin-regulated gene expression. By inhibiting gene expression using RNAi, we found that CAII and clusterin increase cell survival after doxorubicin treatment, whereas Id2 increases susceptibility to doxorubicin. Our results support a model in which highly tumorigenic breast cancer cells induce a transcriptional response to doxorubicin that is distinct from less malignant cells. The induced genes regulate drug susceptibility positively and negatively and may be novel targets for therapeutic intervention.