Discriminatory attitudes towards people living with HIV/AIDS are prevalent. A Joint United Nations Program on HIV/AIDS report (2019) indicated that more than 50% of the people surveyed in one of the studies spanning 26 countries expressed unfavorable attitudes towards HIV-positive people. The objective of this study was to assess the attitudes of senior Education Studies students at a university in Spain towards people with HIV/AIDS so as to propose specific educational interventions. The study employed a quantitative methodological approach; a questionnaire with a 14-item attitude score served as the analytical instrument. The study sample comprised 613 students from the School of Education at the University of Huelva, Spain. The results showed that more than 50% of the School’s senior students had discriminatory attitudes towards HIV-positive people, some of whom were fellow classmates. This study proposes several formative approaches to reducing the stigma suffered by HIV-positive people, while also improving senior students’ skills and capabilities in the field of health promotion.

Fanconi anemia (FA) patients have an exacerbated risk of head and neck squamous cell carcinoma (HNSCC). Treatment is challenging as FA patients display enhanced toxicity to standard treatments, including radio/chemotherapy. Therefore better therapies as well as new disease models are urgently needed. We have used CRISPR/Cas9 editing tools in order to interrupt the human FANCA gene by the generation of insertions/deletions (indels) in exon 4 in two cancer cell lines from sporadic HNSCC having no mutation in FA-genes: CAL27 and CAL33 cells. Our approach allowed efficient editing, subsequent purification of single-cell clones, and Sanger sequencing validation at the edited locus. Clones having frameshift indels in homozygosis did not express FANCA protein and were selected for further analysis. When compared with parental CAL27 and CAL33, FANCA-mutant cell clones displayed a FA-phenotype as they i) are highly sensitive to DNA interstrand crosslink (ICL) agents such as mitomycin C (MMC) or cisplatin, ii) do not monoubiquitinate FANCD2 upon MMC treatment and therefore iii) do not form FANCD2 nuclear foci, and iv) they display increased chromosome fragility and G2 arrest after diepoxybutane (DEB) treatment. These FANCA-mutant clones display similar growth rates as their parental cells. Interestingly, mutant cells acquire phenotypes associated with more aggressive disease, such as increased migration in wound healing assays. Therefore, CAL27 and CAL33 cells with FANCA mutations are phenocopies of FA-HNSCC cells.