Birgitta E. Michels

Abstract Epstein-Barr virus (EBV) and human papillomavirus (HPV) are common oncoviruses that infect similar anatomical sites, persist as latent infections, and contribute to oncogenesis. However, the role of EBV as a cofactor in HPV infection outcomes remains unclear. This study assessed the implications of EBV serology on oral and genital HPV infections in a longitudinal setting. The study included 280 women from the Finnish Family HPV cohort, followed for three years.

To the Editor: Acute myeloid leukemia (AML), an aggressive hematological malignancy, is frequently associated with mutations in genes encoding enzymes that regulate epigenetic patterns. Additionally, AML is associated with genomic rearrangements, including translocations [1]. Structural rearrangements can activate oncogenes by repositioning cis-regulatory elements into the vicinity of genes, normally not expressed in a certain cell lineage, a mechanism termed enhancer hijacking [2].

Abstract Intratumoral heterogeneity impacts the success or failure of anti-cancer therapies. Here, we investigated the evolution and mechanistic heterogeneity in clonal populations of cell models for estrogen receptor positive breast cancer. To this end, we established barcoded models of luminal breast cancer and rendered them resistant to commonly applied first line endocrine therapies.