MIT researchers found a way to measure cell density quickly and accurately — measuring up to 30,000 cells in a single hour. They also showed density changes could be used to make useful predictions, including whether T cells have become activated to kill tumors or whether tumor cells are susceptible to a specific drug.

A combination of two drugs could improve outcomes and reduce the need for toxic chemotherapy for B-cell acute lymphoblastic leukaemia (B-ALL), the commonest cancer in childhood and one that can be particularly difficult to treat in older patients, according to Cambridge scientists. Although the research has so far only been conducted in cell lines and mice, the team is seeking funding to begin clinical trials in patients shortly.

PAX3 is a transcription factor (proteins involved in converting DNA into RNA) that drives melanoma progression by promoting cell growth, migration and survival, while inhibiting cellular terminal differentiation, which is the final stage where a cell becomes specialized and cell division ends. However, known PAX3 target genes are limited and cannot fully explain the wide impact of PAX3 function, suggesting that there are most likely many other genes that PAX3 controls that are undiscovered.

The PAX3 protein can regulate DNA through two separate binding domains, the paired domain (PD) and homeodomain (HD), which bind different DNA motifs, short recurring sequences within a DNA strand that regulate gene expression. It is not clear if these two domains bind and work together to regulate genes and if they promote all or only a subset of downstream cellular events.

A new study by researchers at Boston University Chobanian & Avedisian School of Medicine has discovered that PAX3 mainly uses the PD to bind to the DNA, and that it mostly turns on genes—many of which help cells grow and make other proteins – activities that support cancer growth.