Over the past two decades, the idea of targeting transcription factors to combat malignancies has turned into a clinical reality. Targeting oncogenes and their interactive partners is an effective approach to developing novel targeted therapies for cancer and other chronic diseases. The MYC family of proteins, which are transcription factors, play a pivotal role in many cellular processes. However, dysregulation of MYC, such as amplification of MYCN, is associated with tumorigenesis, especially for neuroblastoma. MDM2, on the other hand, is one of the most frequently studied oncogenes and is an excellent target for cancer therapy, based on its p53-dependent and p53-independent oncogenic activities in various cancers. 

A team led by the Cancer Immunogenomics group at the Josep Carreras Leukaemia Research Institute, the Computational Biology group at the Barcelona Supercomputing Center and the Germans Trias i Pujol Research Institute shows, for the first time, that within a tumour, the expression of the different hallmarks of cancer is not cell-specific, but rather position-specific. Under this new light, tumour architecture emerges as a valuable source of information to understand tumour dynamics and predict its sensitivity to anticancer drugs.

In a recent study, researchers demonstrated that Z526, a novel dithiocarbamate-like compound, mitigates cancer-associated cachexia (CAC) both in vitro and in vivo. Oral administration of Z526 slowed weight loss and improved muscle atrophy, fat loss, and grip force. Furthermore, the authors elucidated that Z526 potentiates anti-CAC effects by regulating NF-κB signaling and suppressing oxidative stress.