With fewer than 5% of pancreatic cancer patients surviving for 5 years, this devastating disease remains a leading cause of cancer-related deaths. A recent and comprehensive analysis of mutations in all of the protein-coding regions of DNA from 99 pancreatic tumors promises to improve the detection and therapeutic options for this disease (link).
The study, which was conducted by an international team of more than100 researchers and led by Sean Grimmond of the University of Queensland, Australia, revealed heterogeneity between the tumors both in terms of the number of mutations in each tumor and the number of genes that these mutations affected. This finding underscored the need to develop personalized cancer therapies.
Previous studies had implicated many of the mutations in different types of malignancies. Strikingly, more than 20% of the tumors carried mutations in the SLIT2 and/or ROBO1/2 genes, which are best known for their roles in neuronal migration and positioning in embryos. This is the first time that researchers have causally linked defective SLIT/ROBO signaling to pancreatic cancer, and the first demonstration of the frequency of defects in the SLIT/ROBO pathway for any type of cancer.
Whether drugs developed to promote neuronal regeneration after injury could be repurposed as cancer therapeutics is not yet clear.