Researchers have developed analogues of vancomycin with three independent and synergistic mechanisms of action. Developing antibiotics that overcome resistance often focuses on improving a drug's fit with its binding pocket, but much like in the development of antitumor drugs, bacteria can evolve resistance to such second-generation inhibitors as well.

CHICAGO – At the 2017 annual meeting of the American Society of Clinical Oncology (ASCO), immunotherapy was front and center, as it is wont to be these days.

In the quest to understand what determines whether checkpoint blockade will work for a given patient, new research points to epigenetic factors.

So wrote the Australian University of Melbourne's Samuel Berkovic, telling it like it is with respect to the medical use of cannabinoids in epileptic patients. Despite spectacular anecdotes in the lay press, peer-reviewed data supporting the practice has been sorely lacking.

Keytruda (pembrolizumab, Merck & Co. Inc.) has become the first drug to be approved based solely on the presence of a molecular biomarker without regard to tumor location.

At least one of the abstracts highlighted at the press briefing of the American Society of Clinical Oncology (ASCO) last week threw an involuntary highlight on the problems that can beset cancer treatment even in successful trials.

"With the advent of targeted cancer therapies, what we've found is that many of them are cardiotoxic," Saptarsi Haldar told BioWorld Today. "Pathways that are effective in cancer are toxic in the heart."

There are 64 possible three-letter combinations of the four DNA bases that are the building blocks of the genetic code, but only 20 amino acids that are the building blocks of proteins. Some amino acids can be coded for by several different three-base combinations – for example, the triplets ACA, ACC, ACG and ACT all code for the amino acid threonine. When one of those bases changes, the resulting single-nucleotide polymorphism is called synonymous (sSNP). It has been assumed that sSNPs have no effect on proteins. Now, researchers from the German University of Hamburg and the British University of Bristol have shown that a change from ACT to ACG in the cystic fibrosis transmembrane conductance regulator (CFTR) affected CFTR function.