Michael Boyd, M.D., Ph.D.
Former Associate Director, DTP

The 60 Cell Screen was introduced in an attempt to provide a greater level of biological diversity in the very first stage of biological evaluation and a tumor evaluation of compounds in a manner that was distinctly different than the screening system that it replaced as a primary screen, which was based on an animal tumor model, called the P388, a mouse leukemia model, which had proven to have considerable utility in drug discovery research.

However, an empirical observation was that many of the agents that the mouse leukemia primary screen guided us toward had any tumor activity in a limited spectrum of tumors, especially, for example, in leukemia when treated clinically in human patients and typically much less activity, if any at all, in solid tumors, the majority of which are the major problem in adult cancer, of course.

The very simplistic idea is that, and also a limitation of the P388 screen or a challenging part of uses of that screen, was it involved living animals and that was very cost-intensive, laborious relative to purely in vitro or test-tube-type assays that would have their own limitations unless one were able to mimic, at least on a small scale, some of the diversity, cellular and biological diversity, that resides in any tumor but particularly across a spectrum of human solid tumor types.

So in essence, that was the reason for replacing one type of screen as a first stage or primary screen with the NCI 60 Cell Screen, to introduce a broader diversity of biology at the earliest stages of screening to try to spread a broader net to catch potential anti-tumor compounds that had different mechanisms of action, potentially different profiles of activity against the commonest types of tumors that cancer patients suffer.