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Down-regulation of (neo)antigens limits the efficacy of immune-checkpoint inhibitors. Interferon-g is a potent stimulator of MHC expression and antigen-presentation. Administration of systemic IFNg may boost checkpoint-inhibitors.
Breakthroughs happen at the level of pure science (=theory) but cancer research has degenerated into an entrepreneurial frenzy of technology-driven data collection. Pairing this expensive activity with inexpensive theory could boost progress.
Cancer progression is assumed to be driven by somatic Darwinian evolution and there is a myopic focus on mutations. However, non-Darwinian, Lamarckian-like mechanisms also play a role which offers a wealth of lever points for molecular intervention.
Every dead cancer cell sends signals to its neighbor cells that makes them resilient to drugs. This is one reason why targeted therapy is inherently limited. This collective cell population level response could be a target for a new class of drugs.
The NCI lacks structure and intellectual capacity to promote outside-the-box (yet scientifically rigorous) ideas despite good intentions. See http://tinyurl.com/gostn3o .
A simple reform of peer-review could unleash enormous innovative potential.
All therapies seek to kill tumor cells. But killing is probabilistic. The inevitable surviving cancer cells are stressed to become cancer stem-cells. Therapy backfires in hidden ways. Targeting this cell response will improve existing therapies.