Yet no resistance arose to endostatin. Every time the mice received the blood vessel inhibitor, their tumors shrank as rapidly as after the first dosage. Because it is not affecting the mutating tumor cells directly, the inhibitor can sustain its effectiveness. Mixson is trying to use genetic therapy to stimulate production of anti-angiogenesis factors in mice. Such resistance accounts for a common tragedy.
Cancer patients benefit at first from chemotherapy, then the drug loses potency over time.
Furthermore, while it's not possible to assess all side effects in mice, the overall signs were positive. There is no accepted explanation for this dormancy. Alternatively, it may cause programmed cell death in tumor cells. Nor is it clear why a chemical that inhibits blood vessel growth would cause tumors to actually shrink, as endostatin did. These results, combined with increasing scientific acceptance of Folkman's view that angiogenesis plays a key role in cancer, sparked the recent flood of attention to angiogenesis inhibitors.