Acute myeloid leukemia is almost diabolically adaptable, able to resist chemotherapy and other formidable drug weapons doctors use to fight it.
But now researchers at the University of Colorado Cancer Center believe that they've cracked the cancer's code, according to the medical center's blog, Coloradocancerblogs.org. They've figured out the cellular mechanism that AML uses to veer out of the way of chemotherapy treatments and also how to stop it from resisting those treatments. (Details are published in the journal Leukemia.)
The group started with a simple question: Which genes, once they are switched off, make AML cells vulnerable to chemo? To answer this, they simultaneously turned off a different gene in several populations of AML cells, and then blasted them with AML-related chemotherapy. Soon it became clear that turning off the WEE1 gene helped kill a lot more AML cells. The hope is that inhibiting WEE1 takes away the cancer cells' ability for self-preservation, but won't harm healthy cells. Scientists found their preclinical study with mouse AML models to be promising enough that they are already planning human clinical trials.
Let's be cautiously optimistic here: Researchers can't always repeat in people the success they had in studies with mice. Additionally, it remains to be seen whether turning off the cancer's ability to fight chemotherapy affects nearby healthy cells. Nevertheless, notion of halting AML's ability to resist chemotherapy is a tantalizing thought. This would be a huge accomplishment that could allow for long-term remission from a cancer which, due to its many variations, can be very difficult to treat. It may be too early to tell, so we look forward to hearing how subsequent trials fare.
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