Here’s an aggravating fact about medical education – a large chunk of what’s taught in medical school is useless trivia:
- The muscle that elevates your palate is called the tensor veli palatini…
- Here’s the best way to treat leprosy…
- Adults whose acute leukemia cells carry an internal tandem mutation of the FLT3 surface tyrosine kinase have a worse prognosis…
I and other cancer specialists have known that last little nugget for about ten years, but haven’t been able to do squat with it:
“So should I use a different induction chemotherapy for FLT3-mutants?” (No)
“Should all FLT3 mutants get a stem cell transplant?” (Not necessarily)
“Is there anything I can do differently for these patients?” (Silence)
Thanks. Thanks a fricken’ lot.
It’s a little unfair to rant, I know. There’s a long lag time between discovery and new treatments for cancer -but the wait is hard, especially with new leukemia patients coming in the door every month.
But last week finally – finally – a drug targeting this specific molecular defect was approved by the FDA.
See, FLT3 is like an “on” switch for cell division. It’s supposed to only be on when it gets a particular environmental signal, and not every cell even carries the switch. But about 35% of acute myeloid leukemia patients have FLT3 abnormally expressed in their cancers – and the switch is stuck in the “on” position, driving cancer cell growth.
Happily, the new FLT3-inhibiting drug midostaurin (given as a twice-daily pill) markedly improved response and survival rates in AML when added to the standard chemotherapy cocktail. The benefits seemed most pronounced among people who ultimately went on to receive a stem cell transplant – but a higher percentage of patients were able to achieve the remission usually required as a first step before transplant.
So now I can re-categorize the FLT3 information from “trivia” to “critical information” in my brain, as I impatiently wait for more breakthroughs.
FDA Press Release 4/28/17: click here