The mutation occurs in the enzyme isocitrate dehydrogenase 1 (IDH 1), found in glioma, blood, skin and soft tissue tumours.
The team, from NYU Langone Medical Center, Laura and Isaac Perlmutter Cancer Center and Massachusetts General Hospital, have discovered that cells which contain IDH 1 typically have very low levels of an essential metabolic chemical called nicotinamide adenine dinucleotide (NAD).
This is an essential chemical that cells use to convert sugar and nutrients into energy and to repair cell DNA.
The researchers then tested the theory that by lowering NAD levels, thereby starving tumour cells of energy, they could halt tumour cell growth.
Drugs called NAMPT inhibitors appeared to do just this in lab tests on mice and when tested on cells from patients with IDH 1 brain tumours.
Further clinical trials with selected cancer patients are planned within the next couple of years, with a patent pending on the use of NAMPT inhibitors on IDH 1 cancer.
“Our findings raise the possibility that NAMPT inhibitors might be effective against such tumours, which are impervious to current anti-cancer drugs,” said Andrew Chi, assistant professor at NYU Langone.
“The work is urgent because no curative treatment exists for IDH1 mutant gliomas, a specific type of brain tumour which often strike people in their 20s and 30s.
“Our findings provide yet another example of the need to personalize cancer therapy.”
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