A drug combination that targets genes that make lung cancer treatment resistant can still shrink tmors – even after two prior treatments have failed, a new study finds.
It is not uncommon for lung cancer to become resistant to treatment (though an exact frequency is hard to pin down), usally due to genetically driven mutations.
Personalzed medicie is one of the most promising recent developments in cancer treatment, allowing doctors to specifically target the mutations making an individual patient’s cancer untreatable.
In the latest advancement for targeted therapy, Massachusetts General Hospital discovered a targeted therapy that targets the gene that drives as much as 25 percent of treatment resistance.
And it even works after a patient has become resistent to two previous treatments.
Massachusetts General Hospital tested the genetics of lung cancer patients’ tumors and developed a treatment combination that works even when a cancer has become resistant to not just one, but two treatments, a new study reveals
‘Targeted therapy in the last 15 years has really moved from the academic to be part of the mainstream,’ lead study author, Dr Lecia Sequist told Daily Mail Online.
‘Here, we’re showing that [targeted therapy] can work as a second or third line of treatment, as long as you match treatment to genotype of trhe patient at that moment.’
In recent years, scientists have discovered that cancers – even of the same tissues or organs – are actually a diverse set of diseases.
Environmental factors interplay with genetics to lead to mutating cancer cells.
But these disparate sub-types of cancers each have their own genetic drivers.
One of these is a gene called MET, which is involved in some mutations to at least nine types of cancer, including lung, breast and colorectal cancer – three of the 10 most common cancers in the US.
Some 10 to 25 percent of lung cancer treatment resistance in lung cancer cases is driven by this gene, Dr Sequist estimates.
Sometimes these mutations develop in cancers that are already fueled by and treament resistant becaus of a mutation in the EFGR gene.
So Dr Sequist and hre team experimented with targeting both genes at once, using a widely used targeted therapy for EFGR positive tumors plus a new drug to counteract MET mutations, called Savolitinib.
Together, the two drugs substantially reduced tumor growth in more than half of the 46 patients involved in the study.
The researchers haven’t done a long-term analysis, but the drug combination dcontinued to work for nearly 10 months for some patients.
Both drugs are pills, which meant that patients didn’t ahve to make frquent, arduous trips to the hospital – they could get treatment from the comfort of their homes.
‘It’s proof of the concept that, if patients take drugs specifically targeted toward mutations showing up at that moment,’ the treatments can work, says Dr Sequist.
But that ‘if’ is a clinical sticking point.
Although genomic sequencing is now a recommended standard part of cancr treatment, it doesn’t happen uniformly, and it’s hard to get a handle on what treatment centers do and don’t do it, why or why not.
Without hard data, Dr Sequist estimates that some 50 to 60 percent of diagnosed cancers are tested for their genetic profiles.
‘That’s instead of 100 percent, so we have a long way to go,’ she says.
And even if they do gene sequence a patient’s tumors when they’re first diagnosed, that doesn’t guarantee that a doctor will bother to run another analysis after the patient becomes resistant to the first treatment – let alone to a second.
‘What I’m suggesting is not only testing at time of diagnosis, but testing again when it stops working’ says Dr Sequist.
‘And even if a patient receives second targeted theary, our stdy says you should now test them again.’
Because further testing might reveal that patients are eligible for new treatments like the one that Dr Sequist and her team tested in their latest work.
Given its efficacy and limited side effects, Dr Sequist is hopeful that the treatment protocol could get FDA approval in udner five years.
‘We don’t have many treatments in our armamement that could be considered curative in patients with metastatic cancer, but this certainly looks like it could be substanttial in disese control,’ she says.