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A new study reveals that a combination of drugs that targets genes that make treatment of lung cancer resistant can still reduce the size of tumors. Even after two previous treatments, the results have failed.
It is not uncommon for lung cancer to become resistant to treatment (although an exact frequency is difficult to pin down), usually because of genetic mutations.
Personalized medicine is one of the most promising recent developments in cancer treatment, allowing doctors to specifically target mutations that make a patient's cancer incurable.
In recent advances in targeted therapy, Massachusetts General Hospital has discovered a therapy targeting the gene responsible for 25% of treatment resistance.
And it works even when a patient has become resistant to the two previous treatments.
The Massachusetts General Hospital has tested the tumor genetics of lung cancer patients and has developed a combination of treatments that works even when a cancer has become resistant to two treatments, according to a new study.
"Targeted therapy over the past 15 years has really left the academic world to become part of the mainstream," said Dr. Lecia Sequist, lead author of the study, at Daily Mail Online.
& # 39; Here, we show that [targeted therapy] can be used as a second or third line of treatment, provided the treatment matches the patient's genotype at that time. & # 39;
In recent years, scientists have discovered that cancers, even those of the same tissues or organs, actually constitute a diverse set of diseases.
Environmental factors interact with genetics to lead to the mutation of cancer cells.
But these different subtypes of cancer each have their own genetic factor.
One of them is a gene called MET, implicated in some mutations of at least nine types of cancer, including lung cancer, breast cancer and colorectal cancer, three of the 10 most cancers. most common in the United States.
According to Dr. Sequist, about 10 to 25% of the resistance to lung cancer treatment in lung cancer cases is due to this gene.
Sometimes, these mutations develop in cancers that are already fed and resistant to treatment because of a mutation in the EFGR gene.
Dr. Sequist and his team therefore experimented with the simultaneous targeting of both genes, using a widely used therapy for EFGR-positive tumors, as well as a new drug against mutations in the MET gene, called Savolitinib.
Together, the two drugs significantly reduced tumor growth in more than half of the 46 patients participating in the study.
The researchers did not do a long-term analysis, but the combination of drugs continued to work for nearly 10 months for some patients.
Both drugs are pills, which means that patients do not have to make frequent and painful trips to the hospital: they can be treated in the comfort of their own home.
"This is proof of the concept that, if patients take drugs specifically targeted at the mutations occurring at that time, the treatments may work," Dr. Sequist says.
But this "if" is a clinical stumbling block.
Although genomic sequencing is now a standard recommended part of cancer treatment, it is not uniform, and it is difficult to know what treatment centers do and do not do, why or why not.
In the absence of reliable data, Dr. Sequist estimates that about 50-60% of diagnosed cancers are tested for their genetic profile.
"It's 100% instead, so we have a long way to go," she says.
And even if the tumors of a patient are sequenced at the initial diagnosis, this does not guarantee that a doctor will take charge of another analysis once the patient has developed resistance to the first treatment – even less than a second.
"What I'm suggesting is not just testing at the time of diagnosis, but testing again when it's not working," says Dr. Sequist.
"And even if a patient receives a second targeted therapy, our study indicates that you should now test it again& # 39;
Additional tests may reveal that patients are eligible for new treatments, such as the one that Dr. Sequist and her team tested in their latest work. She invites clinicians to paint a picture of the tumors of their patients each time they become resistant to treatment.
Given his limited efficacy and side effects, Dr. Sequist hopes the treatment protocol will be approved by the FDA in less than five years.
"We do not have many treatments in our armament that could be considered curative in patients with metastatic cancer, but this certainly seems to be substantial in the control of the disease," she says. .
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