Some lung cancer patients can respond brilliantly to treatment, but sadly this is not always the case. Cancer can be sneaky and develop ways to avoid the treatment but now thanks to you, researchers have found a possible way they could outsmart the cancer. This breakthrough opens a new path toward treatments that are tailored to each patient's cancer, giving more people a better chance of beating it.
To everyone who has supported Worldwide Cancer Research — thank you. Because of you, we can keep going — working to translate these findings into real improvements for patients who desperately need better options.
Sometimes cancer drugs stop working for non-smoking lung cancer patients and doctors are not sure why
You might expect that two people with the same type of cancer would both respond the same way to a drug. Unfortunately, for people with a particular type of non-smoking lung cancer, this is not the case, and the reason has long been a mystery.
Lung cancer is one of the most common cancers worldwide. While smoking is its biggest risk factor, lung cancer affects non-smokers too. Like other cancers, it is caused by changes in our genes that instruct cells to grow uncontrollably, forming tumours.
One of the most common gene changes that drives non-smoking lung cancer is where two genes called EML4 and ALK fuse together. Patients with this mutation are treated with drugs called ALK inhibitors. These drugs can be highly effective but. Unfortunately, some patients become resistant to these drugs meaning the treatment becomes less effective or worse, not effective at all.
Tiny changes in the same gene can have a big impact on how cancer responds to treatment
Not all EML4-ALK fusions are identical. Just as two people can share the same surname but come from very different families, the EML4 gene can break and fuse with ALK at different points, creating distinct variants of the fusion. Until now, these variants were treated as one and the same disease, and patients were given the same drugs regardless of which variant they had.
Professor Sotillo used powerful genetic tools to study how different variants of the cancer behaved. What they found was striking. Tumours with certain variants grew significantly faster and more aggressively than others.
Answering today’s challenges offers us more tomorrows
These findings could help explain why some people stop responding to treatment while others continue to benefit.
This research is an important step toward what scientists call precision oncology — matching a patient's specific cancer biology to the treatment most likely to work most effectively for them.
This breakthrough takes us a step closer to outsmarting cancer cells and tackling treatment resistance. Thanks to Curestarters, projects like Professor Sotillo’s will bring us closer to a world where the clinical challenges we face today, are no longer worries for tomorrow’s patients.
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